TY - JOUR T1 - Kappa Opioid receptor ligands regulate angiogenesis in development and in tumours AN - 1837294725; 21214314 AB - Opioid systems mainly regulate physiological functions such as pain, emotional tone and reward circuitry in neural tissues (brain and spinal cord). These systems are also found in extraneural tissues (ganglia, gut, spleen, stomach, lung, pancreas, liver, heart, blood and blood vessels), and recent studies have elucidated their roles in various organs. The current review focuses on the roles of opioid systems in blood vessels, especially angiogenesis, during development and tumour malignancy. The balance between endogenous activators and inhibitors of angiogenesis delicately maintains a normally quiescent vasculature to sustain homeostasis. Disturbance of this balance causes pathogenic angiogenesis and, especially in tumours, several activators such as VEGF are highly expressed in the tumour microenvironment and strongly induce tumour angiogenesis, the so-called angiogenic switch. Recently, we demonstrated that Kappa opioid receptor agonists function as anti-angiogenic factors, which impede the angiogenic switch, in vascular development and tumour angiogenesis by inhibiting the expression of receptors for VEGF. In clinical medicine, angiogenesis inhibitors that target VEGF signalling such as bevacizumab are used as anti-cancer drugs. Although therapies that inhibit tumour angiogenesis have been highly successful for tumour therapy, most patients eventually develop resistance to this anti-angiogenic therapy. Thus, we must identify novel targets for anti-angiogenic agents to sustain inhibition of angiogenesis for tumour therapy. The regulation of responses to Kappa opioid receptor ligands could be useful for controlling vascular formation under physiological conditions and in cancers, and thus could offer therapeutic benefits beyond the relief of pain. Linked Articles This article is part of a themed section on Opioids: New Pathways to Functional Selectivity. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-2 JF - British Journal of Pharmacology AU - Yamamizu, Kohei AU - Hamada, Yusuke AU - Narita, Minoru AD - Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 268 EP - 276 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 172 IS - 2 SN - 0007-1188, 0007-1188 KW - Toxicology Abstracts KW - Vascular endothelial growth factor KW - Opioid receptors KW - Heart KW - Receptor mechanisms KW - Spinal cord KW - Pancreas KW - angiogenesis inhibitors KW - Angiogenesis KW - Spleen KW - Pain KW - Tumors KW - Homeostasis KW - Bevacizumab KW - Digestive tract KW - Blood vessels KW - Lung KW - Reinforcement KW - Ganglia KW - Signal transduction KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1837294725?accountid=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=Kappa+Opioid+receptor+ligands+regulate+angiogenesis+in+development+and+in+tumours&rft.au=Yamamizu%2C+Kohei%3BHamada%2C+Yusuke%3BNarita%2C+Minoru&rft.aulast=Yamamizu&rft.aufirst=Kohei&rft.date=2015-01-01&rft.volume=172&rft.issue=2&rft.spage=268&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Pharmacology&rft.issn=00071188&rft_id=info:doi/10.1111%2Fbph.12573 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-11-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Heart; Opioid receptors; Vascular endothelial growth factor; Receptor mechanisms; Spinal cord; angiogenesis inhibitors; Pancreas; Angiogenesis; Spleen; Pain; Bevacizumab; Homeostasis; Tumors; Digestive tract; Blood vessels; Lung; Reinforcement; Ganglia; Signal transduction DO - http://dx.doi.org/10.1111/bph.12573 ER - TY - JOUR T1 - Expression signature of microRNA-155 in hepatitis C virus genotype 4 infection. AN - 1826606642; 25469255 AB - Hepatits C virus (HCV) genotype 4 (GT4) shows low treatment response rates and discrepancies when compared to other genotypes. However, the reason underlying these discrepancies remains unclear due to the limited number of studies on GT4. microRNA-155 (miR-155) is a noteworthy example of a discrepancy in GT4, as it was found to be upregulated in genotypes 1, 2 and 3 HCV infection, but downregulated in GT4-HCV-infected peripheral blood mononuclear cells (PBMCs). The present study aimed to investigate the expression of miR-155 in PBMCs, serum and liver tissues of GT4-HCV-infected patients. miR-155 expression was assessed using reverse transcription-quantitative polymerase chain reaction in GT4-HCV-infected PBMCs, serum and liver tissues, as well as GT2- and GT4-infected Huh7 cells, and compared to the healthy controls. There was no difference in miR-155 expression observed between naïve GT4-HCV patients and healthy controls in the PBMCs and serum. In HCV-infected liver tissues, however, a significant downregulation was observed. The unique miR-155 expression pattern during GT4 infection was confirmed in the infected Huh7 cell lines when compared to GT2 infection. Clinical data showed a positive correlation between liver transaminases and serum miR-155 expression. In addition, serum miR-155 expression was significantly lower in naïve non-responders (NRs) than naïve sustained virological responders (SVRs), and in post-treatment NRs compared to post-treatment SVRs. In conclusion, miR-155 was not only proven to be a genotype-specific microRNA that is not induced during GT4-HCV infection, but also a good prognostic factor and predictor of response to treatment enabling a non-invasive differentiation between NRs and SVRs during GT4-HCV infection. JF - Biomedical reports AU - Riad, Sarah Ehab AU - El-Ekiaby, Nada AU - Mekky, Radwa Yehia AU - Ahmed, Rasha AU - El Din, Mohammad Ahmed Mohey AU - El-Sayed, Mohammad AU - Abouelkhair, Mahmoud Mohammad AU - Salah, Ayman AU - Zekri, Abdel Rahman AU - Esmat, Gamal AU - Abdelaziz, Ahmed Ihab AD - The Molecular Pathology Research Group, Department of Pharmacology and Toxicology, German University in Cairo, New Cairo 11835, Egypt. ; Departments of Endemic Medicine and Hepatology and Egypt. ; Departments of Surgery, Cairo University, Cairo 11562, Egypt. ; Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo 11976, Egypt. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 93 EP - 97 VL - 3 IS - 1 SN - 2049-9434, 2049-9434 KW - microRNA-155 KW - genotype 4 KW - treatment response KW - hepatitis C virus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826606642?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomedical+reports&rft.atitle=Expression+signature+of+microRNA-155+in+hepatitis+C+virus+genotype+4+infection.&rft.au=Riad%2C+Sarah+Ehab%3BEl-Ekiaby%2C+Nada%3BMekky%2C+Radwa+Yehia%3BAhmed%2C+Rasha%3BEl+Din%2C+Mohammad+Ahmed+Mohey%3BEl-Sayed%2C+Mohammad%3BAbouelkhair%2C+Mahmoud+Mohammad%3BSalah%2C+Ayman%3BZekri%2C+Abdel+Rahman%3BEsmat%2C+Gamal%3BAbdelaziz%2C+Ahmed+Ihab&rft.aulast=Riad&rft.aufirst=Sarah&rft.date=2015-01-01&rft.volume=3&rft.issue=1&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Biomedical+reports&rft.issn=20499434&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2014-12-03 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Short food safety videos promote peer networking and behavior change AN - 1815692745; PQ0003313174 AB - Purpose - The purpose of this paper is to create a series of 30-60-second short videos to promote improved food safety behaviors of middle school youth, determine the feasibility of disseminating the videos through peer networks, and measure their effects on food safety attitudes, perceived social norms, and behaviors of youth. Design/methodology/approach - Food safety content specialists, learning experts, programmers, illustrators, project managers, instructional designers, scriptwriters, and stakeholders were involved in creation of the Don't Be Gross short videos before evaluation by middle school youth (sixth to eighth grades). The experimental group ( n =220) completed the following activities at about one-week intervals: pre-test, viewed videos, post-test, and follow-up test. The control group ( n =112) completed the same activities at similar intervals but did not have access to the videos until after the follow-up test. Findings - Controlling for grade and gender, linear mixed-effects models revealed significant time by group effects for participants' perceived susceptibility to foodborne illness; intentions to perform recommended food safety behaviors approached significance. Additionally, compared to the pre-test, the experimental group perceived their friends as being significantly more confident in performing food safety behaviors at post- and follow-up tests. Google Analytics data revealed that the bounce rate from the home page of the videos was low (38 percent) suggesting that the videos were engaging. Originality/value - The Don't Be Gross videos were liked by youth and shared among their peers and may have the potential to promote positive food safety behaviors and intentions among youth. JF - British Food Journal AU - Quick, Virginia AU - Corda, Kirsten W AU - Martin-Biggers, Jennifer AU - Chamberlin, Barbara AU - Schaffner, Donald W AU - Byrd-Bredbenner, Carol AD - Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development/ National Institutes of Health, Bethesda, Maryland, USA Y1 - 2015///0, PY - 2015 DA - 0, 2015 SP - 78 EP - 93 PB - Emerald Group Publishing Limited, 60-62 Toller Lane Bradford West Yorkshire BD8 9BY United Kingdom VL - 117 IS - 1 SN - 0007-070X, 0007-070X KW - Biotechnology and Bioengineering Abstracts KW - Food safety KW - Youth UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1815692745?accountid=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=British+Food+Journal&rft.atitle=Short+food+safety+videos+promote+peer+networking+and+behavior+change&rft.au=Quick%2C+Virginia%3BCorda%2C+Kirsten+W%3BMartin-Biggers%2C+Jennifer%3BChamberlin%2C+Barbara%3BSchaffner%2C+Donald+W%3BByrd-Bredbenner%2C+Carol&rft.aulast=Quick&rft.aufirst=Virginia&rft.date=2015-01-01&rft.volume=117&rft.issue=1&rft.spage=78&rft.isbn=&rft.btitle=&rft.title=British+Food+Journal&rft.issn=0007070X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-08-01 N1 - Number of references - 55 N1 - Last updated - 2016-09-01 ER - TY - JOUR T1 - Endothelial Expression of Scavenger Receptor Class B, Type I Protects against Development of Atherosclerosis in Mice AN - 1758247233; PQ0002448370 AB - The role of scavenger receptor class B, type I (SR-BI) in endothelial cells (EC) was examined in several novel transgenic mouse models expressing SR-BI in endothelium of mice with normal C57Bl6/N, apoE-KO, or Scarb1 -KO backgrounds. Mice were also created expressing SR-BI exclusively in endothelium and liver. Endothelial expression of the Tie2-Scarb1 transgene had no significant effect on plasma lipoprotein levels in mice on a normal chow diet but on an atherogenic diet, significantly decreased plasma cholesterol levels, increased plasma HDL cholesterol (HDL-C) levels, and protected mice against atherosclerosis. In 8-month-old apoE-KO mice fed a normal chow diet, the Tie2-Scarb1 transgene decreased aortic lesions by 24%. Mice expressing SR-BI only in EC and liver had a 1.5 plus or minus 0.1-fold increase in plasma cholesterol compared to mice synthesizing SR-BI only in liver. This elevation was due mostly to increased HDL-C. In EC culture studies, SR-BI was found to be present in both basolateral and apical membranes but greater cellular uptake of cholesterol from HDL was found in the basolateral compartment. In summary, enhanced expression of SR-BI in EC resulted in a less atherogenic lipoprotein profile and decreased atherosclerosis, suggesting a possible role for endothelial SR-BI in the flux of cholesterol across EC. JF - BioMed Research International AU - Vaisman, Boris L AU - Vishnyakova, Tatyana G AU - Freeman, Lita A AU - Amar, Marcelo J AU - Demosky, Stephen J AU - Liu, Chengyu AU - Stonik, John A AU - Sampson, Maureen L AU - Pryor, Milton AU - Bocharov, Alexander V AU - Eggerman, Thomas L AU - Patterson, Amy P AU - Remaley, Alan T AD - Lipoprotein Metabolism Section, Cardiovascular-Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA, borisv@mail.nih.gov Y1 - 2015/01// PY - 2015 DA - January 2015 PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States VL - 2015 SN - 2314-6133, 2314-6133 KW - Biotechnology and Bioengineering Abstracts KW - Diets KW - Atherogenic diet KW - Aorta KW - Transgenes KW - Lipoproteins (high density) KW - Animal models KW - Cell culture KW - Arteriosclerosis KW - Cholesterol KW - Transgenic mice KW - Endothelial cells KW - Endothelium KW - Lipoproteins KW - Liver KW - scavenger receptors KW - W 30925:Genetic Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1758247233?accountid=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=BioMed+Research+International&rft.atitle=Endothelial+Expression+of+Scavenger+Receptor+Class+B%2C+Type+I+Protects+against+Development+of+Atherosclerosis+in+Mice&rft.au=Vaisman%2C+Boris+L%3BVishnyakova%2C+Tatyana+G%3BFreeman%2C+Lita+A%3BAmar%2C+Marcelo+J%3BDemosky%2C+Stephen+J%3BLiu%2C+Chengyu%3BStonik%2C+John+A%3BSampson%2C+Maureen+L%3BPryor%2C+Milton%3BBocharov%2C+Alexander+V%3BEggerman%2C+Thomas+L%3BPatterson%2C+Amy+P%3BRemaley%2C+Alan+T&rft.aulast=Vaisman&rft.aufirst=Boris&rft.date=2015-01-01&rft.volume=2015&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2015%2F607120 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 1 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Diets; Atherogenic diet; Aorta; Lipoproteins (high density); Transgenes; Animal models; Cell culture; Cholesterol; Arteriosclerosis; Transgenic mice; Endothelial cells; Lipoproteins; Endothelium; Liver; scavenger receptors DO - http://dx.doi.org/10.1155/2015/607120 ER - TY - JOUR T1 - Acceptable Approaches to Enrolling Adults Who Cannot Consent in More Than Minimal Risk Research AN - 1753465623; PQ0002370724 JF - American Journal of Bioethics AU - Danis, Marion AU - Wendler, David AU - Kim, Scott AD - National Institutes of Health Clinical Center PY - 2015 SP - 70 EP - 71 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 15 IS - 10 SN - 1526-5161, 1526-5161 KW - Environment Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753465623?accountid=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=American+Journal+of+Bioethics&rft.atitle=Acceptable+Approaches+to+Enrolling+Adults+Who+Cannot+Consent+in+More+Than+Minimal+Risk+Research&rft.au=Danis%2C+Marion%3BWendler%2C+David%3BKim%2C+Scott&rft.aulast=Danis&rft.aufirst=Marion&rft.date=2015-01-01&rft.volume=15&rft.issue=10&rft.spage=70&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Bioethics&rft.issn=15265161&rft_id=info:doi/10.1080%2F15265161.2015.1075806 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-01-06 DO - http://dx.doi.org/10.1080/15265161.2015.1075806 ER - TY - JOUR T1 - Prospective study on nanoparticle albumin-bound paclitaxel in advanced breast cancer: clinical results and biological observations in taxane-pretreated patients AN - 1753464302; PQ0002418717 AB - There is a deep need to improve the care of metastatic breast cancer (MBC) patients, since even today it remains an incurable disease. Taxanes are considered the most effective cytotoxic drugs for the treatment of MBC, both in monotherapy and in combined schedules, but the need for synthetic solvents contributes to the severe toxicities and may have a negative impact on the efficacy. Nanoparticle albumin-bound paclitaxel (Nab-paclitaxel) is a colloidal suspension of paclitaxel and human serum albumin initially developed to avoid the toxicities associated with conventional taxanes. The aim of this prospective, single-center open-label, noncomparative study was to evaluate the efficacy and safety of nab-paclitaxel in MBC patients pretreated with taxanes. The patients were treated with nab-paclitaxel as a single agent, 260 mg/m2 on day 1 of each 3-week cycle or 125 mg/m2 weekly. The primary endpoint was the overall response rate (ORR). Secondary objectives were duration of response, clinical benefit rate, progression-free survival (PFS), overall survival, and safety. A total of 42 patients (median age 48 years, median Eastern Cooperative Oncology Group performance status 0, triple-negative MBC 19%, all pretreated with a taxane-based therapy, mainly in advanced disease) were enrolled in the study. The ORR was 23.8%, including one complete response (2.4%) and nine partial responses (21.4%); the disease control rate was 50%. The median duration of response was 7.2 months. After a median follow-up of 9 months, the median PFS was 4.6 months. ORR and PFS were similar irrespective of the previous chemotherapy lines, metastatic sites, and biomolecular expression. Nab-paclitaxel was well tolerated, and the most frequent treatment-related toxicities were mild to moderate (grades 1-2). This real-life study shows that nab-paclitaxel has a significant antitumor activity and a manageable safety profile in patients pretreated with taxanes and experiencing a treatment failure after at least one line of chemotherapy. JF - Drug Design, Development and Therapy AU - Fabi, Alessandra AU - Giannarelli, Diana AU - Malaguti, Paola AU - Ferretti, Gianluigi AU - Vari, Sabrina AU - Papaldo, Paola AU - Nistico, Cecilia AU - Caterino, Mauro AU - De Vita, Roy AU - Mottolese, Marcella AU - Iacorossi, Laura AU - Cognetti, Francesco AD - Department of Medical Oncology, Regina Elena National Cancer Institute, Rome, Italy PY - 2015 SP - 6177 EP - 6183 PB - Dove Medical Press Ltd, Beechfield House Macclesfield SK11 0JL United Kingdom VL - 9 KW - Biotechnology and Bioengineering Abstracts KW - nab-paclitaxel KW - metastatic breast cancer KW - anthracyclines KW - Age KW - Chemotherapy KW - Disease control KW - Solvents KW - Survival KW - taxanes KW - human serum albumin KW - Drug development KW - Oncology KW - Toxicity KW - Metastases KW - Cytotoxicity KW - Paclitaxel KW - Breast cancer KW - nanoparticles KW - Antitumor activity KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753464302?accountid=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=Drug+Design%2C+Development+and+Therapy&rft.atitle=Prospective+study+on+nanoparticle+albumin-bound+paclitaxel+in+advanced+breast+cancer%3A+clinical+results+and+biological+observations+in+taxane-pretreated+patients&rft.au=Fabi%2C+Alessandra%3BGiannarelli%2C+Diana%3BMalaguti%2C+Paola%3BFerretti%2C+Gianluigi%3BVari%2C+Sabrina%3BPapaldo%2C+Paola%3BNistico%2C+Cecilia%3BCaterino%2C+Mauro%3BDe+Vita%2C+Roy%3BMottolese%2C+Marcella%3BIacorossi%2C+Laura%3BCognetti%2C+Francesco&rft.aulast=Fabi&rft.aufirst=Alessandra&rft.date=2015-01-01&rft.volume=9&rft.issue=&rft.spage=6177&rft.isbn=&rft.btitle=&rft.title=Drug+Design%2C+Development+and+Therapy&rft.issn=1177-8881&rft_id=info:doi/10.2147%2FDDDT.S89575 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Age; Chemotherapy; Solvents; Disease control; human serum albumin; taxanes; Survival; Oncology; Drug development; Toxicity; Metastases; Cytotoxicity; Paclitaxel; Breast cancer; nanoparticles; Antitumor activity DO - http://dx.doi.org/10.2147/DDDT.S89575 ER - TY - JOUR T1 - Quantitative assessment of myocardial fibrosis in an age-related rat model by ex vivo late gadolinium enhancement magnetic resonance imaging with histopathological correlation AN - 1751214996; PQ0002336595 AB - Late gadolinium enhanced (LGE) cardiac magnetic resonance (CMR) imaging can detect the presence of myocardial infarction from ischemic cardiomyopathies (ICM). However, it is more challenging to detect diffuse myocardial fibrosis from non-ischemic cardiomyopathy (NICM) with this technique due to more subtle and heterogeneous enhancement of the myocardium. This study investigates whether high-resolution LGE CMR can detect age-related myocardial fibrosis using quantitative texture analysis with histological validation. LGE CMR of twenty-four rat hearts (twelve 6-week-old and twelve 2-year-old) was performed using a 7T MRI scanner. Picrosirius red was used as the histopathology reference for collagen staining. Fibrosis in the myocardium was quantified with standard deviation (SD) threshold methods from the LGE CMR images and 3D contrast texture maps that were computed from gray level co-occurrence matrix of the CMR images. There was a significant increase of collagen fibers in the aged compared to the young rat histology slices (2.60 plus or minus 0.27 %LV vs. 1.24 plus or minus 0.29 %LV, p<0.01). Both LGE CMR and texture images showed a significant increase of myocardial fibrosis in the elderly compared to the young rats. Fibrosis in the LGE CMR images correlated strongly with histology with the 3 SD threshold (r=0.84, y=0.99x+0.00). Similarly, fibrosis in the contrast texture maps correlated with the histology using the 4 SD threshold (r=0.89, y=1.01x+0.00). High resolution ex-vivo LGE CMR can detect the presence of diffuse fibrosis that naturally developed in elderly rat hearts. Our results suggest that texture analysis may improve the assessment of myocardial fibrosis in LGE CMR images. JF - Computers in Biology and Medicine AU - Beliveau, Pascale AU - Cheriet, Farida AU - Anderson, Stasia A AU - Taylor, Joni L AU - Arai, Andrew E AU - Hsu, Li-Yueh AD - National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA PY - 2015 SP - 103 EP - 113 PB - Elsevier B.V., P.O. Box 800 Kidlington Oxford OX5 1DX United Kingdom VL - 65 SN - 0010-4825, 0010-4825 KW - Biotechnology and Bioengineering Abstracts KW - CMR cardiac magnetic resonance KW - DTI diffusion tensor imaging KW - DTPA diethylenetriamine pentaacetic acid KW - ECV extracellular volume fraction KW - Gd gadolinium KW - GLCM gray level co-occurrence matrix KW - HSV hue-saturation-value KW - ICM ischemic cardiomyopathies KW - LGE late gadolinium enhancement KW - LV left ventricular KW - NICM non-ischemic cardiomyopathy KW - NS not statically significant KW - ROI region of interest KW - SA short-axis KW - SI signal intensity KW - SD standard deviation KW - Diffuse myocardial fibrosis KW - Gadolinium KW - Magnetic resonance imaging KW - Texture analysis KW - Computer quantification KW - Aging KW - Heart KW - Age KW - Fibrosis KW - Ischemia KW - Maps KW - Computer applications KW - Myocardial infarction KW - Collagen KW - Cardiomyopathy KW - Fibers KW - Standard deviation KW - Geriatrics KW - Myocardium KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751214996?accountid=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=Computers+in+Biology+and+Medicine&rft.atitle=Quantitative+assessment+of+myocardial+fibrosis+in+an+age-related+rat+model+by+ex+vivo+late+gadolinium+enhancement+magnetic+resonance+imaging+with+histopathological+correlation&rft.au=Beliveau%2C+Pascale%3BCheriet%2C+Farida%3BAnderson%2C+Stasia+A%3BTaylor%2C+Joni+L%3BArai%2C+Andrew+E%3BHsu%2C+Li-Yueh&rft.aulast=Beliveau&rft.aufirst=Pascale&rft.date=2015-01-01&rft.volume=65&rft.issue=&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=Computers+in+Biology+and+Medicine&rft.issn=00104825&rft_id=info:doi/10.1016%2Fj.compbiomed.2015.07.027 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 48 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Heart; Age; Fibrosis; Magnetic resonance imaging; Gadolinium; Ischemia; Computer applications; Maps; Myocardial infarction; Collagen; Fibers; Cardiomyopathy; Standard deviation; Geriatrics; Myocardium DO - http://dx.doi.org/10.1016/j.compbiomed.2015.07.027 ER - TY - JOUR T1 - Structure of RC1339/APRc from Rickettsia conorii, a retropepsin-like aspartic protease AN - 1746874544; PQ0002167264 AB - The crystal structures of two constructs of RC1339/APRc from Rickettsia conorii, consisting of either residues 105-231 or 110-231 followed by a His tag, have been determined in three different crystal forms. As predicted, the fold of a monomer of APRc resembles one-half of the mandatory homodimer of retroviral pepsin-like aspartic proteases (retropepsins), but the quaternary structure of the dimer of APRc differs from that of the canonical retropepsins. The observed dimer is most likely an artifact of the expression and/or crystallization conditions since it cannot support the previously reported enzymatic activity of this bacterial aspartic protease. However, the fold of the core of each monomer is very closely related to the fold of retropepsins from a variety of retroviruses and to a single domain of pepsin-like eukaryotic enzymes, and may represent a putative common ancestor of monomeric and dimeric aspartic proteases. JF - Acta Crystallographica Section D AU - Li, Mi AU - Gustchina, Alla AU - Cruz, Rui AU - Simoes, Marisa AU - Curto, Pedro AU - Martinez, Juan AU - Faro, Carlos AU - Simoes, Isaura AU - Wlodawer, Alexander AD - Protein Structure Section, Macromolecular Crystallography Laboratory, National Cancer Institute, Frederick, MD 21702, USA. PY - 2015 SP - 2109 EP - 2118 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 71 IS - 10 SN - 1399-0047, 1399-0047 KW - Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746874544?accountid=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+RC1339%2FAPRc+from+Rickettsia+conorii%2C+a+retropepsin-like+aspartic+protease&rft.au=Li%2C+Mi%3BGustchina%2C+Alla%3BCruz%2C+Rui%3BSimoes%2C+Marisa%3BCurto%2C+Pedro%3BMartinez%2C+Juan%3BFaro%2C+Carlos%3BSimoes%2C+Isaura%3BWlodawer%2C+Alexander&rft.aulast=Li&rft.aufirst=Mi&rft.date=2015-01-01&rft.volume=71&rft.issue=10&rft.spage=2109&rft.isbn=&rft.btitle=&rft.title=Acta+Crystallographica+Section+D&rft.issn=13990047&rft_id=info:doi/10.1107%2FS1399004715013905 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Last updated - 2015-12-09 DO - http://dx.doi.org/10.1107/S1399004715013905 ER - TY - JOUR T1 - Does focal incidental super(18)F-FDG PET/CT uptake in the prostate have significance? AN - 1735922376; PQ0002271374 AB - super(18)F-FDG PET/CT is used to characterize many malignancies, but is not recommended for localized prostate cancer. This study explores the value of multi-parametric MRI (mpMRI) in characterizing incidental prostate super(18)F-FDG uptake. Thirty-one patients who underwent super(18)F-FDG PET/CT for reasons unrelated to prostate cancer and prostate mpMRI were eligible for this retrospective study. The mpMRI included T2-weighted (T2W), dynamic contrast enhancement (DCE), apparent diffusion coefficient (ADC), and MR spectroscopy (MRS) sequences. Fourteen patients were excluded (n = 8 insufficient histopathology, n = 6 radical prostatectomy before PET), and final analysis included 17 patients. A nuclear medicine physician, blinded to clinicopathologic findings, identified suspicious areas and maximum standardized uptake values (SUVmax) on super(18)F-FDG PET/CT. Sector-based imaging findings were correlated with annotated histopathology from whole-mount or MRI/transrectal ultrasound fusion biopsy samples. Positive predictive values (PPVs) were estimated using generalized estimating equations with logit link. Results were evaluated with Kruskal-Wallis and Dunn's multiple comparisons tests. The PPV of super(18)F-FDG PET alone in detecting prostate cancer was 0.65. Combining super(18)F-FDG PET as a base parameter with mpMRI (T2W, DCE, ADC, and MRS) increased the PPV to 0.82, 0.83, 0.83, and 0.94, respectively. All benign lesions had SUVmax 6. Using mpMRI to further evaluate incidental super(18)F-FDG uptake aids the diagnosis of prostate cancer. JF - Abdominal Imaging AU - Brown, Anna M AU - Lindenberg, Maria L AU - Sankineni, Sandeep AU - Shih, Joanna H AU - Johnson, Linda M AU - Pruthy, Suneha AU - Kurdziel, Karen A AU - Merino, Maria J AU - Wood, Bradford J AU - Pinto, Peter A AU - Choyke, Peter L AU - Turkbey, Baris AD - Molecular Imaging Program, National Cancer Institute, NIH, 10 Center Drive, Room B3B85, Bethesda, MD, 20892, USA, turkbeyi@mail.nih.gov PY - 2015 SP - 3222 EP - 3229 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 40 IS - 8 SN - 0942-8925, 0942-8925 KW - Biotechnology and Bioengineering Abstracts KW - Mathematical models KW - Magnetic resonance imaging KW - Biopsy KW - Malignancy KW - Prostate cancer KW - Magnetic resonance spectroscopy KW - Computed tomography KW - Positron emission tomography KW - Nuclear medicine KW - Diffusion coefficient KW - Ultrasound KW - Benign KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735922376?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Abdominal+Imaging&rft.atitle=Does+focal+incidental+super%2818%29F-FDG+PET%2FCT+uptake+in+the+prostate+have+significance%3F&rft.au=Brown%2C+Anna+M%3BLindenberg%2C+Maria+L%3BSankineni%2C+Sandeep%3BShih%2C+Joanna+H%3BJohnson%2C+Linda+M%3BPruthy%2C+Suneha%3BKurdziel%2C+Karen+A%3BMerino%2C+Maria+J%3BWood%2C+Bradford+J%3BPinto%2C+Peter+A%3BChoyke%2C+Peter+L%3BTurkbey%2C+Baris&rft.aulast=Brown&rft.aufirst=Anna&rft.date=2015-01-01&rft.volume=40&rft.issue=8&rft.spage=3222&rft.isbn=&rft.btitle=&rft.title=Abdominal+Imaging&rft.issn=09428925&rft_id=info:doi/10.1007%2Fs00261-015-0520-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Number of references - 14 N1 - Last updated - 2015-12-09 N1 - SubjectsTermNotLitGenreText - Malignancy; Mathematical models; Prostate cancer; Magnetic resonance spectroscopy; Magnetic resonance imaging; Computed tomography; Positron emission tomography; Nuclear medicine; Biopsy; Diffusion coefficient; Ultrasound; Benign DO - http://dx.doi.org/10.1007/s00261-015-0520-y ER - TY - JOUR T1 - Performance of the BG1Luc ER TA method in a qHTS format. AN - 1733191246; 26117232 AB - In 2012, the BG1Luc4E2 estrogen receptor (ER) transactivation (TA) method (BG1Luc ER TA) was accepted by U.S. regulatory agencies and the Organisation for Economic Co-operation and Development to detect substances with ER agonist activity. The method is now part of the Tier 1 testing battery in the Environmental Protection Agency's Endocrine Disruptor Screening Program. The BG1Luc ER TA method uses the BG1 ovarian cell line that endogenously expresses full-length ER (α and β) and is stably transfected with a plasmid containing four estrogen responsive elements upstream of a luciferase reporter gene. To allow increased throughput and testing efficiency, the BG1Luc ER TA ("BG1 manual") method was adapted for quantitative high-throughput screening (BG1 qHTS) in the U.S. Tox21 testing program. The BG1 qHTS test method was used to test approximately 10,000 chemicals three times each, and concentration-response data (n=15) were analyzed to evaluate test method performance. The balanced accuracy of the BG1 qHTS test method (97% [32/33]) was determined by comparing results to ER TA performance standards for the BG1 manual method. Concordance between the BG1 manual and qHTS methods was 92% (57/62) when calculated for a larger set of non-reference chemicals tested in both methods. These data demonstrate that the performance of the BG1 qHTS is similar to the currently accepted BG1 manual method, thereby establishing the utility of the BG1 qHTS method for identifying ER active environmental chemicals. JF - ALTEX AU - Ceger, Patricia AU - Allen, David AU - Huang, Ruili AU - Xia, Menghang AU - Casey, Warren AD - Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, USA. ; National Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, Maryland, USA. ; National Toxicology Program Interagency Center for the Evaluation of Alternative Toxicological Methods, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. Y1 - 2015 PY - 2015 DA - 2015 SP - 287 EP - 296 VL - 32 IS - 4 SN - 1868-596X, 1868-596X KW - Endocrine Disruptors KW - 0 KW - Estrogen Receptor alpha KW - Index Medicus KW - EDSP KW - quantitative high-throughput screening KW - BG1Luc ER TA KW - Tox21 KW - United States KW - Animal Testing Alternatives KW - United States Environmental Protection Agency KW - Protein Binding -- drug effects KW - Humans KW - Signal Transduction -- drug effects KW - Cell Line KW - High-Throughput Screening Assays -- methods KW - Estrogen Receptor alpha -- agonists KW - Endocrine Disruptors -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1733191246?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ALTEX&rft.atitle=Performance+of+the+BG1Luc+ER+TA+method+in+a+qHTS+format.&rft.au=Ceger%2C+Patricia%3BAllen%2C+David%3BHuang%2C+Ruili%3BXia%2C+Menghang%3BCasey%2C+Warren&rft.aulast=Ceger&rft.aufirst=Patricia&rft.date=2015-01-01&rft.volume=32&rft.issue=4&rft.spage=287&rft.isbn=&rft.btitle=&rft.title=ALTEX&rft.issn=1868596X&rft_id=info:doi/http%3A%2F%2Fdx.doi.org%2F10.14573%2Faltex.1505121 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-20 N1 - Date created - 2015-11-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Erratum In: ALTEX. 2016;33(1):79 [26776439] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.14573/altex.1505121 ER - TY - JOUR T1 - Enhanced T-cell activation and differentiation in lymphocytes from transgenic mice expressing ubiquitination-resistant 2KR LAT molecules AN - 1732826766; PQ0002242120 AB - Linker for activation of T cells (LAT) is critical for the propagation of T-cell signals upon T-cell receptor (TCR) activation. Previous studies demonstrated that substitution of LAT lysines with arginines (2KR LAT) resulted in decreased LAT ubiquitination and elevated T-cell signaling, indicating that LAT ubiquitination is a molecular checkpoint for attenuation of T-cell signaling. To investigate the role of LAT ubiquitination in vivo, we have generated transgenic mice expressing WT and ubiquitin-defective 2KR LAT. On TCR stimulation of T cells from these mice, proximal signaling and cytokine production was elevated in 2KR versus wild-type (WT) LAT mice. Enhanced cytolytic activity as well as T-helper responses were observed on LAT expression, which were further elevated by 2KR LAT expression. Despite greater T-effector function, WT or 2KR LAT expression did not have any effect on clearance of certain pathogens or tumors. Our data support the model that lack of tumor clearance is due to increased differentiation and acquisition of effector phenotype that is associated with suboptimal immunity in an immunotherapy model. Thus, our data further reinforce the role of LAT ubiquitination in TCR signaling and uncovers a novel role for LAT in driving T-cell differentiation. JF - Gene Therapy AU - Rodriguez-Pena, A B AU - Gomez-Rodriguez, J AU - Kortum, R L AU - Palmer, D C AU - Yu, Z AU - Guittard, G C AU - Wohlfert, E A AU - Silver, P B AU - Misplon, J A AU - Sommers, C L AU - Feigenbaum, L AU - Epstein, S L AU - Caspi, R R AU - Belkaid, Y AU - Restifo, N P AU - Samelson, L E AU - Balagopalan, L AD - Cell Signaling and Immunity Section, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA PY - 2015 SP - 781 EP - 792 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 22 IS - 10 SN - 0969-7128, 0969-7128 KW - Immunology Abstracts; Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - T-cell receptor KW - Data processing KW - Gene therapy KW - Arginine KW - Immunotherapy KW - Animal models KW - Lysine KW - Pathogens KW - Tumors KW - Transgenic mice KW - Cell activation KW - Differentiation KW - ubiquitination KW - Cytolytic activity KW - Lymphocytes T KW - Cytokines KW - G 07720:Immunogenetics KW - W 30905:Medical Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732826766?accountid=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=Enhanced+T-cell+activation+and+differentiation+in+lymphocytes+from+transgenic+mice+expressing+ubiquitination-resistant+2KR+LAT+molecules&rft.au=Rodriguez-Pena%2C+A+B%3BGomez-Rodriguez%2C+J%3BKortum%2C+R+L%3BPalmer%2C+D+C%3BYu%2C+Z%3BGuittard%2C+G+C%3BWohlfert%2C+E+A%3BSilver%2C+P+B%3BMisplon%2C+J+A%3BSommers%2C+C+L%3BFeigenbaum%2C+L%3BEpstein%2C+S+L%3BCaspi%2C+R+R%3BBelkaid%2C+Y%3BRestifo%2C+N+P%3BSamelson%2C+L+E%3BBalagopalan%2C+L&rft.aulast=Rodriguez-Pena&rft.aufirst=A&rft.date=2015-01-01&rft.volume=22&rft.issue=10&rft.spage=781&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2015.48 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2015-12-09 N1 - SubjectsTermNotLitGenreText - T-cell receptor; Data processing; Gene therapy; Arginine; Immunotherapy; Animal models; Lysine; Tumors; Pathogens; Transgenic mice; Cell activation; ubiquitination; Differentiation; Cytolytic activity; Lymphocytes T; Cytokines DO - http://dx.doi.org/10.1038/gt.2015.48 ER - TY - JOUR T1 - Entrectinib: a potent new TRK, ROS1, and ALK inhibitor. AN - 1728673900; 26457764 AB - Receptor tyrosine kinases (RTKs) and their signaling pathways, control normal cellular processes; however, their deregulation play important roles in malignant transformation. In advanced non-small cell lung cancer (NSCLC), the recognition of oncogenic activation of specific RTKs, has led to the development of molecularly targeted agents that only benefit roughly 20% of patients. Entrectinib is a pan-TRK, ROS1 and ALK inhibitor that has shown potent anti-neoplastic activity and tolerability in various neoplastic conditions, particularly NSCLC. This review outlines the pharmacokinetics, pharmacodynamics, mechanism of action, safety, tolerability, pre-clinical studies and clinical trials of entrectinib, a promising novel agent for the treatment of advanced solid tumors with molecular alterations of Trk-A, B and C, ROS1 or ALK. Among the several experimental drugs under clinical development, entrectinib is emerging as an innovative and promising targeted agent. The encouraging antitumor activity reported in the Phase 1 studies, together with the acceptable toxicity profile, suggest that entrectinib, thanks to its peculiar mechanism of action, could play an important role in the treatment-strategies of multiple TRK-A, B, C, ROS1, and ALK- dependent solid tumors, including NSCLC and colorectal cancer. That being said, further evidence for its clinical use is still needed. JF - Expert opinion on investigational drugs AU - Rolfo, Christian AU - Ruiz, Rossana AU - Giovannetti, Elisa AU - Gil-Bazo, Ignacio AU - Russo, Antonio AU - Passiglia, Francesco AU - Giallombardo, Marco AU - Peeters, Marc AU - Raez, Luis AD - a Phase I - Early Clinical Trials Unit, Oncology Department , Antwerp University Hospital and Center for Oncological Research (CORE), Antwerp University , Edegem , Belgium. ; b Oncology Department , National Cancer Institute (INEN) , Lima , Peru. ; c Department Medical Oncology , VU University Medical Center , Amsterdam , The Netherlands. ; d Department of Oncology , Clínica Universidad de Navarra , Pamplona , Spain. ; e Department of Surgical, Oncological and Oral Sciences, Section of Medical Oncology , University of Palermo , Palermo , Italy. ; f Thoracic Oncology Program , Memorial Cancer Institute, Memorial Health Care System , Pembroke Pines , FL , USA. Y1 - 2015 PY - 2015 DA - 2015 SP - 1493 EP - 1500 VL - 24 IS - 11 KW - Antineoplastic Agents KW - 0 KW - Benzamides KW - Indazoles KW - Proto-Oncogene Proteins KW - entrectinib KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - ROS1 protein, human KW - Receptor Protein-Tyrosine Kinases KW - Receptor, trkA KW - Receptor, trkB KW - Receptor, trkC KW - anaplastic lymphoma kinase KW - Index Medicus KW - non-small cell lung cancer KW - salivary gland cancer KW - colorectal cancer KW - ALK KW - NTRK3 KW - precision medicine KW - NTRK1 KW - NTRK2 KW - TrkC KW - ROS1 KW - TrkA KW - Entrectinib KW - TrkB KW - Protein-Tyrosine Kinases -- antagonists & inhibitors KW - Receptor, trkC -- antagonists & inhibitors KW - Receptor, trkB -- antagonists & inhibitors KW - Animals KW - Proto-Oncogene Proteins -- antagonists & inhibitors KW - Humans KW - Receptor Protein-Tyrosine Kinases -- antagonists & inhibitors KW - Receptor, trkA -- antagonists & inhibitors KW - Neoplasms -- drug therapy KW - Benzamides -- adverse effects KW - Indazoles -- adverse effects KW - Neoplasms -- pathology KW - Benzamides -- pharmacology KW - Indazoles -- pharmacology KW - Indazoles -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - Benzamides -- therapeutic use KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728673900?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Entrectinib%3A+a+potent+new+TRK%2C+ROS1%2C+and+ALK+inhibitor.&rft.au=Rolfo%2C+Christian%3BRuiz%2C+Rossana%3BGiovannetti%2C+Elisa%3BGil-Bazo%2C+Ignacio%3BRusso%2C+Antonio%3BPassiglia%2C+Francesco%3BGiallombardo%2C+Marco%3BPeeters%2C+Marc%3BRaez%2C+Luis&rft.aulast=Rolfo&rft.aufirst=Christian&rft.date=2015-01-01&rft.volume=24&rft.issue=11&rft.spage=1493&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+investigational+drugs&rft.issn=1744-7658&rft_id=info:doi/10.1517%2F13543784.2015.1096344 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-23 N1 - Date created - 2015-10-31 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1517/13543784.2015.1096344 ER - TY - JOUR T1 - Transgenic mice and metabolomics for study of hepatic xenobiotic metabolism and toxicity AN - 1727673452; PQ0002136369 AB - Introduction: The study of xenobiotic metabolism and toxicity has been greatly aided by the use of genetically modified mouse models and metabolomics. Areas covered: Gene knockout mice can be used to determine the enzymes responsible for the metabolism of xenobiotics in vivo and to examine the mechanisms of xenobiotic-induced toxicity. Humanized mouse models are especially important because there exist marked species differences in the xenobiotic-metabolizing enzymes and the nuclear receptors that regulate these enzymes. Humanized mice expressing CYPs and nuclear receptors including the pregnane X receptor, the major regulator of xenobiotic metabolism and transport were produced. With genetically modified mouse models, metabolomics can determine the metabolic map of many xenobiotics with a level of sensitivity that allows the discovery of even minor metabolites. This technology can be used for determining the mechanism of xenobiotic toxicity and to find early biomarkers for toxicity. Expert opinion: Metabolomics and genetically modified mouse models can be used for the study of xenobiotic metabolism and toxicity by: i) comparison of the metabolomics profiles between wild-type and genetically modified mice, and searching for genotype-dependent endogenous metabolites; ii) searching for and elucidating metabolites derived from xenobiotics; and iii) discovery of specific alterations of endogenous compounds induced by xenobiotics-induced toxicity. JF - Expert Opinion on Drug Metabolism and Toxicology AU - Gonzalez, Frank J AU - Fang, Zhong-Ze AU - Ma, Xiaochao AD - National Institutes of Health, National Cancer Institute, Center for Cancer Research, Laboratory of Metabolism, Bethesda, MD 20892, USA Y1 - 2015///0, PY - 2015 DA - 0, 2015 SP - 869 EP - 881 PB - Informa Healthcare VL - 11 IS - 6 SN - 1742-5255, 1742-5255 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; Toxicology Abstracts KW - CYP KW - CYP3A4 KW - genetically modified mice KW - metabolomics KW - pregnane X receptor KW - UPLC-ESI-QTOFMS KW - xenobiotics KW - Protein transport KW - Nuclear receptors KW - Animal models KW - Enzymes KW - Metabolites KW - Toxicity KW - pregnane X receptors KW - Transgenic mice KW - biomarkers KW - X 24310:Pharmaceuticals KW - G 07870:Mammals KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727673452?accountid=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=Expert+Opinion+on+Drug+Metabolism+and+Toxicology&rft.atitle=Transgenic+mice+and+metabolomics+for+study+of+hepatic+xenobiotic+metabolism+and+toxicity&rft.au=Gonzalez%2C+Frank+J%3BFang%2C+Zhong-Ze%3BMa%2C+Xiaochao&rft.aulast=Gonzalez&rft.aufirst=Frank&rft.date=2015-01-01&rft.volume=11&rft.issue=6&rft.spage=869&rft.isbn=&rft.btitle=&rft.title=Expert+Opinion+on+Drug+Metabolism+and+Toxicology&rft.issn=17425255&rft_id=info:doi/10.1517%2F17425255.2015.1032245 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Protein transport; Nuclear receptors; Animal models; Enzymes; Metabolites; pregnane X receptors; Toxicity; Transgenic mice; biomarkers; metabolomics DO - http://dx.doi.org/10.1517/17425255.2015.1032245 ER - TY - JOUR T1 - GNormPlus: An Integrative Approach for Tagging Genes, Gene Families, and Protein Domains AN - 1722175691; PQ0002026600 AB - The automatic recognition of gene names and their associated database identifiers from biomedical text has been widely studied in recent years, as these tasks play an important role in many downstream text-mining applications. Despite significant previous research, only a small number of tools are publicly available and these tools are typically restricted to detecting only mention level gene names or only document level gene identifiers. In this work, we report GNormPlus: an end-to-end and open source system that handles both gene mention and identifier detection. We created a new corpus of 694 PubMed articles to support our development of GNormPlus, containing manual annotations for not only gene names and their identifiers, but also closely related concepts useful for gene name disambiguation, such as gene families and protein domains. GNormPlus integrates several advanced text-mining techniques, including SimConcept for resolving composite gene names. As a result, GNormPlus compares favorably to other state-of-the-art methods when evaluated on two widely used public benchmarking datasets, achieving 86.7% F1-score on the BioCreative II Gene Normalization task dataset and 50.1% F1-score on the BioCreative III Gene Normalization task dataset. The GNormPlus source code and its annotated corpus are freely available, and the results of applying GNormPlus to the entire PubMed are freely accessible through our web-based tool PubTator. JF - BioMed Research International AU - Wei, Chih-Hsuan AU - Kao, Hung-Yu AU - Lu, Zhiyong AD - National Center for Biotechnology Information (NCBI), 8600 Rockville Pike, Bethesda, MD 20894, USA, zhiyong.lu@nih.gov Y1 - 2015/01// PY - 2015 DA - January 2015 PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States VL - 2015 SN - 2314-6133, 2314-6133 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Databases KW - G 07730:Development & Cell Cycle KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722175691?accountid=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=BioMed+Research+International&rft.atitle=GNormPlus%3A+An+Integrative+Approach+for+Tagging+Genes%2C+Gene+Families%2C+and+Protein+Domains&rft.au=Wei%2C+Chih-Hsuan%3BKao%2C+Hung-Yu%3BLu%2C+Zhiyong&rft.aulast=Wei&rft.aufirst=Chih-Hsuan&rft.date=2015-01-01&rft.volume=2015&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2015%2F918710 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Number of references - 10 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Databases DO - http://dx.doi.org/10.1155/2015/918710 ER - TY - JOUR T1 - Hierarchical decision making: resource distribution exhibits stronger effect on crayfish dominance relationships and shelter occupation than prior social experience and resource ownership AN - 1722169703; PQ0002040446 AB - The outcome of agonistic interactions is critical to the acquisition of vital resources. These behaviours can be influenced by several intrinsic and extrinsic factors, and multi-faceted studies are necessary for ecologically relevant studies. The aim of this study was to combine the effects of past social experience, resource ownership, and the distribution of shelter resources to examine the combination of these effects on various measures of agonism in crayfish (Orconectes rusticus). Crayfish were assigned to one of three social conditioning treatments (naive, subordinate, dominant) and then introduced to an arena where they were assigned to a resident or intruder treatment. An intruder shelter was then positioned 20, 60 or 120 cm from the resident shelter. We found that resource distribution (shelter distance) played a larger role in influencing agonistic behaviour than did past social experience or current social status. JF - Behaviour AU - Chibucos, K AU - Wofford, S J AU - Moore, P A AD - Program for Genomics Differentiation, Eunice K. Shiver Institute for Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA, pmoore@bgsu.edu Y1 - 2015///0, PY - 2015 DA - 0, 2015 SP - 1063 EP - 1082 PB - Brill Academic Publishers, P.O. Box 9000 Leiden PA 2300 Netherlands VL - 152 SN - 0005-7959, 0005-7959 KW - Ecology Abstracts; ASFA 1: Biological Sciences & Living Resources; Animal Behavior Abstracts KW - crayfish KW - dominance KW - prior residence KW - resource ownership KW - shelter KW - social status KW - status reversal KW - Predation KW - Cambaridae KW - Shelter KW - Freshwater KW - Agonistic behaviour KW - Orconectes rusticus KW - Dominance hierarchies KW - Social interactions KW - Dominance KW - Decision making KW - Intruder KW - Freshwater crustaceans KW - Shelters KW - Property rights KW - Territoriality KW - D 04040:Ecosystem and Ecology Studies KW - Q1 08604:Stock assessment and management KW - Y 25070:Learning, Memory, Reinforcement, and Motivation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722169703?accountid=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=Behaviour&rft.atitle=Hierarchical+decision+making%3A+resource+distribution+exhibits+stronger+effect+on+crayfish+dominance+relationships+and+shelter+occupation+than+prior+social+experience+and+resource+ownership&rft.au=Chibucos%2C+K%3BWofford%2C+S+J%3BMoore%2C+P+A&rft.aulast=Chibucos&rft.aufirst=K&rft.date=2015-01-01&rft.volume=152&rft.issue=&rft.spage=1063&rft.isbn=&rft.btitle=&rft.title=Behaviour&rft.issn=00057959&rft_id=info:doi/10.1163%2F1568539X-00003292 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Predation; Freshwater crustaceans; Property rights; Shelters; Territoriality; Agonistic behaviour; Dominance hierarchies; Decision making; Intruder; Shelter; Dominance; Social interactions; Cambaridae; Orconectes rusticus; Freshwater DO - http://dx.doi.org/10.1163/1568539X-00003292 ER - TY - JOUR T1 - Genetic and Phenotypic Properties of Vero Cell-Adapted Japanese Encephalitis Virus SA14-14-2 Vaccine Strain Variants and a Recombinant Clone, Which Demonstrates Attenuation and Immunogenicity in Mice AN - 1722168082; PQ0002059450 AB - The live-attenuated Japanese encephalitis virus CEV) SA14-14-2 vaccine, produced in primary hamster kidney cells, is safe and effective. Past attempts to adapt this virus to replicate in cells that are more favorable for vaccine production resulted in mutations that significantly reduced immunogenicity. In this study, 10 genetically distinct Vero cell-adapted JEV SA14-14-2 variants were isolated and a recombinant wild-type JEV clone, modified to contain the JEV SA14-14-2 polyprotein amino acid sequence, was recovered in Vero cells. A single capsid protein mutation (S66L) was important for Vero cell-adaptation. Mutations were also identified that modulated virus sensitivity to type I interferon-stimulation in Vero cells. A subset of JEV SA14-14-2 variants and the recombinant clone were evaluated in vivo and exhibited levels of attenuation that varied significantly in suckling mice, but were avirulent and highly immunogenic in weanling mice and are promising candidates for the development of a second-generation, recombinant vaccine. JF - American Journal of Tropical Medicine and Hygiene AU - Gromowski, Gregory D AU - Firestone, Cai-Yen AU - Bustos-Arriaga, Jose AU - Whitehead, Stephen S AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, gromowskig@niaid.nih.gov Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 98 EP - 107 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 92 IS - 1 SN - 0002-9637, 0002-9637 KW - Genetics Abstracts; CSA Neurosciences Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Immunology Abstracts; Virology & AIDS Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality KW - Clones KW - polyproteins KW - Vero cells KW - Mutations KW - Disease control KW - Suckling behavior KW - Attenuation KW - Kidneys KW - Phenotypes KW - Encephalitis KW - Recombinants KW - Immunogenicity KW - Kidney KW - Japanese encephalitis virus KW - Vaccines KW - Hygiene KW - Mutation KW - Capsid protein KW - Amino acid sequence KW - K 03410:Animal Diseases KW - Q5 08503:Characteristics, behavior and fate KW - N3 11029:Neurophysiology & biophysics KW - F 06905:Vaccines KW - V 22350:Immunology KW - J 02350:Immunology KW - Q1 08485:Species interactions: pests and control KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722168082?accountid=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=Genetic+and+Phenotypic+Properties+of+Vero+Cell-Adapted+Japanese+Encephalitis+Virus+SA14-14-2+Vaccine+Strain+Variants+and+a+Recombinant+Clone%2C+Which+Demonstrates+Attenuation+and+Immunogenicity+in+Mice&rft.au=Gromowski%2C+Gregory+D%3BFirestone%2C+Cai-Yen%3BBustos-Arriaga%2C+Jose%3BWhitehead%2C+Stephen+S&rft.aulast=Gromowski&rft.aufirst=Gregory&rft.date=2015-01-01&rft.volume=92&rft.issue=1&rft.spage=98&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.14-0427 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Clones; Recombinants; Mutations; Disease control; Attenuation; Kidneys; Vaccines; Hygiene; Phenotypes; polyproteins; Vero cells; Immunogenicity; Kidney; Suckling behavior; Mutation; Encephalitis; Amino acid sequence; Capsid protein; Japanese encephalitis virus DO - http://dx.doi.org/10.4269/ajtmh.14-0427 ER - TY - JOUR T1 - Chondroitin sulfate proteoglycan 4 as a target for chimeric antigen receptor-based T-cell immunotherapy of solid tumors. AN - 1713527622; 26190756 AB - Proteoglycans are critical molecules involved in multiple physiological cell functions, but also key players in cancer development and progression. In particular, chondroitin sulfate proteoglycan 4 (CSPG4) is recognized as an attractive target for antibody-based approaches because of its high expression on cancer cells in several types of human malignancies and its restricted distribution in normal tissues. Adoptive transfer of genetically modified T cells is emerging as a powerful therapeutic approach in cancer patients. In this regard, the selection of the appropriate antigen to be targeted in solid tumors becomes a critical aspect in promoting potent antitumor effects while preventing toxicities. This review summarizes the authors' current knowledge on the expression and function of CSPG4 in normal tissues and malignant tumors, with a particular focus on the potential use of CSPG4 as a target for antigen-specificity redirected T cells. T cells expressing a CSPG4-specific chimeric antigen receptor (CAR) offer the possibility to target a broad spectrum of solid tumors for which no curative treatment is currently available. In addition, since CSPG4 is also selectively up-regulated on tumor-associated pericytes, targeting this antigen may also contribute to tumor regression via inhibition of neoangiogenesis. Preclinical experiments to date justify the clinical translation of CSPG4-specific CAR-T cells. JF - Expert opinion on therapeutic targets AU - Wang, Yangyang AU - Geldres, Claudia AU - Ferrone, Soldano AU - Dotti, Gianpietro AD - a 1 Massachusetts General Hospital, Harvard Medical School, Department of Surgery , 55 Fruit Street, Boston, MA 02114, USA Sferrone@MGH.Harvard.edu. ; b 2 National Cancer Institute, Experimental Transplantation and Immunology Branch , Bethesda, MD 20892, USA. ; c 3 University of North Carolina, Lineberger Comprehensive Cancer Center , Chapel Hill, NC, USA gdotti@med.unc.edu. Y1 - 2015 PY - 2015 DA - 2015 SP - 1339 EP - 1350 VL - 19 IS - 10 KW - Antigens KW - 0 KW - Proteoglycans KW - Receptors, Antigen, T-Cell KW - chondroitin sulfate proteoglycan 4 KW - Index Medicus KW - T-cell therapies KW - solid tumors KW - chimeric antigen receptor KW - CSPG4 KW - Animals KW - Humans KW - Molecular Targeted Therapy KW - Receptors, Antigen, T-Cell -- immunology KW - T-Lymphocytes -- immunology KW - Neoplasms -- pathology KW - Neoplasms -- therapy KW - Antigens -- immunology KW - Proteoglycans -- immunology KW - Neoplasms -- immunology KW - Immunotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1713527622?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+targets&rft.atitle=Chondroitin+sulfate+proteoglycan+4+as+a+target+for+chimeric+antigen+receptor-based+T-cell+immunotherapy+of+solid+tumors.&rft.au=Wang%2C+Yangyang%3BGeldres%2C+Claudia%3BFerrone%2C+Soldano%3BDotti%2C+Gianpietro&rft.aulast=Wang&rft.aufirst=Yangyang&rft.date=2015-01-01&rft.volume=19&rft.issue=10&rft.spage=1339&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+therapeutic+targets&rft.issn=1744-7631&rft_id=info:doi/10.1517%2F14728222.2015.1068759 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-05 N1 - Date created - 2015-09-16 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1517/14728222.2015.1068759 ER - TY - JOUR T1 - The Implementation Road: Engaging Community Partnerships in Evidence-Based Cancer Control Interventions AN - 1708526700; 2011-842022 AB - Southern rural and underserved counties have high proportions of individuals with increased mortality for cervical and breast cancers. To improve the integration of behavioral research into practice, the dissemination and implementation of efficacious interventions to encourage the use of screening have increased in recent years. This study addressed gaps in the dissemination and implementation of evidence-based interventions with a pilot called Team Up. Qualitative interviews with 24 key individuals in six state-level partnerships explored partnership characteristics that influenced selection and use of evidence-based interventions among low-income, rarely or never screened women. Guided by diffusion of innovations theory and the Lasker and Weiss partnership functioning model, interviews about the intervention centered on (a) knowledge surrounding evidence base; (b) identification, selection, and adoption; (c) planning and adaptation; (d) implementation; and (e) partnership reflections and impact. Using grounded theory and content analysis, data revealed that lack of communication and high partner turnover hindered adoption and adaptation, whereas failure of partnership leaders to engage local stakeholders and lack of sufficient funds hampered implementation. Delivery of evidence-based interventions was more effective when partnerships included local partners in early decision making and when coaches were introduced to facilitate strategic thinking about translating evidence-based interventions into practice. A challenge for public health partnerships was the translation of interventions into successful programs, such that underserved communities benefited from early detection intervention research. [Reprinted by permission of Sage Publications Inc., copyright holder.] JF - Health Promotion Practice AU - Breslau, Erica S AU - Weiss, Elisa S AU - Williams, Abigail AU - Burness, Allison AU - Kepka, Deanna AD - National Cancer Institute, Bethesda, MD, USA Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 46 EP - 54 PB - Sage Publications, Thousand Oaks CA VL - 16 IS - 1 SN - 1524-8399, 1524-8399 KW - Business and service sector - Business organization and administration KW - Health conditions and policy - Health and health policy KW - Population groups, population policy, and demographics - Women KW - Population groups, population policy, and demographics - Demography and census KW - Health conditions and policy - Diseases and disorders KW - Science and technology policy - Technology and technology policy KW - Social conditions and policy - Communication KW - cancer prevention and control health disparities health education health promotion partnerships/coalitions program planning and evaluation women's health KW - Mortality KW - Partnership KW - Women KW - Communication KW - Diffusion of innovations KW - Breast cancer KW - Health policy KW - Cancer KW - Public health KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1708526700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apais&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Promotion+Practice&rft.atitle=The+Implementation+Road%3A+Engaging+Community+Partnerships+in+Evidence-Based+Cancer+Control+Interventions&rft.au=Breslau%2C+Erica+S%3BWeiss%2C+Elisa+S%3BWilliams%2C+Abigail%3BBurness%2C+Allison%3BKepka%2C+Deanna&rft.aulast=Breslau&rft.aufirst=Erica&rft.date=2015-01-01&rft.volume=16&rft.issue=1&rft.spage=46&rft.isbn=&rft.btitle=&rft.title=Health+Promotion+Practice&rft.issn=15248399&rft_id=info:doi/10.1177%2F1524839914528705 LA - English DB - PAIS Index N1 - Date revised - 2015-09-01 N1 - Last updated - 2016-09-28 N1 - SubjectsTermNotLitGenreText - Partnership; Public health; Women; Mortality; Breast cancer; Diffusion of innovations; Cancer; Health policy; Communication DO - http://dx.doi.org/10.1177/1524839914528705 ER - TY - JOUR T1 - Combined Analysis of SNP Array Data Identifies Novel CNV Candidates and Pathways in Ependymoma and Mesothelioma AN - 1701500771; PQ0001772704 AB - Copy number variation is a class of structural genomic modifications that includes the gain and loss of a specific genomic region, which may include an entire gene. Many studies have used low-resolution techniques to identify regions that are frequently lost or amplified in cancer. Usually, researchers choose to use proprietary or non-open-source software to detect these regions because the graphical interface tends to be easier to use. In this study, we combined two different open-source packages into an innovative strategy to identify novel copy number variations and pathways associated with cancer. We used a mesothelioma and ependymoma published datasets to assess our tool. We detected previously described and novel copy number variations that are associated with cancer chemotherapy resistance. We also identified altered pathways associated with these diseases, like cell adhesion in patients with mesothelioma and negative regulation of glutamatergic synaptic transmission in ependymoma patients. In conclusion, we present a novel strategy using open-source software to identify copy number variations and altered pathways associated with cancer. JF - BioMed Research International AU - Wajnberg, Gabriel AU - Carvalho, Benilton S AU - Ferreira, Carlos G AU - Passetti, Fabio AD - Bioinformatics Unit, Clinical Research Coordination, National Cancer Institute of Brazil (INCA), 20231-050 Rio de Janeiro, RJ, Brazil, passetti@fiocruz.br Y1 - 2015/01// PY - 2015 DA - Jan 2015 PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States VL - 2015 SN - 2314-6133, 2314-6133 KW - Biotechnology and Bioengineering Abstracts KW - Data processing KW - Chemotherapy KW - Cancer KW - copy number KW - Cell adhesion KW - Computer programs KW - software KW - Glutamatergic transmission KW - Single-nucleotide polymorphism KW - mesothelioma KW - genomics KW - Synaptic transmission KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701500771?accountid=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=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Lipid+exhange+at+contact+sites&rft.au=Prinz%2C+Will&rft.aulast=Prinz&rft.aufirst=Will&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Computer programs; Glutamatergic transmission; software; Data processing; Single-nucleotide polymorphism; Chemotherapy; mesothelioma; Synaptic transmission; genomics; Cancer; Cell adhesion; copy number DO - http://dx.doi.org/10.1155/2015/902419 ER - TY - JOUR T1 - The Implementation Road: Engaging Community Partnerships in Evidence-Based Cancer Control Interventions AN - 1683509130 AB - Southern rural and underserved counties have high proportions of individuals with increased mortality for cervical and breast cancers. To improve the integration of behavioral research into practice, the dissemination and implementation of efficacious interventions to encourage the use of screening have increased in recent years. This study addressed gaps in the dissemination and implementation of evidence-based interventions with a pilot called Team Up. Qualitative interviews with 24 key individuals in six state-level partnerships explored partnership characteristics that influenced selection and use of evidence-based interventions among low-income, rarely or never screened women. Guided by diffusion of innovations theory and the Lasker and Weiss partnership functioning model, interviews about the intervention centered on (a) knowledge surrounding evidence base; (b) identification, selection, and adoption; (c) planning and adaptation; (d) implementation; and (e) partnership reflections and impact. Using grounded theory and content analysis, data revealed that lack of communication and high partner turnover hindered adoption and adaptation, whereas failure of partnership leaders to engage local stakeholders and lack of sufficient funds hampered implementation. Delivery of evidence-based interventions was more effective when partnerships included local partners in early decision making and when coaches were introduced to facilitate strategic thinking about translating evidence-based interventions into practice. A challenge for public health partnerships was the translation of interventions into successful programs, such that underserved communities benefited from early detection intervention research. JF - Health Promotion Practice AU - Breslau, Erica S AU - Weiss, Elisa S AU - Williams, Abigail AU - Burness, Allison AU - Kepka, Deanna AD - National Cancer Institute, Bethesda, MD, USA ; The Leukemia & Lymphoma Society, White Plains, NY, USA ; Mayor’s Office to Combat Domestic Violence, The City of New York, New York, NY, USA ; National Cancer Institute, Bethesda, MD, USA, MedStar Washington Hospital Center, Washington, DC, USA ; National Cancer Institute, Bethesda, MD, USA, University of Utah, Salt Lake City, UT, USA ; National Cancer Institute, Bethesda, MD, USA Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 46 EP - 54 CY - Thousand Oaks PB - SAGE PUBLICATIONS, INC. VL - 16 IS - 1 SN - 1524-8399 KW - Public Health And Safety KW - cancer prevention and control KW - health disparities KW - health education KW - health promotion KW - partnerships/coalitions KW - program planning and evaluation KW - women’s health KW - Adaptation KW - Breast cancer KW - Cervical cancer KW - Early warnings KW - Evidence based KW - Evidence based medicine KW - Funds KW - Grounded theory KW - Health education KW - Identification KW - Innovations KW - Interventions KW - Low income people KW - Low income women KW - Mortality KW - Partnerships KW - Public health KW - Public health policy KW - Rural communities KW - Screening KW - Behaviour KW - Cancer KW - Coalitions KW - Communication KW - Content analysis KW - Decision making KW - Detection KW - Dissemination KW - Early intervention programmes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683509130?accountid=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=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Imaging+the+molecular+architecture+of+the+plasma+membrane+with+correlative+3D+super+resolution+light+and+electron+microscopy&rft.au=Taraska%2C+Justin&rft.aulast=Taraska&rft.aufirst=Justin&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-05-14 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1177/1524839914528705 ER - TY - JOUR T1 - Novel dosing strategies increase exposures of the potent antituberculosis drug rifapentine but are poorly tolerated in healthy volunteers. AN - 1681266550; 25824215 AB - Rifapentine is a potent antituberculosis drug currently in phase III trials. Bioavailability decreases with increasing dose, yet high daily exposures are likely needed to improve efficacy and shorten the tuberculosis treatment duration. Further, the limits of tolerability are poorly defined. The phase I multicenter trial in healthy adults described here investigated two strategies to increase rifapentine exposures: dividing the dose or giving the drug with a high-fat meal. In arm 1, rifapentine was administered at 10 mg/kg of body weight twice daily and 20 mg/kg once daily, each for 14 days, separated by a 28-day washout; the dosing sequence was randomized. In arm 2, 15 mg/kg rifapentine once daily was given with a high-fat versus a low-fat breakfast. Sampling for pharmacokinetic analysis was performed on days 1 and 14. Population pharmacokinetic analyses were performed. This trial was stopped early for poor tolerability and because of safety concerns. Of 44 subjects, 20 discontinued prematurely; 11 of these discontinued for protocol-defined toxicity (a grade 3 or higher adverse event or grade 2 or higher rifamycin hypersensitivity). Taking rifapentine with a high-fat meal increased the median steady-state area under the concentration-time curve from time zero to 24 h (AUC0-24ss) by 31% (relative standard error, 6%) compared to that obtained when the drug was taken with a low-fat breakfast. Dividing the dose increased exposures substantially (e.g., 38% with 1,500 mg/day). AUC0-24ss was uniformly higher in our study than in recent tuberculosis treatment trials, in which toxicity was rare. In conclusion, two strategies to increase rifapentine exposures, dividing the dose or giving it with a high-fat breakfast, successfully increased exposures, but toxicity was common in healthy adults. The limits of tolerability in patients with tuberculosis remain to be defined. (AIDS Clinical Trials Group study A5311 has been registered at ClinicalTrials.gov under registration no. NCT01574638.). Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Antimicrobial agents and chemotherapy AU - Dooley, Kelly E AU - Savic, Radojka M AU - Park, Jeong-Gun AU - Cramer, Yoninah AU - Hafner, Richard AU - Hogg, Evelyn AU - Janik, Jennifer AU - Marzinke, Mark A AU - Patterson, Kristine AU - Benson, Constance A AU - Hovind, Laura AU - Dorman, Susan E AU - Haas, David W AU - ACTG A5311 Study Team AD - Johns Hopkins University School of Medicine, Baltimore, Maryland, USA kdooley1@jhmi.edu. ; University of California, San Francisco, California, USA. ; Center for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, Massachusetts, USA. ; Division of AIDS, National Institutes of Health, Bethesda, Maryland, USA. ; Social & Scientific Systems, Inc., Silver Spring, Maryland, USA. ; Frontier Science Foundation, Amherst, New York, USA. ; Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. ; University of North Carolina, Chapel Hill, North Carolina, USA. ; University of California, San Diego, California, USA. ; Vanderbilt University School of Medicine, Nashville, Tennessee, USA. ; ACTG A5311 Study Team Y1 - 2015 PY - 2015 DA - 2015 SP - 3399 EP - 3405 VL - 59 IS - 6 KW - Antitubercular Agents KW - 0 KW - Rifampin KW - VJT6J7R4TR KW - rifapentine KW - XJM390A33U KW - Index Medicus KW - Young Adult KW - Drug Administration Schedule KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Healthy Volunteers KW - Adolescent KW - Male KW - Female KW - Antitubercular Agents -- pharmacokinetics KW - Rifampin -- analogs & derivatives KW - Rifampin -- adverse effects KW - Antitubercular Agents -- administration & dosage KW - Rifampin -- pharmacokinetics KW - Rifampin -- administration & dosage KW - Antitubercular Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681266550?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+agents+and+chemotherapy&rft.atitle=Novel+dosing+strategies+increase+exposures+of+the+potent+antituberculosis+drug+rifapentine+but+are+poorly+tolerated+in+healthy+volunteers.&rft.au=Dooley%2C+Kelly+E%3BSavic%2C+Radojka+M%3BPark%2C+Jeong-Gun%3BCramer%2C+Yoninah%3BHafner%2C+Richard%3BHogg%2C+Evelyn%3BJanik%2C+Jennifer%3BMarzinke%2C+Mark+A%3BPatterson%2C+Kristine%3BBenson%2C+Constance+A%3BHovind%2C+Laura%3BDorman%2C+Susan+E%3BHaas%2C+David+W%3BACTG+A5311+Study+Team&rft.aulast=Dooley&rft.aufirst=Kelly&rft.date=2015-01-01&rft.volume=59&rft.issue=6&rft.spage=3399&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+agents+and+chemotherapy&rft.issn=1098-6596&rft_id=info:doi/10.1128%2FAAC.05128-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-16 N1 - Date created - 2015-05-15 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01574638; ClinicalTrials.gov N1 - SuppNotes - Cited By: Medicine (Baltimore). 1999 Nov;78(6):361-9 [10575418] Antimicrob Agents Chemother. 2012 Aug;56(8):4331-40 [22664964] MMWR Morb Mortal Wkly Rep. 2003 Aug 8;52(31):735-9 [12904741] Rev Infect Dis. 1983 Jul-Aug;5 Suppl 3:S440-50 [6356277] Clin Pharmacol Ther. 2005 Oct;78(4):342-50 [16198653] Antimicrob Agents Chemother. 2007 Aug;51(8):2994-6 [17517849] PLoS Med. 2007 Dec;4(12):e344 [18092886] Antimicrob Agents Chemother. 2010 Aug;54(8):3390-4 [20516273] Am J Respir Crit Care Med. 2011 May 1;183(9):1254-61 [21330452] Int J Tuberc Lung Dis. 2011 Aug;15(8):1133 [21740683] Antimicrob Agents Chemother. 2011 Sep;55(9):4122-7 [21709081] J Infect Dis. 2012 Oct 1;206(7):1030-40 [22850121] Lancet Infect Dis. 2013 Jan;13(1):27-35 [23103177] Int J Tuberc Lung Dis. 2013 May;17(5):590-6 [23575322] Antimicrob Agents Chemother. 2014 Jun;58(6):3035-42 [24614383] Antimicrob Agents Chemother. 2003 Jul;47(7):2118-24 [12821456] N Engl J Med. 2011 Dec 8;365(23):2155-66 [22150035] Clin Pharmacol Ther. 2012 May;91(5):881-8 [22472995] Am J Respir Crit Care Med. 2015 Feb 1;191(3):333-43 [25489785] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/AAC.05128-14 ER - TY - JOUR T1 - Inositol pyrophosphates: Why so many phosphates? AN - 1680451541; PQ0001535628 AB - The inositol pyrophosphates (PP-InsPs) are a specialized group of "energetic" signaling molecules found in yeasts, plants and animals. PP-InsPs boast the most crowded three dimensional phosphate arrays found in Nature; multiple phosphates and diphosphates are crammed around the six-carbon, inositol ring. Yet, phosphate esters are also a major energy currency in cells. So the synthesis of PP-InsPs, and the maintenance of their levels in the face of a high rate of ongoing turnover, all requires significant bioenergetic input. What are the particular properties of PP-InsPs that repay this investment of cellular energy? Potential answers to that question are discussed here, against the backdrop of a recent hypothesis that signaling by PP-InsPs is evolutionarily ancient. The latter idea is extended herein, with the proposal that the primordial origins of PP-InsPs is reflected in the apparent lack of isomeric specificity of certain of their actions. Nevertheless, there are other aspects of signaling by these polyphosphates that are more selective for a particular PP-InsP isomer. Consideration of the nature of both specific and non-specific effects of PP-InsPs can help rationalize why such molecules possess so many phosphates. JF - Advances in Biological Regulation AU - Shears, Stephen B AD - Inositol Signaling Group, Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, NIH, DHHS, PO Box 12233, Research Triangle Park, NC 27709, USA, Shears@niehs.nih.gov Y1 - 2015 PY - 2015 DA - 2015 SP - 203 EP - 216 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 57 SN - 2212-4926, 2212-4926 KW - Biotechnology and Bioengineering Abstracts KW - Inositol pyrophosphates KW - Structure KW - Analogs KW - Diphosphoinositol polyphosphates KW - Cell-signaling KW - Kinase KW - Phosphorylation KW - Phosphate KW - Bioenergetics KW - Energy KW - Inositol KW - polyphosphates KW - Esters KW - pyrophosphates KW - Evolution KW - Isomers KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680451541?accountid=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=Advances+in+Biological+Regulation&rft.atitle=Inositol+pyrophosphates%3A+Why+so+many+phosphates%3F&rft.au=Shears%2C+Stephen+B&rft.aulast=Shears&rft.aufirst=Stephen&rft.date=2015-01-01&rft.volume=57&rft.issue=&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Advances+in+Biological+Regulation&rft.issn=22124926&rft_id=info:doi/10.1016%2Fj.jbior.2014.09.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Phosphate; Bioenergetics; Energy; polyphosphates; Inositol; Esters; Evolution; pyrophosphates; Isomers DO - http://dx.doi.org/10.1016/j.jbior.2014.09.015 ER - TY - JOUR T1 - Molecular mechanism behind the synergistic activity of diphenylmethyl selenocyanate and Cisplatin against murine tumor model. AN - 1677894407; 25584690 AB - Various preclinical, clinical and epidemiological studies have already well established the cancer chemopreventive and chemoprotective potential of selenium compounds. In addition to its protective efficacy, recent studies have also proved the abilities of selenium compounds to induce cell death specifically in malignant cells. Therefore, our intention is to improve the therapeutic efficacy of an alkylating agent, cisplatin, by the adjuvant use of an organoselenium compound, diphenylmethyl selenocyanate (DMSE). It was observed that combined treatment decreased the tumor burden significantly through reactive oxygen species generation and modulation of antioxidant and detoxifying enzyme system in tumor cells. These activities ultimately led to significant DNA damage and apoptosis in tumor cells. Study of the molecular pathway disclosed that the adjuvant treatment caused induction of p53, Bax and suppressed Bcl-2 followed by the activation of caspase cascade. Furthermore, a concomitant decrease in cisplatin-induced nephrotoxicity and hematopoietic toxicity by DMSE might also have enhanced the efficacy of cisplatin and provided survival advantage to the host. Results suggested that the combination treatment with DMSE and cisplatin may offer potential therapeutic benefit, and utilization of cisplatin in cancer chemotherapy exempt of its limitations. JF - Anti-cancer agents in medicinal chemistry AU - Chakraborty, Pramita AU - Roy, Somnath Singha AU - Bhattacharya, Sudin AD - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37- S. P. Mukherjee Road, Kolkata-700026, India. sudinb19572004@yahoo.co.in. Y1 - 2015 PY - 2015 DA - 2015 SP - 501 EP - 510 VL - 15 IS - 4 KW - Antineoplastic Agents KW - 0 KW - Organoselenium Compounds KW - Proto-Oncogene Proteins c-bcl-2 KW - Reactive Oxygen Species KW - Tumor Suppressor Protein p53 KW - diphenylmethyl selenocyanate KW - Caspases KW - EC 3.4.22.- KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Apoptosis KW - Enzyme Activation KW - DNA Damage KW - Proto-Oncogene Proteins c-bcl-2 -- metabolism KW - Tumor Burden KW - Mice KW - Drug Synergism KW - Tumor Suppressor Protein p53 -- metabolism KW - Male KW - Caspases -- metabolism KW - Organoselenium Compounds -- pharmacology KW - Cisplatin -- therapeutic use KW - Organoselenium Compounds -- therapeutic use KW - Carcinoma, Ehrlich Tumor -- pathology KW - Carcinoma, Ehrlich Tumor -- drug therapy KW - Cisplatin -- pharmacology KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1677894407?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anti-cancer+agents+in+medicinal+chemistry&rft.atitle=Molecular+mechanism+behind+the+synergistic+activity+of+diphenylmethyl+selenocyanate+and+Cisplatin+against+murine+tumor+model.&rft.au=Chakraborty%2C+Pramita%3BRoy%2C+Somnath+Singha%3BBhattacharya%2C+Sudin&rft.aulast=Chakraborty&rft.aufirst=Pramita&rft.date=2015-01-01&rft.volume=15&rft.issue=4&rft.spage=501&rft.isbn=&rft.btitle=&rft.title=Anti-cancer+agents+in+medicinal+chemistry&rft.issn=1875-5992&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-21 N1 - Date created - 2015-05-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Targeting the HIV RNA genome: high-hanging fruit only needs a longer ladder. AN - 1675876016; 25735922 AB - Small molecules targeting the enzymes responsible for human immunodeficiency virus (HIV) maturation, DNA synthesis and its subsequent chromosomal integration as ribonucleotide-free double-stranded DNA remain the mainstay of combination antiretroviral therapy. For infected individuals harboring drug-susceptible virus, this approach has afforded complete or near-complete viral suppression. However, in the absence of a curative strategy, the predictable emergence of drug-resistant variants requires continued development of improved antiviral strategies, inherent to which is the necessity of identifying novel targets. Regulatory elementsRegulatory elements that mediate transcription, translation, nucleocytoplasmic transport, dimerization, packaging and reverse transcription of the (+) strand RNA genomeRNA genome should now be considered viable targets for small molecule, peptide- and oligonucleotide-based therapeuticsTherapeutics . Where target specificity and cellular penetration and toxicity have been the primary obstacle to successful "macromolecule therapeutics", this chapter summarizes (a) novel approaches targeting RNA motifs whose three-dimensional structure is critical for biological function and consequently may be less prone to resistance-conferring mutations and (b) improved methods for deliveryDelivery . JF - Current topics in microbiology and immunology AU - Le Grice, Stuart F J AD - RT Biochemistry Section, Basic Research Laboratory, National Cancer Institute, Frederick, MD, 21702, USA, legrices@mail.nih.gov. Y1 - 2015 PY - 2015 DA - 2015 SP - 147 EP - 169 VL - 389 SN - 0070-217X, 0070-217X KW - Anti-HIV Agents KW - 0 KW - DNA, Viral KW - RNA, Viral KW - Viral Proteins KW - Index Medicus KW - Virus Assembly KW - HIV Long Terminal Repeat KW - DNA, Viral -- biosynthesis KW - Virus Replication -- drug effects KW - Active Transport, Cell Nucleus -- drug effects KW - Humans KW - Viral Proteins -- biosynthesis KW - Reverse Transcription -- drug effects KW - Genome, Viral -- drug effects KW - Anti-HIV Agents -- pharmacology KW - RNA, Viral -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1675876016?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+topics+in+microbiology+and+immunology&rft.atitle=Targeting+the+HIV+RNA+genome%3A+high-hanging+fruit+only+needs+a+longer+ladder.&rft.au=Le+Grice%2C+Stuart+F+J&rft.aulast=Le+Grice&rft.aufirst=Stuart+F&rft.date=2015-01-01&rft.volume=389&rft.issue=&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=Current+topics+in+microbiology+and+immunology&rft.issn=0070217X&rft_id=info:doi/10.1007%2F82_2015_434 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-09 N1 - Date created - 2015-04-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/82_2015_434 ER - TY - JOUR T1 - Is Visual Registration Equivalent to Semiautomated Registration in Prostate Biopsy? AN - 1668253471; PQ0001292482 AB - In magnetic resonance iimaging- (MRI-) ultrasound (US) guided biopsy, suspicious lesions are identified on MRI, registered on US, and targeted during biopsy. The registration can be performed either by a human operator (visual registration) or by fusion software. Previous studies showed that software registration is fairly accurate in locating suspicious lesions and helps to improve the cancer detection rate. Here, the performance of visual registration was examined for ability to locate suspicious lesions defined on MRI. This study consists of 45 patients. Two operators with differing levels of experience (<1 and 18 years) performed visual registration. The overall spatial difference by the two operators in 72 measurements was 10.6 plus or minus 6.0 mm. Each operator showed a spatial difference of 9.4 plus or minus 5.1 mm (experienced; 39 lesions) and 12.1 plus or minus 6.6 mm (inexperienced; 33 lesions), respectively. In a head-to-head comparison of the same 16 lesions from 12 patients, the spatial differences were 9.7 mm plus or minus 4.9 mm (experienced) and 13.4 mm plus or minus 7.4 mm (inexperienced). There were significant differences between the two operators (unpaired, P value = 0.042; paired, P value = 0.044). The substantial differences by the two operators suggest that visual registration could improperly and inaccurately target many tumors, thereby potentially leading to missed diagnosis or false characterization on pathology. JF - BioMed Research International AU - Kwak, Jin Tae AU - Hong, Cheng William AU - Pinto, Peter A AU - Williams, Molly AU - Xu, Sheng AU - Kruecker, Jochen AU - Yan, Pingkun AU - Turkbey, Baris AU - Choyke, Peter L AU - Wood, Bradford J AD - Center for Interventional Oncology, National Institutes of Health Clinical Center, Bethesda, MD 20892, USA, bwood@cc.nih.gov Y1 - 2015/01// PY - 2015 DA - Jan 2015 PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States VL - 2015 SN - 2314-6133, 2314-6133 KW - Biotechnology and Bioengineering Abstracts KW - Computer programs KW - software KW - Magnetic resonance imaging KW - Biopsy KW - N.M.R. KW - Tumors KW - Ultrasound KW - Prostate KW - Cancer KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668253471?accountid=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=BioMed+Research+International&rft.atitle=Is+Visual+Registration+Equivalent+to+Semiautomated+Registration+in+Prostate+Biopsy%3F&rft.au=Kwak%2C+Jin+Tae%3BHong%2C+Cheng+William%3BPinto%2C+Peter+A%3BWilliams%2C+Molly%3BXu%2C+Sheng%3BKruecker%2C+Jochen%3BYan%2C+Pingkun%3BTurkbey%2C+Baris%3BChoyke%2C+Peter+L%3BWood%2C+Bradford+J&rft.aulast=Kwak&rft.aufirst=Jin&rft.date=2015-01-01&rft.volume=2015&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=BioMed+Research+International&rft.issn=23146133&rft_id=info:doi/10.1155%2F2015%2F394742 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Computer programs; software; Magnetic resonance imaging; N.M.R.; Biopsy; Tumors; Prostate; Ultrasound; Cancer DO - http://dx.doi.org/10.1155/2015/394742 ER - TY - JOUR T1 - Measuring Outcome Expectancy Value of Leisure-Time Physical Activity for African Americans AN - 1665150732 AB - A scale was adapted from existing scales to measure the outcome expectancy value (EV) as one of contributory factors to leisure-time physical activity (LTPA) and was administered to 649 African American adults. The eligible participants (N = 569) for the analysis were split into three subsamples (rate = 0.5 : 0.25 : 0.25) respectively for Exploratory Factor Analysis (N = 285) and cross-validation (N = 142 for the calibration group and N = 142 for the validation group) to evaluate the psychometric properties of the scale. Item analysis of the scale provided adequate psychometric properties. The 2-factor solution with positive and negative outcome EV subscales was supported based on the exploratory factor analysis and the multiple-group confirmatory factor analysis for both the calibration and validation samples. The results support the factorial construct validity and criterion validity of the outcome EV scale applied to assess LTPA in a sample of church-going African Americans. JF - Behavioral Medicine AU - Li, Kaigang AU - Seo, Dong-Chul AU - Torabi, Mohammad R AD - National Institute of Child Health and Human Development, Ewha Womans University, College of Health Sciences, Indiana University School of Public Health-Bloomington ; National Institute of Child Health and Human Development; Ewha Womans University, College of Health Sciences; Indiana University School of Public Health-Bloomington Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 33 EP - 39 CY - Washington PB - Taylor & Francis Ltd. VL - 41 IS - 1 SN - 0896-4289 KW - Psychology KW - American people KW - Analysis KW - Leisure activities KW - Time use KW - Black American people KW - Confirmatory factor analysis KW - Construct validity KW - Exploratory factor analysis KW - Factor analysis KW - Leisure KW - Physical activity KW - Psychometric properties KW - Validation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665150732?accountid=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=Behavioral+Medicine&rft.atitle=Measuring+Outcome+Expectancy+Value+of+Leisure-Time+Physical+Activity+for+African+Americans&rft.au=Li%2C+Kaigang%3BSeo%2C+Dong-Chul%3BTorabi%2C+Mohammad+R&rft.aulast=Li&rft.aufirst=Kaigang&rft.date=2015-01-01&rft.volume=41&rft.issue=1&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Behavioral+Medicine&rft.issn=08964289&rft_id=info:doi/10.1080%2F08964289.2014.881775 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1080/08964289.2014.881775 ER - TY - JOUR T1 - Intramuscular delivery of heterodimeric IL-15 DNA in macaques produces systemic levels of bioactive cytokine inducing proliferation of NK and T cells AN - 1664207399; PQ0001182263 AB - Interleukin-15 (IL-15) is a common gamma -chain cytokine that has a significant role in the activation and proliferation of T and NK cells and holds great potential in fighting infection and cancer. We have previously shown that bioactive IL-15 in vivo comprises a complex of the IL-15 chain with the soluble or cell-associated IL-15 receptor alpha (IL-15R alpha ) chain, which together form the IL-15 heterodimer. We have generated DNA vectors expressing the heterodimeric IL-15 by optimizing mRNA expression and protein trafficking. Repeated administration of these DNA plasmids by intramuscular injection followed by in vivo electroporation in rhesus macaques resulted in sustained high levels of IL-15 in plasma, with no significant toxicity. Administration of DNAs expressing heterodimeric IL-15 also resulted in an increased frequency of NK and T cells undergoing proliferation in peripheral blood. Heterodimeric IL-15 led to preferential expansion of CD8 super(+)NK cells, all memory CD8 super(+) T-cell subsets and effector memory CD4 super(+) T cells. Expression of heterodimeric IL-15 by DNA delivery to the muscle is an efficient procedure to obtain high systemic levels of bioactive cytokine, without the toxicity linked to the high transient cytokine peak associated with protein injection. JF - Gene Therapy AU - Bergamaschi, C AU - Kulkarni, V AU - Rosati, M AU - Alicea, C AU - Jalah, R AU - Chen, S AU - Bear, J AU - Sardesai, N Y AU - Valentin, A AU - Felber, B K AU - Pavlakis, G N AD - Human Retrovirus Pathogenesis Section, Vaccine Branch, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, USA Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 76 EP - 86 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 22 IS - 1 SN - 0969-7128, 0969-7128 KW - Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Protein transport KW - Interleukin 15 receptors KW - Gene therapy KW - Electroporation KW - Immunological memory KW - Memory cells KW - Natural killer cells KW - Muscles KW - Peripheral blood KW - Toxicity KW - CD8 antigen KW - Infection KW - Plasmids KW - Cancer KW - Gene expression KW - Expression vectors KW - CD4 antigen KW - Interleukin 15 KW - Lymphocytes T KW - DNA KW - Macaca mulatta KW - Cell proliferation KW - G 07720:Immunogenetics KW - W 30905:Medical Applications KW - N 14810:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664207399?accountid=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=Intramuscular+delivery+of+heterodimeric+IL-15+DNA+in+macaques+produces+systemic+levels+of+bioactive+cytokine+inducing+proliferation+of+NK+and+T+cells&rft.au=Bergamaschi%2C+C%3BKulkarni%2C+V%3BRosati%2C+M%3BAlicea%2C+C%3BJalah%2C+R%3BChen%2C+S%3BBear%2C+J%3BSardesai%2C+N+Y%3BValentin%2C+A%3BFelber%2C+B+K%3BPavlakis%2C+G+N&rft.aulast=Bergamaschi&rft.aufirst=C&rft.date=2015-01-01&rft.volume=22&rft.issue=1&rft.spage=76&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2014.84 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Protein transport; Interleukin 15 receptors; Electroporation; Gene therapy; Muscles; Natural killer cells; Memory cells; Immunological memory; Peripheral blood; CD8 antigen; Toxicity; Plasmids; Infection; Cancer; Expression vectors; Gene expression; CD4 antigen; Interleukin 15; DNA; Lymphocytes T; Cell proliferation; Macaca mulatta DO - http://dx.doi.org/10.1038/gt.2014.84 ER - TY - JOUR T1 - Primary mediastinal B-cell lymphoma and mediastinal gray zone lymphoma: do they require a unique therapeutic approach? AN - 1657315530; 25499450 AB - Primary mediastinal B-cell lymphoma (PMBL) is a subtype of diffuse large B-cell lymphoma (DLBCL) that is putatively derived from a thymic B cell. Accounting for up to 10% of cases of DLBCL, this subtype predominantly affects women in the third and fourth decades of life. Its clinical and molecular characteristics are distinct from other subtypes of DLBCL and, in fact, closely resemble those of nodular sclerosing Hodgkin lymphoma (NSHL). Recently, mediastinal lymphomas with features intermediate between PMBL and NSHL, called mediastinal gray-zone lymphomas, have been described. The optimal management of PMBL is controversial, and most standard approaches include a combination of immunochemotherapy and mediastinal radiation. Recently, the recognition that mediastinal radiation is associated with significant long-term toxicities has led to the development of novel approaches for PMBL that have shown excellent efficacy and challenge the need for routine mediastinal radiation. JF - Blood AU - Dunleavy, Kieron AU - Wilson, Wyndham H AD - Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD. Y1 - 2015/01/01/ PY - 2015 DA - 2015 Jan 01 SP - 33 EP - 39 VL - 125 IS - 1 KW - Antibodies, Monoclonal, Murine-Derived KW - 0 KW - Fluorodeoxyglucose F18 KW - 0Z5B2CJX4D KW - Rituximab KW - 4F4X42SYQ6 KW - Abridged Index Medicus KW - Index Medicus KW - Positron-Emission Tomography KW - B-Lymphocytes -- cytology KW - Fluorodeoxyglucose F18 -- chemistry KW - Humans KW - Decision Making KW - Hodgkin Disease -- therapy KW - Recurrence KW - Mediastinum -- radiation effects KW - Immunotherapy -- methods KW - Gene Expression Profiling KW - Antibodies, Monoclonal, Murine-Derived -- therapeutic use KW - Treatment Outcome KW - Drug Therapy -- methods KW - Lymphoma -- metabolism KW - Immunophenotyping KW - Male KW - Female KW - Lymphoma, B-Cell -- therapy KW - Mediastinal Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1657315530?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Primary+mediastinal+B-cell+lymphoma+and+mediastinal+gray+zone+lymphoma%3A+do+they+require+a+unique+therapeutic+approach%3F&rft.au=Dunleavy%2C+Kieron%3BWilson%2C+Wyndham+H&rft.aulast=Dunleavy&rft.aufirst=Kieron&rft.date=2015-01-01&rft.volume=125&rft.issue=1&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=1528-0020&rft_id=info:doi/10.1182%2Fblood-2014-05-575092 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-13 N1 - Date created - 2015-01-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Haematol. 2005 Sep;130(5):691-9 [16115124] Histopathology. 2005 Jul;47(1):101-10 [15982329] Ann Oncol. 2006 Jan;17(1):123-30 [16236753] Clin Cancer Res. 2008 May 15;14(10):3044-51 [18483370] J Clin Oncol. 2008 Jun 1;26(16):2717-24 [18378569] J Clin Oncol. 2010 Mar 1;28(7):1232-9 [20124178] Int J Surg Pathol. 2010 Apr;18(2):121-8 [19223373] Blood. 2010 Oct 28;116(17):3268-77 [20628145] Cancer Cell. 2010 Dec 14;18(6):590-605 [21156283] Blood. 2011 Feb 10;117(6):1806-16 [21037086] Ann Oncol. 2011 Mar;22(3):664-70 [20724576] Haematologica. 2011 Apr;96(4):558-66 [21454882] Mod Pathol. 2011 Dec;24(12):1586-97 [21822207] Curr Hematol Malig Rep. 2012 Sep;7(3):241-7 [22833351] Clin Cancer Res. 2012 Nov 1;18(21):5845-9 [22962441] N Engl J Med. 2013 Apr 11;368(15):1408-16 [23574119] N Engl J Med. 2013 Jul 18;369(3):282 [23863060] Oncotarget. 2013 Jul;4(7):1093-102 [23852366] Leuk Lymphoma. 2014 Mar;55(3):538-43 [23734654] Blood. 2014 Mar 27;123(13):2062-5 [24497532] Nat Genet. 2014 Apr;46(4):329-35 [24531327] Clin Cancer Res. 2014 May 15;20(10):2674-83 [24610827] J Clin Oncol. 2014 Jun 10;32(17):1769-75 [24799481] Ann Hematol. 2014 Aug;93(8):1297-304 [24595734] Blood. 2014 Sep 4;124(10):1563-9 [25024303] Blood. 1999 Nov 15;94(10):3289-93 [10552937] Am J Surg Pathol. 2001 Mar;25(3):297-306 [11224599] N Engl J Med. 2002 Jan 24;346(4):235-42 [11807147] Haematologica. 2002 Dec;87(12):1258-64 [12495899] Am J Pathol. 2003 Jan;162(1):243-53 [12507907] J Exp Med. 2003 Sep 15;198(6):851-62 [12975453] Blood. 2003 Dec 1;102(12):3871-9 [12933571] Br J Cancer. 2004 Jan 26;90(2):372-6 [14735179] Leuk Lymphoma. 2003;44 Suppl 3:S21-6 [15202521] Blood. 2004 Jul 15;104(2):543-9 [15044251] Blood. 1987 Apr;69(4):1087-95 [3103712] Am J Pathol. 1991 Sep;139(3):475-83 [1716042] Am J Pathol. 1991 Oct;139(4):701-7 [1656757] N Engl J Med. 1993 Apr 8;328(14):1002-6 [7680764] J Clin Oncol. 1993 Aug;11(8):1573-82 [7687667] N Engl J Med. 1993 Sep 30;329(14):987-94 [8141877] Blood. 1996 Feb 15;87(4):1571-8 [8608249] J Clin Oncol. 1998 Jan;16(1):63-9 [9440724] Blood. 1998 Feb 15;91(4):1178-84 [9454747] Histopathology. 2004 Dec;45(6):619-24 [15569053] Blood. 2005 Mar 15;105(6):2535-42 [15572583] Am J Surg Pathol. 2005 Nov;29(11):1411-21 [16224207] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1182/blood-2014-05-575092 ER - TY - JOUR T1 - Successful Protection against Tularemia in C57BL/6 Mice Is Correlated with Expansion of Francisella tularensis-Specific Effector T Cells AN - 1654694323; 21328243 AB - Francisella tularensis is an intracellular, Gram-negative bacterium that causes the fatal disease tularemia. Currently, there are no licensed vaccines for tularemia and the requirements for protection against infection are poorly defined. To identify correlates of vaccine-induced immunity against tularemia, we compared different strains of the live vaccine strain (LVS) for their relative levels of virulence and ability to protect C57BL/6 mice against challenge with virulent F. tularensis strain SchuS4. Successful vaccination, as defined by survival of C57BL/6 mice, was correlated with significantly greater numbers of effector T cells in the spleen and lung. Further, lung cells and splenocytes from fully protected animals were more effective than lung cells and splenocytes from vaccinated but nonimmune animals in limiting intracellular replication of SchuS4 in vitro. Together, our data provide a unique model to compare efficacious vaccines to nonefficacious vaccines, which will enable comprehensive identification of host and bacterial components required for immunization against tularemia. JF - Clinical and Vaccine Immunology AU - Griffin, Amanda J AU - Crane, Deborah D AU - Wehrly, Tara D AU - Bosio, Catharine M Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 119 EP - 128 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 22 IS - 1 SN - 1556-6811, 1556-6811 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Cell survival KW - Data processing KW - Replication KW - Animal models KW - Spleen KW - Francisella tularensis KW - Infection KW - Effector cells KW - Virulence KW - Splenocytes KW - Tularemia KW - Lung KW - Lymphocytes T KW - Vaccines KW - F 06905:Vaccines KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654694323?accountid=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=Clinical+and+Vaccine+Immunology&rft.atitle=Successful+Protection+against+Tularemia+in+C57BL%2F6+Mice+Is+Correlated+with+Expansion+of+Francisella+tularensis-Specific+Effector+T+Cells&rft.au=Griffin%2C+Amanda+J%3BCrane%2C+Deborah+D%3BWehrly%2C+Tara+D%3BBosio%2C+Catharine+M&rft.aulast=Griffin&rft.aufirst=Amanda&rft.date=2015-01-01&rft.volume=22&rft.issue=1&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=15566811&rft_id=info:doi/10.1128%2FCVI.00648-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Number of references - 43 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Cell survival; Data processing; Replication; Animal models; Spleen; Infection; Effector cells; Virulence; Splenocytes; Tularemia; Lung; Lymphocytes T; Vaccines; Francisella tularensis DO - http://dx.doi.org/10.1128/CVI.00648-14 ER - TY - JOUR T1 - The role of the microbiota in inflammation, carcinogenesis, and cancer therapy AN - 1654692061; 21333270 AB - Commensal microorganisms colonize barrier surfaces of all multicellular organisms, including those of humans. For more than 500 million years, commensal microorganisms and their hosts have coevolved and adapted to each other. As a result, the commensal microbiota affects many immune and nonimmune functions of their hosts, and de facto the two together comprise one metaorganism. The commensal microbiota communicates with the host via biologically active molecules. Recently, it has been reported that microbial imbalance may play a critical role in the development of multiple diseases, such as cancer, autoimmune conditions, and increased susceptibility to infection. In this review, we focus on the role of the commensal microbiota in the development, progression, and immune evasion of cancer, as well as some modulatory effects on the treatment of cancer. In particular, we discuss the mechanisms of microbiota-mediated regulation of innate and adaptive immune responses to tumors, and the consequences on cancer progression and whether tumors subsequently become resistant or susceptible to different anticancer therapeutic regiments. JF - European Journal of Immunology AU - Dzutsev, Amiran AU - Goldszmid, Romina S AU - Viaud, Sophie AU - Zitvogel, Laurence AU - Trinchieri, Giorgio AD - Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD, USA. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 17 EP - 31 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 45 IS - 1 SN - 0014-2980, 0014-2980 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Immunology Abstracts KW - Carcinogenesis KW - Autoimmune diseases KW - Commensals KW - Microorganisms KW - Tumors KW - Immune response KW - Infection KW - Cancer KW - Inflammation KW - A 01340:Antibiotics & Antimicrobials KW - F 06915:Cancer Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654692061?accountid=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=European+Journal+of+Immunology&rft.atitle=The+role+of+the+microbiota+in+inflammation%2C+carcinogenesis%2C+and+cancer+therapy&rft.au=Dzutsev%2C+Amiran%3BGoldszmid%2C+Romina+S%3BViaud%2C+Sophie%3BZitvogel%2C+Laurence%3BTrinchieri%2C+Giorgio&rft.aulast=Dzutsev&rft.aufirst=Amiran&rft.date=2015-01-01&rft.volume=45&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Immunology&rft.issn=00142980&rft_id=info:doi/10.1002%2Feji.201444972 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Autoimmune diseases; Carcinogenesis; Microorganisms; Commensals; Immune response; Tumors; Infection; Cancer; Inflammation DO - http://dx.doi.org/10.1002/eji.201444972 ER - TY - JOUR T1 - Estimates of benefits and harms of prophylactic use of aspirin in the general population. AN - 1652449494; 25096604 AB - Accumulating evidence supports an effect of aspirin in reducing overall cancer incidence and mortality in the general population. We reviewed current data and assessed the benefits and harms of prophylactic use of aspirin in the general population. The effect of aspirin for site-specific cancer incidence and mortality, cardiovascular events was collated from the most recent systematic reviews. Studies identified through systematic Medline search provided data regarding harmful effects of aspirin and baseline rates of harms like gastrointestinal bleeding and peptic ulcer. The effects of aspirin on cancer are not apparent until at least 3 years after the start of use, and some benefits are sustained for several years after cessation in long-term users. No differences between low and standard doses of aspirin are observed, but there were no direct comparisons. Higher doses do not appear to confer additional benefit but increase toxicities. Excess bleeding is the most important harm associated with aspirin use, and its risk and fatality rate increases with age. For average-risk individuals aged 50-65 years taking aspirin for 10 years, there would be a relative reduction of between 7% (women) and 9% (men) in the number of cancer, myocardial infarction or stroke events over a 15-year period and an overall 4% relative reduction in all deaths over a 20-year period. Prophylactic aspirin use for a minimum of 5 years at doses between 75 and 325 mg/day appears to have favourable benefit-harm profile; longer use is likely to have greater benefits. Further research is needed to determine the optimum dose and duration of use, to identify individuals at increased risk of bleeding, and to test effectiveness of Helicobacter pylori screening-eradication before starting aspirin prophylaxis. © The Author 2014. Published by Oxford University Press on behalf of the European Society for Medical Oncology. JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Cuzick, J AU - Thorat, M A AU - Bosetti, C AU - Brown, P H AU - Burn, J AU - Cook, N R AU - Ford, L G AU - Jacobs, E J AU - Jankowski, J A AU - La Vecchia, C AU - Law, M AU - Meyskens, F AU - Rothwell, P M AU - Senn, H J AU - Umar, A AD - Centre for Cancer Prevention, Wolfson Institute of Preventive Medicine, Queen Mary University of London, London, UK j.cuzick@qmul.ac.uk. ; Centre for Cancer Prevention, Wolfson Institute of Preventive Medicine, Queen Mary University of London, London, UK. ; Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy. ; Department of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, USA. ; Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK. ; Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston. ; Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda. ; Epidemiology Research Program, American Cancer Society, Atlanta, USA. ; Centre for Biomedical Research-Translational and Stratified Medicine, Peninsula Schools of Medicine and Dentistry, Plymouth University, Plymouth Centre for Digestive Diseases, Blizard Institute of Cell and Molecular Science, Queen Mary University of London, London, UK. ; Department of Epidemiology, IRCCS-Istituto di Ricerche Farmacologiche 'Mario Negri', Milan, Italy Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy. ; Centre for Environmental and Preventive Medicine, Wolfson Institute of Preventive Medicine, Queen Mary University of London, London, UK. ; Chao Family Comprehensive Cancer Center, University of California, Irvine, Irvine, USA. ; Stroke Prevention Research Unit, Nuffield Department of Clinical Neuroscience, University of Oxford, Oxford, UK. ; Tumor and Breast Center ZeTuP, St Gallen, Switzerland. ; Gastrointestinal and Other Cancers Research Group, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, USA. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 47 EP - 57 VL - 26 IS - 1 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Aspirin KW - R16CO5Y76E KW - Index Medicus KW - aspirin KW - benefit-harm KW - cardiovascular disease KW - prevention KW - gastrointestinal bleeding KW - cancer KW - Anti-Inflammatory Agents, Non-Steroidal -- therapeutic use KW - Humans KW - Anti-Inflammatory Agents, Non-Steroidal -- adverse effects KW - Gastrointestinal Hemorrhage -- chemically induced KW - Male KW - Female KW - Aspirin -- adverse effects KW - Aspirin -- therapeutic use KW - Neoplasms -- prevention & control KW - Stroke -- prevention & control KW - Myocardial Infarction -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652449494?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Estimates+of+benefits+and+harms+of+prophylactic+use+of+aspirin+in+the+general+population.&rft.au=Cuzick%2C+J%3BThorat%2C+M+A%3BBosetti%2C+C%3BBrown%2C+P+H%3BBurn%2C+J%3BCook%2C+N+R%3BFord%2C+L+G%3BJacobs%2C+E+J%3BJankowski%2C+J+A%3BLa+Vecchia%2C+C%3BLaw%2C+M%3BMeyskens%2C+F%3BRothwell%2C+P+M%3BSenn%2C+H+J%3BUmar%2C+A&rft.aulast=Cuzick&rft.aufirst=J&rft.date=2015-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-24 N1 - Date created - 2014-12-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 2004 Apr 7;96(7):524-8 [15069114] Health Technol Assess. 2003;7(31):1-94 [14604498] Anticancer Res. 2004 Sep-Oct;24(5B):3177-84 [15510608] N Engl J Med. 1989 Jul 20;321(3):129-35 [2664509] Cancer Res. 1993 Mar 15;53(6):1322-7 [8443812] J Natl Cancer Inst. 1993 Aug 4;85(15):1220-4 [8331682] Lancet. 1996 Jul 20;348(9021):150-4 [8684154] Lancet. 1997 Oct 4;350(9083):975-9 [9329511] JAMA. 2005 Jul 6;294(1):47-55 [15998890] N Engl J Med. 2005 Dec 1;353(22):2373-83 [16319386] BMJ. 2005 Dec 3;331(7528):1310-6 [16322018] Clin Gastroenterol Hepatol. 2006 Feb;4(2):130-42 [16469671] Ann Intern Med. 2006 Mar 7;144(5):326-36 [16520473] Ann Intern Med. 2007 Mar 6;146(5):361-4 [17339621] Arch Intern Med. 2007 Mar 26;167(6):562-72 [17389287] Lancet. 2007 May 12;369(9573):1603-13 [17499602] Gastroenterology. 2008 Jan;134(1):21-8 [18005960] Circulation. 2008 Jun 3;117(22):2875-83 [18506010] N Engl J Med. 2008 Dec 11;359(24):2567-78 [19073976] J Natl Cancer Inst. 2009 Feb 18;101(4):256-66 [19211452] Ann Intern Med. 2009 Mar 17;150(6):396-404 [19293072] Lancet Oncol. 2009 May;10(5):501-7 [19410194] Lancet. 2009 May 30;373(9678):1849-60 [19482214] JAMA. 2009 Aug 12;302(6):649-58 [19671906] Aliment Pharmacol Ther. 2009 Nov 15;30(10):1039-48 [19709097] N Engl J Med. 2010 Jun 10;362(23):2155-65 [20558366] Lancet. 2010 Nov 20;376(9754):1741-50 [20970847] Lancet. 2011 Jan 1;377(9759):31-41 [21144578] Arch Intern Med. 2011 Feb 14;171(3):218-25 [21325111] Int J Cancer. 2011 May 15;128(10):2444-52 [21128233] Clin Gastroenterol Hepatol. 2011 Sep;9(9):762-768.e6 [21699808] J Natl Cancer Inst. 2012 Aug 22;104(16):1208-17 [22888140] J Natl Cancer Inst. 2004 Jun 2;96(11):885-7; author reply 887 [15173278] Health Technol Assess. 2003;7(6):1-86 [12709294] N Engl J Med. 2003 Mar 6;348(10):891-9 [12621133] Lancet. 2011 Dec 17;378(9809):2081-7 [22036019] Ann Intern Med. 2013 Jul 16;159(2):77-85 [23856681] J Gen Intern Med. 2013 Nov;28(11):1483-91 [23681842] Eur J Epidemiol. 2015 Jan;30(1):5-18 [25421783] Lancet. 2012 Aug 11;380(9841):581-90 [22607822] Am J Gastroenterol. 1999 Nov;94(11):3189-96 [10566713] Lancet. 2002 Jan 5;359(9300):9-13 [11809180] Lancet. 2002 Jan 5;359(9300):14-22 [11809181] Lancet. 2012 Apr 28;379(9826):1602-12 [22440946] J Clin Oncol. 2010 Mar 20;28(9):1467-72 [20159825] Lancet. 2012 Apr 28;379(9826):1591-601 [22440947] Lancet Oncol. 2012 May;13(5):518-27 [22440112] Am J Med. 2012 Jun;125(6):560-7 [22513195] Ann Oncol. 2012 Jun;23(6):1403-15 [22517822] Circulation. 2012 Jan 3;125(1):188-97 [22215894] Br J Cancer. 2003 Mar 10;88(5):684-8 [12618874] Comment In: Ann Oncol. 2015 Feb;26(2):442-3 [25403580] BMJ. 2014;349:g5037 [25098322] Ann Oncol. 2015 Feb;26(2):441-2 [25416686] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/annonc/mdu225 ER - TY - JOUR T1 - The evolving field of kinase inhibitors in thyroid cancer. AN - 1652441542; 25240824 AB - Most of the genetic events implicated in the pathogenesis of thyroid cancer (TC) involve genes with kinase activity. Thus, kinase inhibitors (KIs) are very relevant in this field. KIs are considered the most suitable treatment for patients with iodine-refractory differentiated TC; these patients comprise the subgroup with the poorer prognosis. To date, only sorafenib has been approved for this indication, but promising results have been reported with several other KIs. In particular, lenvatinib has demonstrated excellent efficacy, with both progression-free survival and objective tumour response being better than with sorafenib. Despite being considered to be well tolerated, both sorafenib and lenvatinib have shown a remarkable toxicity, which has led to dose reductions in the majority of patients and to treatment discontinuation in a significant proportion of cases. The role of KIs in differentiated TC may be revolutionised by the finding that selumetinib may restore a clinical response to radioactive iodine (RAI). Vandetanib and cabozantinib have been approved for the treatment of advanced, progressive medullary TC (MTC). Nevertheless, the toxicity of both compounds suggests their selective use in those patients with strong disease progression. Treatment with the mTOR-inhibitor everolimus, alone or in combination with somatostatin analogues, should be studied in metastatic MTC patients with slow progression of disease, these representing the vast majority of patients. KIs did not significantly impact on the clinical features of anaplastic TC (ATC). Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Critical reviews in oncology/hematology AU - Marotta, V AU - Sciammarella, C AU - Vitale, M AU - Colao, A AU - Faggiano, A AD - Department of Clinical Medicine and Surgery, Section of Endocrinology, Federico II University of Naples, Italy. Electronic address: vinc.endo@libero.it. ; Department of Clinical Medicine and Surgery, Section of Endocrinology, Federico II University of Naples, Italy. ; Department of Medicine and Surgery, University of Salerno, Baronissi, Italy. ; Department of Clinical Medicine and Surgery, Section of Endocrinology, Federico II University of Naples, Italy; Endocrinology, National Cancer Institute, Fondazione G. Pascale, Naples, Italy. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 60 EP - 73 VL - 93 IS - 1 KW - Angiogenesis Inhibitors KW - 0 KW - Anilides KW - Antineoplastic Agents KW - Phenylurea Compounds KW - Piperidines KW - Protein Kinase Inhibitors KW - Pyridines KW - Quinazolines KW - Quinolines KW - cabozantinib KW - 1C39JW444G KW - Niacinamide KW - 25X51I8RD4 KW - sorafenib KW - 9ZOQ3TZI87 KW - lenvatinib KW - EE083865G2 KW - N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine KW - YO460OQ37K KW - Index Medicus KW - Kinase inhibitors KW - Cancer therapy KW - Anti-angiogenetic therapy KW - Protein kinases KW - Thyroid cancer KW - Piperidines -- therapeutic use KW - Anilides -- therapeutic use KW - Niacinamide -- therapeutic use KW - Quinolines -- therapeutic use KW - Humans KW - Quinazolines -- therapeutic use KW - Phenylurea Compounds -- therapeutic use KW - Niacinamide -- analogs & derivatives KW - Pyridines -- therapeutic use KW - Angiogenesis Inhibitors -- therapeutic use KW - Protein Kinase Inhibitors -- therapeutic use KW - Thyroid Neoplasms -- drug therapy KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652441542?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Critical+reviews+in+oncology%2Fhematology&rft.atitle=The+evolving+field+of+kinase+inhibitors+in+thyroid+cancer.&rft.au=Marotta%2C+V%3BSciammarella%2C+C%3BVitale%2C+M%3BColao%2C+A%3BFaggiano%2C+A&rft.aulast=Marotta&rft.aufirst=V&rft.date=2015-01-01&rft.volume=93&rft.issue=1&rft.spage=60&rft.isbn=&rft.btitle=&rft.title=Critical+reviews+in+oncology%2Fhematology&rft.issn=1879-0461&rft_id=info:doi/10.1016%2Fj.critrevonc.2014.08.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-29 N1 - Date created - 2014-12-16 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.critrevonc.2014.08.007 ER - TY - JOUR T1 - Nontargeted SWATH acquisition for identifying 47 synthetic cannabinoid metabolites in human urine by liquid chromatography-high-resolution tandem mass spectrometry. AN - 1652427170; 25224637 AB - Clandestine laboratories constantly produce new synthetic cannabinoids to circumvent legislative scheduling efforts, challenging and complicating toxicological analysis. Sundstrom et al. (Anal Bioanal Chem 405(26):8463-8474, [9]) and Kronstrand et al. (Anal Bioanal Chem 406(15):3599-3609, [10]) published nontargeted liquid chromatography, high-resolution, quadrupole/time-of-flight mass spectrometric (LC-QTOF) assays with validated detection of 18 and 38 urinary synthetic cannabinoid metabolites, respectively. We developed and validated a LC-QTOF urine method for simultaneously identifying the most current 47 synthetic cannabinoid metabolites from 21 synthetic cannabinoid families (5-fluoro AB-PINACA, 5-fluoro-AKB48, 5-fluoro PB-22, AB-PINACA, ADB-PINACA, AKB48, AM2201, JWH-018, JWH-019, JWH-073, JWH-081, JWH-122, JWH-200, JWH-210, JWH-250, JWH-398, MAM2201, PB-22, RCS-4, UR-144, and XLR11). β-Glucuronidase-hydrolyzed urine was extracted with 1-mL Biotage SLE+ columns. Specimens were reconstituted in 150-μL mobile phase consisting of 80% A (0.1% formic acid in water) and 20% B (0.1% formic acid in acetonitrile). Fifty microliters was injected, and SWATH™ MS data were acquired in positive electrospray mode. The LC-QTOF instrument consisted of a Shimadzu UFLCxr system and an ABSciex 5600+ TripleTOF® mass spectrometer. Gradient chromatographic separation was achieved with a Restek Ultra Biphenyl column with a 0.5-mL/min flow rate and an overall run time of 15 min. Identification criteria included molecular ion mass error, isotopic profiles, retention time, and library fit criteria. Limits of detection were 0.25-5 μg/L (N = 10 unique fortified urine samples), except for two PB-22 metabolites with limits of 10 and 20 μg/L. Extraction efficiencies and matrix effects (N = 10) were 55-104 and -65-107%, respectively. We present a highly useful novel LC-QTOF method for simultaneously confirming 47 synthetic cannabinoid metabolites in human urine. JF - Analytical and bioanalytical chemistry AU - Scheidweiler, Karl B AU - Jarvis, Michael J Y AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Boulevard Suite 200 Room 05A-721, Baltimore, MD, 21224, USA. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 883 EP - 897 VL - 407 IS - 3 KW - (1-hexyl-1H-indol-3-yl)-1-naphthalenylmethanone KW - 0 KW - (1-pentyl-1H-indol-3-yl)(2,2,3,3-tetramethylcyclopropyl)methanone KW - (4-methyl-1-naphthyl)-(1-pentylindol-3-yl)methanone KW - 1-(1- pentyl-1H-indol-3-yl)-2-(2-methoxyphenyl)ethanone KW - 1-(5-fluoropentyl)-3-(1-naphthoyl)indole KW - 1-pentyl-3-(1-naphthoyl)indole KW - 4-ethylnaphthalen-1-yl-(1-pentylindol-3-yl)methanone KW - Anisoles KW - Cannabinoids KW - Indazoles KW - Indoles KW - JWH-073 KW - N-(1-amino-3,3-dimethyl-1-oxobutan-2-yl)-1-pentyl-1H-indazole-3-carboxamide KW - Naphthalenes KW - Index Medicus KW - Sensitivity and Specificity KW - Indazoles -- urine KW - Signal Processing, Computer-Assisted KW - Indoles -- urine KW - Humans KW - Calibration KW - Anisoles -- urine KW - Naphthalenes -- urine KW - Limit of Detection KW - Hydrolysis KW - Substance Abuse Detection -- methods KW - Chromatography, Liquid -- methods KW - Cannabinoids -- metabolism KW - Tandem Mass Spectrometry -- methods KW - Cannabinoids -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652427170?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+bioanalytical+chemistry&rft.atitle=Nontargeted+SWATH+acquisition+for+identifying+47+synthetic+cannabinoid+metabolites+in+human+urine+by+liquid+chromatography-high-resolution+tandem+mass+spectrometry.&rft.au=Scheidweiler%2C+Karl+B%3BJarvis%2C+Michael+J+Y%3BHuestis%2C+Marilyn+A&rft.aulast=Scheidweiler&rft.aufirst=Karl&rft.date=2015-01-01&rft.volume=407&rft.issue=3&rft.spage=883&rft.isbn=&rft.btitle=&rft.title=Analytical+and+bioanalytical+chemistry&rft.issn=1618-2650&rft_id=info:doi/10.1007%2Fs00216-014-8118-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-02 N1 - Date created - 2015-01-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00216-014-8118-8 ER - TY - JOUR T1 - Recognition and repair of chemically heterogeneous structures at DNA ends. AN - 1652415166; 25111769 AB - Exposure to environmental toxicants and stressors, radiation, pharmaceutical drugs, inflammation, cellular respiration, and routine DNA metabolism all lead to the production of cytotoxic DNA strand breaks. Akin to splintered wood, DNA breaks are not "clean." Rather, DNA breaks typically lack DNA 5'-phosphate and 3'-hydroxyl moieties required for DNA synthesis and DNA ligation. Failure to resolve damage at DNA ends can lead to abnormal DNA replication and repair, and is associated with genomic instability, mutagenesis, neurological disease, ageing and carcinogenesis. An array of chemically heterogeneous DNA termini arises from spontaneously generated DNA single-strand and double-strand breaks (SSBs and DSBs), and also from normal and/or inappropriate DNA metabolism by DNA polymerases, DNA ligases and topoisomerases. As a front line of defense to these genotoxic insults, eukaryotic cells have accrued an arsenal of enzymatic first responders that bind and protect damaged DNA termini, and enzymatically tailor DNA ends for DNA repair synthesis and ligation. These nucleic acid transactions employ direct damage reversal enzymes including Aprataxin (APTX), Polynucleotide kinase phosphatase (PNK), the tyrosyl DNA phosphodiesterases (TDP1 and TDP2), the Ku70/80 complex and DNA polymerase β (POLβ). Nucleolytic processing enzymes such as the MRE11/RAD50/NBS1/CtIP complex, Flap endonuclease (FEN1) and the apurinic endonucleases (APE1 and APE2) also act in the chemical "cleansing" of DNA breaks to prevent genomic instability and disease, and promote progression of DNA- and RNA-DNA damage response (DDR and RDDR) pathways. Here, we provide an overview of cellular first responders dedicated to the detection and repair of abnormal DNA termini. © 2014 Wiley Periodicals, Inc. JF - Environmental and molecular mutagenesis AU - Andres, Sara N AU - Schellenberg, Matthew J AU - Wallace, Bret D AU - Tumbale, Percy AU - Williams, R Scott AD - Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, North Carolina. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 1 EP - 21 VL - 56 IS - 1 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - X-ray crystallography KW - DNA damage response KW - neurodegeneration KW - cancer KW - Animals KW - Genomic Instability KW - Humans KW - Disease Progression KW - Nucleic Acid Conformation KW - DNA Repair -- genetics KW - DNA -- genetics KW - DNA -- chemistry KW - DNA Damage -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652415166?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Recognition+and+repair+of+chemically+heterogeneous+structures+at+DNA+ends.&rft.au=Andres%2C+Sara+N%3BSchellenberg%2C+Matthew+J%3BWallace%2C+Bret+D%3BTumbale%2C+Percy%3BWilliams%2C+R+Scott&rft.aulast=Andres&rft.aufirst=Sara&rft.date=2015-01-01&rft.volume=56&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21892 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-19 N1 - Date created - 2015-01-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Parkinsonism Relat Disord. 2007 Apr;13(3):139-42 [17049295] Mol Cell Biol. 2007 May;27(10):3793-803 [17353262] Biochem Cell Biol. 2007 Aug;85(4):509-20 [17713585] J 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[24371269] Cell. 1999 Dec 10;99(6):577-87 [10612394] Nature. 2000 Jan 27;403(6768):451-6 [10667800] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/em.21892 ER - TY - JOUR T1 - Withdrawal from long-term methamphetamine self-administration 'normalizes' neurometabolites in rhesus monkeys: a super(1)H MR spectroscopy study AN - 1647024729; 21213421 AB - super(1)H magnetic resonance spectroscopy has demonstrated alterations in several neurometabolites in methamphetamine (METH)-dependent individuals in brain regions implicated in addiction. Yet, it is unclear whether these neurochemicals return to homeostatic levels after an individual abstains from drug use, a difficult question to address due to high recidivism and poor study retention in human subjects. We thus utilized a non-human primate model of addiction to explore the effects of long-term drug exposure and withdrawal on brain neurochemistry. Ten rhesus macaque monkeys on an active METH self-administration protocol (average use 4.6 plus or minus 0.8 years, average daily intake between 0.4 and 1.2mg/kg) and 10 age- and sex-matched drug-naive controls (CONT) served as subjects. Concentrations of several neurochemicals were evaluated at several timepoints following withdrawal from drug availability (10 monkeys at 1 week and 1 and 3 months, and 6 monkeys at 6 and 12 months; CONT examined at one timepoint). At 1 week following METH withdrawal, we found increases in myo-inositol in anterior cingulate cortex in the METH group relative to CONT. These alterations showed a linear pattern of decreased levels ('normalization') by 1 year of abstinence. We also found decreases in glutamine and Glx (composed mainly of glutamate and glutamine) in the caudate-putamen of the same animals at early withdrawal that showed a similar linear pattern of increasing concentration by 1 year. These results demonstrate that despite protracted, long-term use, neurochemical changes seen following long-term drug administration do not persist following prolonged abstinence, suggesting therapeutic effects of long-term withdrawal from drug use. JF - Addiction Biology AU - Yang, Shaolin AU - Belcher, Annabelle M AU - Chefer, Svetlana AU - Vaupel, DBruce AU - Schindler, Charles W AU - Stein, Elliot A AU - Yang, Yihong AD - Neuroimaging Research Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 69 EP - 79 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 20 IS - 1 SN - 1355-6215, 1355-6215 KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - Glutamine KW - Caudate-putamen KW - Withdrawal KW - Brain KW - Neurochemistry KW - Drug abuse KW - Primates KW - Cortex (cingulate) KW - Methamphetamine KW - Magnetic resonance spectroscopy KW - Self-administration KW - Macaca mulatta KW - Addiction KW - Glutamic acid 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/1647024729?accountid=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=Withdrawal+from+long-term+methamphetamine+self-administration+%27normalizes%27+neurometabolites+in+rhesus+monkeys%3A+a+super%281%29H+MR+spectroscopy+study&rft.au=Yang%2C+Shaolin%3BBelcher%2C+Annabelle+M%3BChefer%2C+Svetlana%3BVaupel%2C+DBruce%3BSchindler%2C+Charles+W%3BStein%2C+Elliot+A%3BYang%2C+Yihong&rft.aulast=Yang&rft.aufirst=Shaolin&rft.date=2015-01-01&rft.volume=20&rft.issue=1&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Addiction+Biology&rft.issn=13556215&rft_id=info:doi/10.1111%2Fadb.12078 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Methamphetamine; Glutamine; Caudate-putamen; Magnetic resonance spectroscopy; Withdrawal; Brain; Self-administration; Neurochemistry; Glutamic acid; Addiction; Drug abuse; Cortex (cingulate); Macaca mulatta; Primates DO - http://dx.doi.org/10.1111/adb.12078 ER - TY - JOUR T1 - OdoCapsule: Next-Generation Wireless Capsule Endoscopy With Accurate Lesion Localization and Video Stabilization Capabilities AN - 1647020562; 21210091 AB - In this paper, we propose a platform to achieve accurate localization of small-bowel lesions and endoscopic video stabilization in wireless capsule endoscopy. Current research modules rely on the use of external magnetic fields and triangulation methods to calculate the position vector of the capsule, leading to considerable error margins. Our platform, entitled OdoCapsule (a synthesis of the words Odometer and Capsule), provides real-time distance information from the point of duodenal entry to the point of exit from the small bowel. To achieve this, OdoCapsule is equipped with three miniature legs. Each leg carries a soft rubber wheel, which is made with human-compliant material. These legs are extendable and retractable thanks to a micromotor and three custom-made torsion springs. The wheels are specifically designed to function as microodometers: each rotation they perform is registered. Hence, the covered distance is measured accurately in real time. Furthermore, with its legs fully extended, OdoCapsule can stabilize itself inside the small-bowel lumen thus offering smoother video capture and better image processing. Recent ex vivo testing of this concept, using porcine small bowel and a commercially available (custom-modified) capsule endoscope, has proved its viability. JF - IEEE Transactions on Biomedical Engineering AU - Karargyris, Alexandros AU - Koulaouzidis, Anastastios AD - , National Library of Medicine National Institutes of Health, Bethesda, MD, USA Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 352 EP - 360 PB - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States VL - 62 IS - 1 SN - 0018-9294, 0018-9294 KW - Biotechnology and Bioengineering Abstracts KW - Leg KW - Magnetic fields KW - Intestine KW - Rubber KW - Image processing KW - Endoscopes KW - Endoscopy KW - W 30905:Medical Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647020562?accountid=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+Biomedical+Engineering&rft.atitle=OdoCapsule%3A+Next-Generation+Wireless+Capsule+Endoscopy+With+Accurate+Lesion+Localization+and+Video+Stabilization+Capabilities&rft.au=Karargyris%2C+Alexandros%3BKoulaouzidis%2C+Anastastios&rft.aulast=Karargyris&rft.aufirst=Alexandros&rft.date=2015-01-01&rft.volume=62&rft.issue=1&rft.spage=352&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Biomedical+Engineering&rft.issn=00189294&rft_id=info:doi/10.1109%2FTBME.2014.2352493 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Leg; Magnetic fields; Intestine; Image processing; Rubber; Endoscopes; Endoscopy DO - http://dx.doi.org/10.1109/TBME.2014.2352493 ER - TY - JOUR T1 - Insecticide Residues in Soil, Water, and Eggplant Fruits and Farmers' Health Effects Due to Exposure to Pesticides AN - 1647008143; 21314194 AB - Objectives: Eggplant (Solanum melongena L.) is an important vegetable crop that is widely cultivated in the tropical and subtropical areas in Asia. Globally, the top three eggplant producers are China, India, and Egypt. The Philippines has been one of the top 10 eggplant-producing countries based on area planted and crop productivity. This study aims to describe the insecticide residues found in soil, water, and eggplant fruits in eggplant farms in Sta. Maria, Pangasinan. Methods: The study design is a cross sectional of randomly selected eggplant farms in Sta. Maria, Pangasinan. Soil, water, and eggplant fruits were collected and subjected to gas chromatography (Shimadzu) analysis for multi-pesticide residues. Results: Farmers from Sta. Maria, Pangasinan were found to be applying a broad spectrum of insecticides on their eggplant crop. Soil samples from 11 (about 42 %) out of the 26 farms tested positive for insecticide residues, six of which from four farms exceeded the acceptable maximum residue limit. These residues were profenofos, triazophos, chlorpyrifos, cypermethrin, and malathion. No insecticide residues were detected from water samples taken from the 26 farms. Cypermethrin and chlorpyrifos were the insecticide residues detected in eggplant fruit samples. A maximum of 20 % of the eggplant samples tested positive for insecticide residues. In the eggplant fruit study, all farmers have been using Prevathon super( registered ) for 24 years at a rate of 10 ml/application, and Malathion super( registered ) for 25 years at about 16.5 ml/application, respectively equivalent to 0.24 liter-years and 0.413 liter-years of exposure. Similarly, to the findings in the soil and water study, although Brodan super( registered ) and Magnum super( registered ) were not prevalently applied, the farmers' liter-years of exposure to these insecticides, and their active ingredients, were highest at about 18.92 and 10.0, respectively. The farmers and farm workers in the soil and water study reported experiencing itchiness of the skin (63.8 %), redness of the eyes (29.3 %), muscle pains (27.6 %), and headaches (27.6 %), as being related to their pesticide exposure. Conclusion: In summary, a maximum of 20 % of the eggplant samples tested positive for insecticide residues at any one stage of sampling done. The farmers and farm workers also reported of pesticide-related illnesses but none of them sought any medical attention. Intervention to reduce the farmers' pesticide exposure can focus on the risk factors identified, primarily the toxicity of pesticides used, the unsafe application practices, and the adverse health effects of pesticide exposure. JF - Environmental Health and Preventive Medicine AU - Del Prado-Lu, Jinky Leilanie AD - Institute of Health Policy and Development Studies, National Institutes of Health, University of the Philippines Manila, NIH Bldg, P. Gil St., UP Manila, Taft Avenue, 1100, Manila, Philippines, jinky_lu@yahoo.com Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 53 EP - 62 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 20 IS - 1 SN - 1342-078X, 1342-078X KW - Toxicology Abstracts; Risk Abstracts; Pollution Abstracts; Health & Safety Science Abstracts KW - Philippines KW - Fruits KW - Egypt, Arab Rep. KW - Vegetables KW - Farms KW - Water sampling KW - Intervention KW - Solanum melongena KW - Crops KW - Malathion KW - India KW - Soil KW - Workers KW - triazophos KW - Insecticides KW - Gas chromatography KW - Risk factors KW - Headache KW - Sampling KW - Occupational exposure KW - Residues KW - Cypermethrin KW - Muscles KW - Insecticide residues KW - Toxicity KW - Chlorpyrifos KW - Pesticides KW - China, People's Rep. KW - H 5000:Pesticides KW - P 2000:FRESHWATER POLLUTION KW - R2 23060:Medical and environmental health KW - X 24330:Agrochemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647008143?accountid=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=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Neurogenetic+insights+into+organelle+biogenesis&rft.au=Blackstone%2C+Craig&rft.aulast=Blackstone&rft.aufirst=Craig&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Number of references - 44 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Fruits; Vegetables; Farms; Cypermethrin; Muscles; Toxicity; Malathion; Crops; Soil; Chlorpyrifos; Workers; triazophos; Insecticides; Gas chromatography; Risk factors; Pesticides; Headache; Sampling; Occupational exposure; Water sampling; Residues; Intervention; Insecticide residues; Solanum melongena; Philippines; Egypt, Arab Rep.; China, People's Rep.; India DO - http://dx.doi.org/10.1007/s12199-014-0425-3 ER - TY - JOUR T1 - Design of self-assembling peptide hydrogelators amenable to bacterial expression AN - 1647006236; 21286534 AB - Hydrogels formed from self-assembling peptides are finding use in tissue engineering and drug delivery applications. Given the notorious difficulties associated with producing self-assembling peptides by recombinant expression, most are typically prepared by chemical synthesis. Herein, we report the design of a family of self-assembling beta -hairpin peptides amenable to efficient production using an optimized bacterial expression system. Expressing peptides, EX1, EX2 and EX3 contain identical eight-residue amphiphilic beta -strands connected by varying turn sequences that are responsible for ensuring chain reversal and the proper intramolecular folding and consequent self-assembly of the peptide into a hydrogel network under physiological conditions. EX1 was initially used to establish and optimize the bacterial expression system by which all the peptides could be eventually individually expressed. Expression clones were designed to allow exploration of possible fusion partners and investigate both enzymatic and chemical cleavage as means to liberate the target peptide. A systematic analysis of possible expression systems followed by fermentation optimization lead to a system in which all three peptides could be expressed as fusions with BAD-BH3, the BH3 domain of the proapoptotic BAD (Bcl-2 Associated Death) Protein. CNBr cleavage followed by purification afforded 50, 31, and 15 mg/L yields of pure EX1, EX2 and EX3, respectively. CD spectroscopy, TEM, and rheological analysis indicate that these peptides fold and assembled into well-defined fibrils that constitute hydrogels having shear-thin/recovery properties. JF - Biomaterials AU - Sonmez, Cem AU - Nagy, Katelyn J AU - Schneider, Joel P AD - National Cancer Institute, Center for Cancer Research, Frederick, MD 21701, United States Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 62 EP - 72 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 37 SN - 0142-9612, 0142-9612 KW - Microbiology Abstracts B: Bacteriology; Biotechnology and Bioengineering Abstracts KW - Hydrogel KW - Peptide KW - Assembly KW - Expression KW - Injectable KW - Bacteria KW - Drug delivery KW - Apoptosis KW - hydrogels KW - Fermentation KW - Self-assembly KW - Bcl-2 protein KW - Tissue engineering KW - Spectroscopy KW - Fibrils KW - J 02310:Genetics & Taxonomy KW - W 30920:Tissue Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647006236?accountid=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=Biomaterials&rft.atitle=Design+of+self-assembling+peptide+hydrogelators+amenable+to+bacterial+expression&rft.au=Sonmez%2C+Cem%3BNagy%2C+Katelyn+J%3BSchneider%2C+Joel+P&rft.aulast=Sonmez&rft.aufirst=Cem&rft.date=2015-01-01&rft.volume=37&rft.issue=&rft.spage=62&rft.isbn=&rft.btitle=&rft.title=Biomaterials&rft.issn=01429612&rft_id=info:doi/10.1016%2Fj.biomaterials.2014.10.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Drug delivery; Apoptosis; hydrogels; Fermentation; Self-assembly; Bcl-2 protein; Spectroscopy; Tissue engineering; Fibrils; Bacteria DO - http://dx.doi.org/10.1016/j.biomaterials.2014.10.011 ER - TY - JOUR T1 - The design of covalent allosteric drugs. AN - 1643407497; 25149918 AB - A key issue in drug discovery is how to reduce drug dosage and increase specificity while retaining or increasing efficacy, as high dosage is often linked to toxicity. There are two types of drugs on the market: orthosteric and allosteric. Orthosteric drugs can be noncovalent or covalent. The latter are advantageous because they may be prescribed in lower doses, but their potential off-target toxicity is a primary concern. The chief advantages of allosteric drugs are their higher specificity and their consequently lower chance of toxic side effects. Covalent allosteric drugs combine the pharmacological merits of covalent drugs with the additional benefit of the higher specificity of allosteric drugs. In a recent promising step in therapeutic drug development, allosteric, disulfide-tethered fragments successfully modulated the activity of a protein kinase and K-Ras. JF - Annual review of pharmacology and toxicology AU - Nussinov, Ruth AU - Tsai, Chung-Jung AD - Cancer and Inflammation Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, National Cancer Institute, Frederick, Maryland 21702; email: NussinoR@helix.nih.gov. Y1 - 2015 PY - 2015 DA - 2015 SP - 249 EP - 267 VL - 55 KW - Enzyme Activators KW - 0 KW - Enzyme Inhibitors KW - Index Medicus KW - allosteric drug discovery KW - toxicity KW - antagonist KW - allosteric modulator KW - agonist KW - pharmacology KW - Molecular Structure KW - Animals KW - Models, Molecular KW - Humans KW - Drug-Related Side Effects and Adverse Reactions -- etiology KW - Protein Binding KW - Structure-Activity Relationship KW - Binding Sites KW - Kinetics KW - Signal Transduction -- drug effects KW - Allosteric Regulation KW - Computer-Aided Design KW - Drug-Related Side Effects and Adverse Reactions -- prevention & control KW - Protein Conformation KW - Enzyme Inhibitors -- adverse effects KW - Enzyme Activators -- chemistry KW - Enzyme Inhibitors -- chemistry KW - Enzyme Inhibitors -- pharmacology KW - Enzyme Activators -- adverse effects KW - Enzyme Activators -- pharmacology KW - Drug Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1643407497?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+review+of+pharmacology+and+toxicology&rft.atitle=The+design+of+covalent+allosteric+drugs.&rft.au=Nussinov%2C+Ruth%3BTsai%2C+Chung-Jung&rft.aulast=Nussinov&rft.aufirst=Ruth&rft.date=2015-01-01&rft.volume=55&rft.issue=&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Annual+review+of+pharmacology+and+toxicology&rft.issn=1545-4304&rft_id=info:doi/10.1146%2Fannurev-pharmtox-010814-124401 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-09 N1 - Date created - 2015-01-07 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1146/annurev-pharmtox-010814-124401 ER - TY - JOUR T1 - Free radical generation from an aniline derivative in HepG2 cells: a possible captodative effect. AN - 1641016976; 25450331 AB - Xenobiotic metabolism can induce the generation of protein radicals, which are believed to play an important role in the toxicity of chemicals and drugs. It is therefore important to identify chemical structures capable of inducing macromolecular free radical formation in living cells. In this study, we evaluated the ability of four structurally related environmental chemicals, aniline, nitrosobenzene, N,N-dimethylaniline, and N,N-dimethyl-4-nitrosoaniline (DMNA), to induce free radicals and cellular damage in the hepatoma cell line HepG2. Cytotoxicity was assessed using lactate dehydrogenase assays, and morphological changes were observed using phase contrast microscopy. Protein free radicals were detected by immuno-spin trapping using in-cell western experiments and confocal microscopy to determine the subcellular locale of free radical generation. DMNA induced free radical generation, lactate dehydrogenase release, and morphological changes in HepG2 cells, whereas aniline, nitrosobenzene, N,N-dimethylaniline did not. Confocal microscopy showed that DMNA induced free radical generation mainly in the cytosol. Preincubation of HepG2 cells with N-acetylcysteine and 2,2'-dipyridyl significantly prevented free radical generation on subsequent incubation with DMNA, whereas preincubation with apocynin and dimethyl sulfoxide had no effect. These results suggest that DMNA is metabolized to reactive free radicals capable of generating protein radicals which may play a critical role in DMNA toxicity. We propose that the captodative effect, the combined action of the electron-releasing dimethylamine substituent, and the electron-withdrawing nitroso substituent, leads to a thermodynamically stabilized radical, facilitating enhanced protein radical formation by DMNA. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Free radical biology & medicine AU - Horinouchi, Yuya AU - Summers, Fiona A AU - Ehrenshaft, Marilyn AU - Mason, Ronald P AD - Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: yuya.h@basic.med.tokushima-u.ac.jp. ; Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: summersfa@niehs.nih.gov. ; Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: ehrensh1@niehs.nih.gov. ; Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: mason4@niehs.nih.gov. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 111 EP - 117 VL - 78 KW - Aniline Compounds KW - 0 KW - Carcinogens KW - Free Radical Scavengers KW - Free Radicals KW - Nitroso Compounds KW - 4-nitrosodimethylaniline KW - 138-89-6 KW - N,N-dimethylaniline KW - 7426719369 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - aniline KW - SIR7XX2F1K KW - nitrosobenzene KW - ZI9W9E8G2Z KW - Index Medicus KW - Cytotoxicity KW - Immuno-spin trapping KW - Confocal microscopy KW - In-cell western KW - Environmental chemicals KW - Captodative effect KW - Microscopy, Confocal KW - Carcinogens -- pharmacology KW - Blotting, Western KW - Spin Trapping KW - Hep G2 Cells KW - Humans KW - Electron Spin Resonance Spectroscopy KW - L-Lactate Dehydrogenase -- metabolism KW - Cell Proliferation -- drug effects KW - Aniline Compounds -- pharmacology KW - Nitroso Compounds -- pharmacology KW - Free Radicals -- metabolism KW - Free Radical Scavengers -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1641016976?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Free+radical+generation+from+an+aniline+derivative+in+HepG2+cells%3A+a+possible+captodative+effect.&rft.au=Horinouchi%2C+Yuya%3BSummers%2C+Fiona+A%3BEhrenshaft%2C+Marilyn%3BMason%2C+Ronald+P&rft.aulast=Horinouchi&rft.aufirst=Yuya&rft.date=2015-01-01&rft.volume=78&rft.issue=&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2014.10.577 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-02 N1 - Date created - 2014-12-29 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2014.10.577 ER - TY - JOUR T1 - Antiviral activity of a single-domain antibody immunotoxin binding to glycoprotein D of herpes simplex virus 2. AN - 1640482632; 25385102 AB - Despite years of research dedicated to preventing the sexual transmission of herpes simplex virus 2 (HSV-2), there is still no protective vaccine or microbicide against one of the most common sexually transmitted infections in the world. Using a phage display library constructed from a llama immunized with recombinant HSV-2 glycoprotein D, we identified a single-domain antibody VHH, R33, which binds to the viral surface glycoprotein D. Although R33 does not demonstrate any HSV-2 neutralization activity in vitro, when expressed with the cytotoxic domain of exotoxin A, the resulting immunotoxin (R33ExoA) specifically and potently kills HSV-2-infected cells, with a 50% neutralizing dilution (IC50) of 6.7 nM. We propose that R33ExoA could be used clinically to prevent transmission of HSV-2 through killing of virus-producing epithelial cells during virus reactivation. R33 could also potentially be used to deliver other cytotoxic effectors to HSV-2-infected cells. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Antimicrobial agents and chemotherapy AU - Geoghegan, Eileen M AU - Zhang, Hong AU - Desai, Prashant J AU - Biragyn, Arya AU - Markham, Richard B AD - The W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA. ; Viral Oncology Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University, Baltimore, Maryland, USA. ; Immunoregulation Section, Laboratory of Molecular Biology and Immunology, National Institute on Aging, Baltimore, Maryland, USA. ; The W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA rmarkha1@jhu.edu. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 527 EP - 535 VL - 59 IS - 1 KW - Antiviral Agents KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Single-Domain Antibodies KW - Viral Envelope Proteins KW - Virulence Factors KW - glycoprotein D-herpes simplex virus type 2 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 - Exotoxins -- genetics KW - ADP Ribose Transferases -- immunology KW - Recombinant Fusion Proteins -- immunology KW - Vero Cells -- drug effects KW - Vero Cells -- virology KW - Virulence Factors -- genetics KW - Bacterial Toxins -- immunology KW - Exotoxins -- immunology KW - Virulence Factors -- immunology KW - ADP Ribose Transferases -- genetics KW - Bacterial Toxins -- genetics KW - Immunotoxins -- immunology KW - Cercopithecus aethiops KW - Recombinant Fusion Proteins -- genetics KW - Neutralization Tests KW - Toxicity Tests -- methods KW - Recombinant Fusion Proteins -- pharmacology KW - Camelids, New World KW - Immunotoxins -- genetics KW - Immunotoxins -- pharmacology KW - Herpesvirus 2, Human -- drug effects KW - Single-Domain Antibodies -- genetics KW - Antiviral Agents -- pharmacology KW - Single-Domain Antibodies -- immunology KW - Single-Domain Antibodies -- pharmacology KW - Viral Envelope Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1640482632?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+agents+and+chemotherapy&rft.atitle=Antiviral+activity+of+a+single-domain+antibody+immunotoxin+binding+to+glycoprotein+D+of+herpes+simplex+virus+2.&rft.au=Geoghegan%2C+Eileen+M%3BZhang%2C+Hong%3BDesai%2C+Prashant+J%3BBiragyn%2C+Arya%3BMarkham%2C+Richard+B&rft.aulast=Geoghegan&rft.aufirst=Eileen&rft.date=2015-01-01&rft.volume=59&rft.issue=1&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+agents+and+chemotherapy&rft.issn=1098-6596&rft_id=info:doi/10.1128%2FAAC.03818-14 LA - 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Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/AAC.03818-14 ER - TY - JOUR T1 - Sirolimus use and cancer incidence among US kidney transplant recipients. AN - 1640330521; 25522018 AB - Sirolimus has anti-carcinogenic properties and can be included in maintenance immunosuppressive therapy following kidney transplantation. We investigated sirolimus effects on cancer incidence among kidney recipients. The US transplant registry was linked with 15 population-based cancer registries and national pharmacy claims. Recipients contributed sirolimus-exposed time when sirolimus claims were filled, and unexposed time when other immunosuppressant claims were filled without sirolimus. Cox regression was used to estimate associations with overall and specific cancer incidence, excluding nonmelanoma skin cancers (not captured in cancer registries). We included 32,604 kidney transplants (5687 sirolimus-exposed). Overall, cancer incidence was suggestively lower during sirolimus use (hazard ratio [HR] = 0.88, 95% confidence interval [CI] = 0.70-1.11). Prostate cancer incidence was higher during sirolimus use (HR = 1.86, 95% CI = 1.15-3.02). Incidence of other cancers was similar or lower with sirolimus use, with a 26% decrease overall (HR = 0.74, 95% CI = 0.57-0.96, excluding prostate cancer). Results were similar after adjustment for demographic and clinical characteristics. This modest association does not provide strong evidence that sirolimus prevents posttransplant cancer, but it may be advantageous among kidney recipients with high cancer risk. Increased prostate cancer diagnoses may result from sirolimus effects on screen detection. © Copyright 2014 The American Society of Transplantation and the American Society of Transplant Surgeons. JF - American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons AU - Yanik, E L AU - Gustafson, S K AU - Kasiske, B L AU - Israni, A K AU - Snyder, J J AU - Hess, G P AU - Engels, E A AU - Segev, D L AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 129 EP - 136 VL - 15 IS - 1 KW - Immunosuppressive Agents KW - 0 KW - Sirolimus KW - W36ZG6FT64 KW - Index Medicus KW - immunosuppressant KW - immunosuppression/immune modulation KW - health services and outcomes research KW - mechanistic target of rapamycin: sirolimus KW - epidemiology KW - clinical research/practice KW - Cancer/malignancy/neoplasia KW - hematology/oncology KW - kidney transplantation/nephrology KW - Kidney Function Tests KW - Humans KW - Prognosis KW - Risk Assessment KW - Registries KW - Glomerular Filtration Rate KW - Adult KW - Graft Rejection -- drug therapy KW - Incidence KW - Follow-Up Studies KW - Middle Aged KW - United States -- epidemiology KW - Female KW - Male KW - Kidney Transplantation KW - Neoplasms -- epidemiology KW - Kidney Failure, Chronic -- surgery KW - Sirolimus -- therapeutic use KW - Immunosuppressive Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1640330521?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+transplantation+%3A+official+journal+of+the+American+Society+of+Transplantation+and+the+American+Society+of+Transplant+Surgeons&rft.atitle=Sirolimus+use+and+cancer+incidence+among+US+kidney+transplant+recipients.&rft.au=Dunleavy%2C+Kieron&rft.aulast=Dunleavy&rft.aufirst=Kieron&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-25 N1 - Date created - 2014-12-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/ajt.12969 ER - TY - JOUR T1 - Class act: safety comparison of approved tyrosine kinase inhibitors for non-small-cell lung carcinoma. AN - 1637568396; 25345687 AB - The past decade has seen the development and widespread use of tyrosine kinase inhibitors (TKIs) targeting a mutated EGFR (mEGFR) for the treatment of metastatic NSCLC. We discuss the main properties of the TKIs currently recommended for the treatment of mEGFR NSCLC: gefitinib, erlotinib and afatinib. The mechanism of action, pharmacodynamics and pharmacokinetics of these drugs, with emphasis on the historical context of their preclinical and clinical development, will be covered, including potential resistance mechanisms to these first-generation TKIs that has driven the trial design for second and third generations of EGFR inhibitors. Six Phase III clinical trials comparing these three TKIs with cisplatin-based chemotherapy upfront for mEGFR NSCLC provide the basis for the comparative safety and toxicity analysis between these agents. Class-related toxicity of these EGFR inhibitors, including life-threatening effects, will be discussed. Toxicity and safety analysis from the Phase III trials of these agents in mEGFR populations suggests that afatinib has more frequent and severe side effects. Given that an efficacy advantage has not yet been demonstrated for afatinib over erlotinib and gefitinib, the consistent class toxicity profile of these agents means that gefitinib and erlotinib are a safer first-line treatment recommendation. JF - Expert opinion on drug safety AU - Burotto, Mauricio AU - Ali, Syed Abbas AU - O'Sullivan Coyne, Geraldine AD - National Cancer Institute, National Institutes of Health National, Center for Cancer Research , Maryland, USA10 Center Dr, 12N226, Bethesda, MD 20892 , USA +1 301 496 4916 ; +1 301 402 0172 ; mauricio.burottopichun@nih.gov. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 97 EP - 110 VL - 14 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Protein Kinase Inhibitors KW - Quinazolines KW - afatinib KW - 41UD74L59M KW - Erlotinib Hydrochloride KW - DA87705X9K KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Receptor, Epidermal Growth Factor KW - gefitinib KW - S65743JHBS KW - Index Medicus KW - tyrosine kinase inhibitor KW - safety KW - toxicity KW - mutated EGFR KW - clinical trial KW - erlotinib KW - Protein Kinase Inhibitors -- therapeutic use KW - Protein Kinase Inhibitors -- adverse effects KW - Humans KW - Antineoplastic Agents -- pharmacokinetics KW - Protein Kinase Inhibitors -- pharmacokinetics KW - Antineoplastic Agents -- therapeutic use KW - Mutation KW - Models, Biological KW - Antineoplastic Agents -- adverse effects KW - Quinazolines -- pharmacokinetics KW - Protein-Tyrosine Kinases -- antagonists & inhibitors KW - Receptor, Epidermal Growth Factor -- antagonists & inhibitors KW - Receptor, Epidermal Growth Factor -- genetics KW - Lung Neoplasms -- drug therapy KW - Quinazolines -- adverse effects KW - Carcinoma, Non-Small-Cell Lung -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1637568396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+drug+safety&rft.atitle=Class+act%3A+safety+comparison+of+approved+tyrosine+kinase+inhibitors+for+non-small-cell+lung+carcinoma.&rft.au=Burotto%2C+Mauricio%3BAli%2C+Syed+Abbas%3BO%27Sullivan+Coyne%2C+Geraldine&rft.aulast=Burotto&rft.aufirst=Mauricio&rft.date=2015-01-01&rft.volume=14&rft.issue=1&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+drug+safety&rft.issn=1744-764X&rft_id=info:doi/10.1517%2F14740338.2014.973400 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-14 N1 - Date created - 2014-12-16 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1517/14740338.2014.973400 ER - TY - JOUR T1 - Acute air pollution exposure and blood pressure at delivery among women with and without hypertension. AN - 1637558422; 24795401 AB - Chronic air pollution exposure increases risk for hypertensive disorders of pregnancy, but the effect of acute air pollution exposure on blood pressure during pregnancy is less well known. We studied 151,276 singleton term deliveries from the Consortium on Safe Labor (2002-2008) with clinical blood pressure measured at admission to labor/delivery and diagnoses of hypertensive disorders collected from electronic medical records and hospital discharge summaries. Air pollution exposures were estimated for the admission hour and the 4 hours preceding admission using a modified version of the Community Multiscale Air Quality models and observed air monitoring data. Blood pressure was categorized as normal; high normal; and mild, moderate, or severe hypertension based on pregnancy cut points. Adjusted ordinal logistic regression estimated the odds of women having a higher admission blood pressure category as a function of air pollutant, hypertensive disorders, and their interaction effect. Odds of high blood pressure at admission to labor/delivery were increased in normotensive women after exposure to nitrogen oxides (by 0.2%/5 units), sulfur dioxide (by 0.3%/1 unit), carbon monoxide and several air toxics (by 3%-4%/high exposure). The effects were often similar or stronger among women with gestational hypertension and preeclampsia. Exposure to particulate matter <10 μm increased odds of high blood pressure in women with preeclampsia by 3%/5 units. Air pollution can influence admission blood pressure in term deliveries and may increase likelihood of preeclampsia screening at delivery admission. © Published by Oxford University Press on behalf of American Journal of Hypertension Ltd 2014. This work is written by (a) US Government employees(s) and is in the public domain in the US. JF - American journal of hypertension AU - Männistö, Tuija AU - Mendola, Pauline AU - Liu, Danping AU - Leishear, Kira AU - Sherman, Seth AU - Laughon, S Katherine AD - Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, Maryland; ; Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, Maryland; pauline.mendola@nih.gov. ; Biostatistics and Bioinformatics Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, Maryland; ; Glotech, Rockville, Maryland; ; The EMMES Corporation, Rockville, Maryland. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 58 EP - 72 VL - 28 IS - 1 KW - Air Pollutants KW - 0 KW - Particulate Matter KW - Index Medicus KW - pregnancy. KW - blood pressure KW - hypertension KW - epidemiology KW - air pollution KW - Severity of Illness Index KW - Young Adult KW - Odds Ratio KW - Patient Admission KW - Humans KW - Particle Size KW - Pregnancy KW - Environmental Monitoring KW - Logistic Models KW - Risk Factors KW - Adult KW - Case-Control Studies KW - United States -- epidemiology KW - Time Factors KW - Female KW - Delivery, Obstetric KW - Hypertension, Pregnancy-Induced -- physiopathology KW - Blood Pressure KW - Hypertension, Pregnancy-Induced -- diagnosis KW - Particulate Matter -- adverse effects KW - Hypertension, Pregnancy-Induced -- epidemiology KW - Environmental Exposure -- adverse effects KW - Air Pollutants -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1637558422?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+hypertension&rft.atitle=Acute+air+pollution+exposure+and+blood+pressure+at+delivery+among+women+with+and+without+hypertension.&rft.au=M%C3%A4nnist%C3%B6%2C+Tuija%3BMendola%2C+Pauline%3BLiu%2C+Danping%3BLeishear%2C+Kira%3BSherman%2C+Seth%3BLaughon%2C+S+Katherine&rft.aulast=M%C3%A4nnist%C3%B6&rft.aufirst=Tuija&rft.date=2015-01-01&rft.volume=28&rft.issue=1&rft.spage=58&rft.isbn=&rft.btitle=&rft.title=American+journal+of+hypertension&rft.issn=1941-7225&rft_id=info:doi/10.1093%2Fajh%2Fhpu077 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-21 N1 - Date created - 2014-12-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Obstet Gynecol. 2013 Nov;122(5):1122-31 [24150027] Hypertension. 2003 Dec;42(6):1206-52 [14656957] Lancet. 1997 May 31;349(9065):1582-7 [9174559] Environ Health Perspect. 2005 Aug;113(8):1052-5 [16079078] Epidemiology. 2005 Nov;16(6):744-50 [16222163] Ann Emerg Med. 2008 Mar;51(3):221-9 [18207606] Hypertension. 2009 May;53(5):853-9 [19273743] Hypertension. 2009 Sep;54(3):659-67 [19620518] Circulation. 2010 Jun 1;121(21):2331-78 [20458016] Occup Environ Med. 2010 Sep;67(9):625-30 [20519749] Am J Obstet Gynecol. 2010 Oct;203(4):326.e1-326.e10 [20708166] Hypertension. 2011 Mar;57(3):406-12 [21220700] Epidemiology. 2011 Jul;22(4):524-31 [21516040] Environ Res. 2011 Jul;111(5):685-92 [21453913] Epidemiology. 2011 Sep;22(5):671-9 [21730862] Environ Res. 2011 Nov;111(8):1309-12 [22000598] Women Health. 2011 Nov 30;51(8):724-38 [22185288] Epidemiology. 2012 Mar;23(2):341-8 [22249240] Hypertension. 2012 May;59(5):943-8 [22431582] Hypertension. 2012 Jun;59(6):1241-8 [22526257] Cardiol Clin. 2012 Aug;30(3):317-29 [22813360] Cardiovasc Toxicol. 2012 Sep;12(3):216-25 [22328329] Am J Epidemiol. 2012 Aug 15;176(4):308-16 [22811493] Environ Res. 2012 Aug;117:60-7 [22717264] Environ Res. 2012 Aug;117:46-53 [22835955] Circulation. 2013 Feb 12;127(6):681-90 [23401113] Matern Child Health J. 2013 Apr;17(3):545-55 [22544506] Environ Res. 2013 May;123:9-16 [23522615] Environ Pollut. 2013 Dec;183:30-9 [23369806] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/ajh/hpu077 ER - TY - JOUR T1 - Fibrillation of β amyloid peptides in the presence of phospholipid bilayers and the consequent membrane disruption. AN - 1634726169; 24769158 AB - Fibrillation of β amyloid (Aβ) peptides and the accumulation of amyloid plaques are considered as an important clinical hallmark to identify Alzheimer's disease (AD). The physiological connection between Aβ plaques and the disruption of neuronal cells has not been clearly understood. One hypothesis to explain the Aβ neurotoxicity is that the fibrillation process induces disruption to the cellular membrane. We studied the Aβ fibrillation process in two biologically relevant conditions with the peptide either pre-incorporated into or externally added to the synthetic phospholipid bilayers. These two sample preparation conditions mimic the physiological membrane proximities of Aβ peptides before and after the enzymatic cleavage of amyloid precursor protein (APP). Using thioflavin T (ThT) fluorescence and transmission electron microscopy (TEM), we were able to monitor the kinetics and morphological evolution of fibril formation, which was highly sensitive to the two sample preparation protocols. While the external addition protocol generates long and mature fibrils through normal fibrillation process, the pre-incubation protocol was found to stabilize the immature protofibrils. Fluorescence spectroscopy studies with doubly-labeled phospholipids indicated that there may be a lipid uptake process associated with the fibril formation. Solid state nuclear magnetic resonance (NMR) spectroscopy provided evidence for high resolution structural variations in fibrils formed with different protocols, and in particular the stabilization of long-range contact between N- and C-terminal β strands. In addition, disruption of phospholipid bilayers was supported by measurements with ³¹P chemical shifts and relaxation time constants. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biochimica et biophysica acta AU - Qiang, Wei AU - Yau, Wai-Ming AU - Schulte, Jürgen AD - Department of Chemistry, Binghamton University, State University of New York, Binghamton, NY 13902-6000, USA; Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0520, USA. Electronic address: wqiang@binghamton.edu. ; Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0520, USA. ; Department of Chemistry, Binghamton University, State University of New York, Binghamton, NY 13902-6000, USA. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 266 EP - 276 VL - 1848 IS - 1 Pt B SN - 0006-3002, 0006-3002 KW - Amyloid beta-Peptides KW - 0 KW - Lipid Bilayers KW - Phospholipids KW - Index Medicus KW - Alzheimer's disease KW - β amyloid fibril KW - Solid state NMR KW - Membrane disruption KW - Neurotoxicity mechanism KW - Protein Aggregation, Pathological KW - Models, Biological KW - Magnetic Resonance Spectroscopy KW - Phospholipids -- chemistry KW - Amyloid beta-Peptides -- toxicity KW - Amyloid beta-Peptides -- chemistry KW - Lipid Bilayers -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1634726169?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fibrillation+of+%CE%B2+amyloid+peptides+in+the+presence+of+phospholipid+bilayers+and+the+consequent+membrane+disruption.&rft.au=Qiang%2C+Wei%3BYau%2C+Wai-Ming%3BSchulte%2C+J%C3%BCrgen&rft.aulast=Qiang&rft.aufirst=Wei&rft.date=2015-01-01&rft.volume=1848&rft.issue=1+Pt+B&rft.spage=266&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbamem.2014.04.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-12 N1 - Date created - 2014-12-06 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbamem.2014.04.011 ER - TY - JOUR T1 - Nucleocytoplasmic shuttling of valosin-containing protein (VCP/p97) regulated by its N domain and C-terminal region. AN - 1629968055; 25447673 AB - Valosin-containing protein (VCP or p97), a member of the AAA family (ATPases associated with diverse cellular activities), plays a key role in many important cellular activities. A genetic deficiency of VCP can cause inclusion body myopathy associated with Paget's disease of bone and frontotemporal dementia (IBMPFD). Previous studies showed that the VCP N domain is essential for the regulation of nuclear entry of VCP. Here we report that IBMPFD mutations, which are mainly located in the N domain, suppress the nuclear entry of VCP. Moreover, the peptide sequence G780AGPSQ in the C-terminal region regulates the retention of VCP in the nucleus. A mutant lacking this sequence can increase the nuclear distribution of IBMPFD VCP, suggesting that this sequence is a potential molecular target for correcting the deficient nucleocytoplasmic shuttling of IBMPFD VCP proteins. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biochimica et biophysica acta AU - Song, Changcheng AU - Wang, Qing AU - Song, Changzheng AU - Lockett, Stephen J AU - Colburn, Nancy H AU - Li, Chou-Chi H AU - Wang, Ji Ming AU - Rogers, Thomas J AD - Center for Inflammation, Translational and Clinical Lung Research, School of Medicine, Temple University, Philadelphia, PA 19140, USA. Electronic address: songc@temple.edu. ; Graduate Center for Toxicology, University of Kentucky, Lexington, KY, USA. ; Erythrocrine Project of Translational Medicine, Shandong Academy of Medical Sciences, Jinan 250062, China. ; Optical Microscopy and Analysis Laboratory, Advanced Technology Program, National Cancer Institute at Frederick, Frederick, MD 21702, USA. ; Laboratory of Cancer Prevention, National Cancer Institute at Frederick, Frederick, MD 21702, USA. ; Laboratory of Cancer Prevention, National Cancer Institute at Frederick, Frederick, MD 21702, USA; Basic Research Program, SAIC-Frederick Inc., National Cancer Institute at Frederick, Frederick, MD 21702, USA. ; Laboratory of Molecular Immunoregulation, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD 21702, USA. ; Center for Inflammation, Translational and Clinical Lung Research, School of Medicine, Temple University, Philadelphia, PA 19140, USA. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 222 EP - 232 VL - 1853 IS - 1 SN - 0006-3002, 0006-3002 KW - Cell Cycle Proteins KW - 0 KW - Adenosine Triphosphatases KW - EC 3.6.1.- KW - CDC48 protein KW - Index Medicus KW - Valosin containing protein KW - Nucleocytoplasmic shuttling KW - Nuclear export signal KW - Inclusion body myopathy associated with Paget's disease of bone and frontotemporal dementia (IBMPFD) KW - Osteitis Deformans -- genetics KW - Active Transport, Cell Nucleus KW - Humans KW - HEK293 Cells KW - Muscular Dystrophies, Limb-Girdle -- genetics KW - Frontotemporal Dementia -- genetics KW - Protein Structure, Tertiary KW - Myositis, Inclusion Body -- genetics KW - Cell Cycle Proteins -- chemistry KW - Cell Cycle Proteins -- genetics KW - Cell Nucleus -- metabolism KW - Adenosine Triphosphatases -- physiology KW - Adenosine Triphosphatases -- metabolism KW - Adenosine Triphosphatases -- chemistry KW - Adenosine Triphosphatases -- genetics KW - Cell Cycle Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629968055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nucleocytoplasmic+shuttling+of+valosin-containing+protein+%28VCP%2Fp97%29+regulated+by+its+N+domain+and+C-terminal+region.&rft.au=Song%2C+Changcheng%3BWang%2C+Qing%3BSong%2C+Changzheng%3BLockett%2C+Stephen+J%3BColburn%2C+Nancy+H%3BLi%2C+Chou-Chi+H%3BWang%2C+Ji+Ming%3BRogers%2C+Thomas+J&rft.aulast=Song&rft.aufirst=Changcheng&rft.date=2015-01-01&rft.volume=1853&rft.issue=1&rft.spage=222&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbamcr.2014.10.019 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-29 N1 - Date created - 2014-12-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncogene. 2011 Feb 17;30(7):790-805 [20956947] Biochem Biophys Res Commun. 2003 Jan 10;300(2):253-60 [12504076] J Biol Chem. 2003 Feb 7;278(6):3648-55 [12446676] J Biol Chem. 2003 Aug 29;278(35):32784-93 [12807884] Nat Struct Biol. 2003 Oct;10(10):856-63 [12949490] Mol Biol Cell. 2003 Oct;14(10):4221-9 [12937274] J Struct Biol. 2004 Apr-May;146(1-2):44-57 [15037236] J Struct Biol. 2004 Apr-May;146(1-2):251-9 [15037256] Nat Genet. 2004 Apr;36(4):377-81 [15034582] J Cell Biol. 1983 Nov;97(5 Pt 1):1389-95 [6355118] Cell. 1995 Aug 11;82(3):463-73 [7634336] J Virol. 1996 Sep;70(9):6442-5 [8709278] J Biol Chem. 1996 Aug 16;271(33):20024-8 [8702720] Science. 1997 Oct 3;278(5335):141-4 [9311922] Mol Biol Cell. 1998 Jan;9(1):131-41 [9436996] FEBS Lett. 1998 Oct 23;437(3):255-7 [9824302] J Biol Chem. 2005 Dec 9;280(49):40515-23 [16216872] Trends Cell Biol. 2007 Apr;17(4):193-201 [17317185] Biochemistry. 2007 Dec 25;46(51):14889-98 [18044963] Biochem Soc Trans. 2008 Feb;36(Pt 1):62-7 [18208387] Toxicol Appl Pharmacol. 2008 May 1;228(3):351-63 [18261755] Mol Cell Biol. 2009 Aug;29(16):4484-94 [19506019] EMBO J. 2010 Jul 7;29(13):2217-29 [20512113] Genes Cells. 2010 Aug;15(8):911-22 [20604808] PLoS One. 2010;5(10). pii: e13183. doi: 10.1371/journal.pone.0013183 [20957154] J Biol Chem. 2011 Jun 17;286(24):21732-41 [21474449] Biochim Biophys Acta. 2012 Jan;1823(1):130-7 [21781992] Nat Cell Biol. 2012 Feb;14(2):117-23 [22298039] J Biol Chem. 2012 Mar 9;287(11):8561-70 [22270372] Biochim Biophys Acta. 2014 Jun;1842(6):848-59 [24269586] Mol Cell. 2000 Dec;6(6):1473-84 [11163219] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbamcr.2014.10.019 ER - TY - JOUR T1 - Conformational dynamics and aggregation behavior of piezoelectric diphenylalanine peptides in an external electric field. AN - 1629964930; 25240398 AB - Aromatic peptides including diphenylalanine (FF) have the capacity to self-assemble into ordered, biocompatible nanostructures with piezoelectric properties relevant to a variety of biomedical applications. Electric fields are commonly applied to align FF nanotubes, yet little is known about the effect of the electric field on the assembly process. Using all-atom molecular dynamics with explicit water molecules, we examine the response of FF monomers to the application of a constant external electric field over a range of intensities. We probe the aggregation mechanism of FF peptides, and find that the presence of even relatively weak fields can accelerate ordered aggregation, primarily by facilitating the alignment of individual molecular dipole moments. This is modulated by the conformational response of individual FF peptides (e.g., backbone stretching) and by the cooperative alignment of neighboring FF and water molecules. These observations may facilitate future studies on the controlled formation of nanostructured aggregates of piezoelectric peptides and the understanding of their electro-mechanical properties. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biophysical chemistry AU - Kelly, Catherine M AU - Northey, Thomas AU - Ryan, Kate AU - Brooks, Bernard R AU - Kholkin, Andrei L AU - Rodriguez, Brian J AU - Buchete, Nicolae-Viorel AD - School of Physics, University College Dublin, Belfield, Dublin 4, Ireland; Complex and Adaptive Systems Laboratory, University College Dublin, Belfield, Dublin 4, Ireland. ; School of Physics, University College Dublin, Belfield, Dublin 4, Ireland; Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Belfield, Dublin 4, Ireland. ; Laboratory of Computational Biology, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, United States. ; Department of Materials and Ceramic Engineering & CICECO, University of Aveiro, Portugal. ; School of Physics, University College Dublin, Belfield, Dublin 4, Ireland; Complex and Adaptive Systems Laboratory, University College Dublin, Belfield, Dublin 4, Ireland. Electronic address: buchete@ucd.ie. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 16 EP - 24 VL - 196 KW - Solvents KW - 0 KW - diphenylalanine KW - Phenylalanine KW - 47E5O17Y3R KW - Index Medicus KW - Peptide aggregate KW - Peptide–peptide interaction KW - Atomistic molecular dynamics KW - Piezoelectric peptide KW - Diphenylalanine peptide KW - External electric field KW - Solvents -- chemistry KW - Nanostructures -- chemistry KW - Electricity KW - Protein Structure, Tertiary KW - Hydrogen Bonding KW - Phenylalanine -- chemistry KW - Phenylalanine -- analogs & derivatives KW - Molecular Dynamics Simulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629964930?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biophysical+chemistry&rft.atitle=Conformational+dynamics+and+aggregation+behavior+of+piezoelectric+diphenylalanine+peptides+in+an+external+electric+field.&rft.au=Kelly%2C+Catherine+M%3BNorthey%2C+Thomas%3BRyan%2C+Kate%3BBrooks%2C+Bernard+R%3BKholkin%2C+Andrei+L%3BRodriguez%2C+Brian+J%3BBuchete%2C+Nicolae-Viorel&rft.aulast=Kelly&rft.aufirst=Catherine&rft.date=2015-01-01&rft.volume=196&rft.issue=&rft.spage=16&rft.isbn=&rft.btitle=&rft.title=Biophysical+chemistry&rft.issn=1873-4200&rft_id=info:doi/10.1016%2Fj.bpc.2014.08.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-27 N1 - Date created - 2014-12-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Chem Soc Rev. 2007 Aug;36(8):1263-9 [17619686] Chemistry. 2001 Dec 3;7(23):5153-9 [11775688] Proteins. 2008 Jan 1;70(1):119-30 [17640067] Angew Chem Int Ed Engl. 2008;47(22):4062-9 [18412209] Electrophoresis. 2008 Dec;29(24):5026-32 [19130587] Phys Chem Chem Phys. 2009 Mar 28;11(12):2068-76 [19280017] Phys Chem Chem Phys. 2009 Mar 28;11(12):2077-86 [19280018] Biopolymers. 2009;92(3):164-72 [19226515] J Comput Chem. 2009 Jul 30;30(10):1545-614 [19444816] Acta Crystallogr B. 2010 Feb;66(Pt 1):84-93 [20101088] ACS Nano. 2010 Feb 23;4(2):610-4 [20131852] Angew Chem Int Ed Engl. 2010 Dec 17;49(51):9939-42 [20878815] ACS Nano. 2011 Jun 28;5(6):4448-54 [21591732] Nat Nanotechnol. 2012 Jun;7(6):351-6 [22581406] Biophys Chem. 2012 Jun;167:1-7 [22609945] J Mol Biol. 2012 Aug 24;421(4-5):572-86 [22281438] J Nanosci Nanotechnol. 2012 Apr;12(4):3077-83 [22849068] Prion. 2012 Sep-Oct;6(4):339-45 [22874669] Biophys J. 2012 Oct 3;103(7):1411-3 [23062332] J Colloid Interface Sci. 2013 Jan 15;390(1):54-61 [23102909] Electrophoresis. 2013 Apr;34(7):1085-96 [23400789] Electrophoresis. 2013 Apr;34(7):1105-12 [23436323] Nanoscale. 2014 Mar 7;6(5):2800-11 [24468750] Biochem Soc Trans. 2014 Aug;42(4):784-90 [25109958] Curr Opin Struct Biol. 2001 Apr;11(2):236-42 [11297934] Science. 2003 Apr 25;300(5619):625-7 [12714741] J Comput Chem. 2004 Aug;25(11):1400-15 [15185334] Nature. 1993 Nov 25;366(6453):324-7 [8247126] J Mol Graph. 1996 Feb;14(1):33-8, 27-8 [8744570] Nano Lett. 2005 Jul;5(7):1343-6 [16178235] Biophys J. 2007 May 1;92(9):3032-9 [17293399] Langmuir. 2006 Jan 31;22(3):1313-20 [16430299] J Comput Chem. 2005 Dec;26(16):1781-802 [16222654] J Mol Biol. 2007 Oct 19;373(2):439-51 [17850816] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bpc.2014.08.009 ER - TY - JOUR T1 - Alcohol and breast cancer: reconciling epidemiological and molecular data. AN - 1628878280; 25427899 AB - Breast cancer is the most diagnosed cancer in women worldwide. Epidemiological studies have suggested a possible causative role of alcohol consumption as a risk factor for breast cancer. However, such conclusions should be interpreted with considerable caution for several reasons. While epidemiological studies can help identify the roots of health problems and disease incidence in a community, they are by necessity associative and cannot determine cause and effect relationships. In addition, all these studies rely on self-reporting to determine the amount and type of alcoholic beverage consumed, which introduces recall bias. This is documented in a recent study which stated that the apparent increased risk of cancer among light-moderate drinkers may be "substantially due to underreporting of intake." Another meta-analysis about alcohol and breast cancer declared "the modest size of the association and variation in results across studies leave the causal role of alcohol in question." Furthermore, breast cancer develops over decades; thus, correlations between alcohol consumption and breast cancer cannot be determined in epidemiological studies with windows of alcohol exposure that captures current or recent alcohol intake, after clinical diagnosis. Numerous risk factors are involved in breast carcinogenesis; some are genetic and beyond the control of a woman; others are influenced by lifestyle factors. Breast cancer is a heterogeneous and polygenic disease which is further influenced by epigenetic mechanisms that affect the transciptomes, proteomes and metabolomes, and ultimately breast cancer evolution. Environmental factors add another layer of complexity by their interactions with the susceptibility genes for breast cancer and metabolic diseases. The current state-of-knowledge about alcohol and breast cancer association is ambiguous and confusing to both a woman and her physician. Confronting the huge global breast cancer issue should be addressed by sound science. It is advised that women with or without a high risk for breast cancer should avoid overconsumption of alcohol and should consult with their physician about risk factors involved in breast cancer. Since studies associating moderate alcohol consumption and breast cancer are contradictory, a woman and her physician should weigh the risks and benefits of moderate alcohol consumption. JF - Advances in experimental medicine and biology AU - Zakhari, Samir AU - Hoek, Jan B AD - Former Director, Division of Metabolism and Health Effects, NIAAA, NIH, Bethesda, MD, 20852, USA, szakhari@discus.org. Y1 - 2015 PY - 2015 DA - 2015 SP - 7 EP - 39 VL - 815 SN - 0065-2598, 0065-2598 KW - Estrogens KW - 0 KW - Ethanol KW - 3K9958V90M KW - Folic Acid KW - 935E97BOY8 KW - Index Medicus KW - Folic Acid -- metabolism KW - Estrogens -- metabolism KW - Epidemiologic Studies KW - Risk Factors KW - Humans KW - Female KW - Ethanol -- toxicity KW - Ethanol -- metabolism KW - Breast Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1628878280?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Alcohol+and+breast+cancer%3A+reconciling+epidemiological+and+molecular+data.&rft.au=Zakhari%2C+Samir%3BHoek%2C+Jan+B&rft.aulast=Zakhari&rft.aufirst=Samir&rft.date=2015-01-01&rft.volume=815&rft.issue=&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/10.1007%2F978-3-319-09614-8_2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-23 N1 - Date created - 2014-11-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/978-3-319-09614-8_2 ER - TY - JOUR T1 - Microglial regulation of immunological and neuroprotective functions of astroglia. AN - 1627078775; 25130274 AB - Microglia and astroglia play critical roles in the development, function, and survival of neurons in the CNS. However, under inflammatory conditions the role of astrogliosis in the inflammatory process and its effects on neurons remains unclear. Here, we used several types of cell cultures treated with the bacterial inflammogen LPS to address these questions. We found that the presence of astroglia reduced inflammation-driven neurotoxicity, suggesting that astrogliosis is principally neuroprotective. Neutralization of supernatant glial cell line-derived neurotrophic factor (GDNF) released from astroglia significantly reduced this neuroprotective effect during inflammation. To determine the immunological role of astroglia, we optimized a highly-enriched astroglial culture protocol and demonstrated that LPS failed to induce the synthesis and release of TNF-α and iNOS/NO. Instead we found significant enhancement of TNF-α and iNOS expression in highly-enriched astroglial cultures required the presence of 0.5-1% microglia, respectively. Thus suggesting that microglial-astroglial interactions are required for LPS to induce the expression of pro-inflammatory factors and GDNF from astroglia. Specifically, we found that microglia-derived TNF-α plays a pivotal role as a paracrine signal to regulate the neuroprotective functions of astrogliosis. Taken together, these findings suggest that astroglia may not possess the ability to directly recognize the innate immune stimuli LPS, but rather depend on crosstalk with microglia to elicit release of neurotrophic factors as a counterbalance to support neuronal survival from the collateral damage generated by activated microglia during neuroinflammation. © 2014 Wiley Periodicals, Inc. JF - Glia AU - Chen, Shih-Heng AU - Oyarzabal, Esteban A AU - Sung, Yueh-Feng AU - Chu, Chun-Hsien AU - Wang, Qingshan AU - Chen, Shiou-Lan AU - Lu, Ru-Band AU - Hong, Jau-Shyong AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 118 EP - 131 VL - 63 IS - 1 KW - Glial Cell Line-Derived Neurotrophic Factor KW - 0 KW - Lipopolysaccharides KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - astroglia KW - microglia KW - glial cell line-derived neurotrophic factor KW - neuroprotection KW - glial interaction KW - neuroinflammation KW - Gliosis -- metabolism KW - Animals KW - Rats, Inbred F344 KW - Glial Cell Line-Derived Neurotrophic Factor -- metabolism KW - Cells, Cultured KW - Lipopolysaccharides -- pharmacology KW - Tumor Necrosis Factor-alpha -- metabolism KW - Female KW - Neurons -- metabolism KW - Microglia -- immunology KW - Astrocytes -- immunology KW - Microglia -- metabolism KW - Astrocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627078775?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Glia&rft.atitle=Microglial+regulation+of+immunological+and+neuroprotective+functions+of+astroglia.&rft.au=Chen%2C+Shih-Heng%3BOyarzabal%2C+Esteban+A%3BSung%2C+Yueh-Feng%3BChu%2C+Chun-Hsien%3BWang%2C+Qingshan%3BChen%2C+Shiou-Lan%3BLu%2C+Ru-Band%3BHong%2C+Jau-Shyong&rft.aulast=Chen&rft.aufirst=Shih-Heng&rft.date=2015-01-01&rft.volume=63&rft.issue=1&rft.spage=118&rft.isbn=&rft.btitle=&rft.title=Glia&rft.issn=1098-1136&rft_id=info:doi/10.1002%2Fglia.22738 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-14 N1 - Date created - 2014-11-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Neurosci Res. 1996 Jan;24(2):131-8 [8929919] Glia. 1997 Mar;19(3):190-8 [9063726] Exp Neurol. 1998 Feb;149(2):301-9 [9500953] Neurochem Res. 1998 May;23(5):759-65 [9566616] Glia. 1998 Aug;23(4):316-28 [9671962] J Physiol. 2004 Nov 15;561(Pt 1):109-22 [15358811] Glia. 2005 Feb;49(3):360-74 [15538753] J Neuroimmunol. 2005 Feb;159(1-2):12-9 [15652398] J Neurosci. 2005 Feb 16;25(7):1788-96 [15716415] Expert Opin Drug Saf. 2005 May;4(3):433-42 [15934851] J Neurosci Methods. 2006 Jan 15;150(1):128-37 [16105687] Glia. 2006 Feb;53(3):248-56 [16265667] Glia. 2006 Jul;54(1):35-46 [16673374] J Gastroenterol Hepatol. 2006 Jul;21(7):1136-42 [16824065] Brain Res. 2006 Oct 20;1116(1):12-8 [16956589] J Neurosci Res. 2007 Jan;85(1):205-12 [17061254] Trends Immunol. 2007 Mar;28(3):138-45 [17276138] J Neuroinflammation. 2007;4:26 [17937799] Glia. 2008 Aug 15;56(11):1187-98 [18449943] Brain Res Bull. 2008 Sep 5;77(1):19-26 [18639741] Acta Neurobiol Exp (Wars). 2008;68(4):526-34 [19112477] Genesis. 2008 Dec;46(12):743-57 [18924152] Brain Res Rev. 2009 Mar;59(2):278-92 [18822314] J Neurochem. 2009 May;109 Suppl 1:117-25 [19393017] Brain Behav Immun. 2010 Jan;24(1):102-9 [19735725] Neuroscience. 2010 Jan 20;165(2):386-94 [19878709] Mol Neurobiol. 2010 Jun;41(2-3):232-41 [20148316] J Neuroimmunol. 2010 Aug 25;225(1-2):43-51 [20471698] Neuron. 2011 Sep 8;71(5):799-811 [21903074] Br J Pharmacol. 2012 Jan;165(2):494-505 [21726209] J Neurosci Methods. 2012 May 30;207(1):59-71 [22483759] Neurobiol Dis. 2012 Sep;47(3):407-15 [22579772] Glia. 2012 Sep;60(9):1417-26 [22648602] J Neuroinflammation. 2012;9:95 [22607552] Glia. 2012 Oct;60(10):1506-17 [22740309] Neurochem Int. 2013 Jul;63(1):47-53 [23619393] Methods Mol Biol. 2013;1041:231-40 [23813383] Glia. 2013 Sep;61(9):1429-42 [23832717] Nat Neurosci. 2014 Jan;17(1):131-43 [24316888] Glia. 2014 Jun;62(6):841-54 [24590682] Prog Neurobiol. 2000 Dec;62(6):649-71 [10880854] J Virol. 2000 Oct;74(19):9214-21 [10982368] FASEB J. 2001 Jan;15(1):155-163 [11149903] Trends Neurosci. 2001 Jan;24(1):39-47 [11163886] Brain Res. 2001 Aug 3;909(1-2):92-101 [11478925] Glia. 2001 Nov;36(2):180-90 [11596126] J Neurosci Res. 2002 Jan 1;67(1):21-9 [11754077] Proc Natl Acad Sci U S A. 2012 Jan 24;109(4):E197-205 [22167804] Glia. 2012 Apr;60(4):630-8 [22271465] J Pharmacol Exp Ther. 2000 May;293(2):607-17 [10773035] Neurochem Int. 2000 Aug-Sep;37(2-3):317-29 [10812217] J Neurosci. 2002 Feb 1;22(3):876-85 [11826117] J Neurosci. 2002 Apr 1;22(7):2478-86 [11923412] J Pharmacol Exp Ther. 2002 Sep;302(3):1212-9 [12183682] Eur J Neurosci. 2002 Oct;16(7):1275-83 [12405988] Cell Tissue Res. 2003 Apr;312(1):135-9 [12712323] J Neurochem. 2003 Jul;86(1):228-37 [12807442] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8514-9 [12824464] Glia. 2003 Sep;43(3):281-91 [12898707] Neuroreport. 2003 Aug 6;14(11):1529-34 [12960779] J Neurochem. 2004 Feb;88(3):746-58 [14720224] Am J Pathol. 2004 Jun;164(6):2067-75 [15161641] J Immunol. 2004 Aug 15;173(4):2762-70 [15294995] J Neurochem. 2004 Oct;91(1):119-32 [15379893] Brain Res. 2004 Oct 29;1025(1-2):186-93 [15464759] J Cell Biol. 1980 Jun;85(3):890-902 [6248568] J Neurosci. 1986 Aug;6(8):2163-78 [3018187] Proc Natl Acad Sci U S A. 1989 Aug;86(16):6348-52 [2474832] J Immunol. 1990 Apr 15;144(8):2999-3007 [2109008] Science. 1993 May 21;260(5111):1130-2 [8493557] J Neurosci Res. 1994 Feb 15;37(3):406-14 [7513765] J Neurocytol. 1994 Oct;23(10):605-13 [7836955] Dev Neurosci. 1994;16(3-4):128-36 [7535679] J Neuropathol Exp Neurol. 1996 May;55(5):515-21 [8627341] J Immunol. 1996 Mar 15;156(6):2247-55 [8690915] J Neurochem. 2006 Feb;96(3):893-907 [16405499] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/glia.22738 ER - TY - JOUR T1 - Identifying gender differences in reported occupational information from three US population-based case-control studies AN - 1808615939; PQ0003453858 AB - ObjectivesGrowing evidence suggests that gender-blind assessment of exposure may introduce exposure misclassification, but few studies have characterised gender differences across occupations and industries. We pooled control responses to job-specific, industry-specific and exposure-specific questionnaires (modules) that asked detailed questions about work activities from three US population-based case-control studies to examine gender differences in work tasks and their frequencies.MethodsWe calculated the ratio of female-to-male controls that completed each module. For four job modules (assembly worker, machinist, health professional, janitor/cleaner) and for subgroups of jobs that completed those modules, we evaluated gender differences in task prevalence and frequency using chi 2 and Mann-Whitney U tests, respectively.ResultsThe 1360 female and 2245 male controls reported 6033 and 12083 jobs, respectively. Gender differences in female:male module completion ratios were observed for 39 of 45 modules completed by greater than or equal to 20 controls. Gender differences in task prevalence varied in direction and magnitude. For example, female janitors were significantly more likely to polish furniture (79% vs 44%), while male janitors were more likely to strip floors (73% vs 50%). Women usually reported more time spent on tasks than men. For example, the median hours per week spent degreasing for production workers in product manufacturing industries was 6.3 for women and 3.0 for men.ConclusionsObserved gender differences may reflect actual differences in tasks performed or differences in recall, reporting or perception, all of which contribute to exposure misclassification and impact relative risk estimates. Our findings reinforce the need to capture subject-specific information on work tasks. JF - Occupational and Environmental Medicine AU - Locke, Sarah J AU - Colt, Joanne S AU - Stewart, Patricia A AU - Armenti, Karla R AU - Baris, Dalsu AU - Blair, Aaron AU - Cerhan, James R AU - Chow, Wong-Ho AU - Cozen, Wendy AU - Davis, Faith AU - De Roos, Anneclaire J AU - Hartge, Patricia AU - Karagas, Margaret R AU - Johnson, Alison AU - Purdue, Mark P AU - Rothman, Nathaniel AU - Schwartz, Kendra AU - Schwenn, Molly AU - Severson, Richard AU - Silverman, Debra T AU - Friesen, Melissa C AD - Occupational and Environmental Epidemiology, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA Y1 - 2014/12/28/ PY - 2014 DA - 2014 Dec 28 SP - 855 EP - 864 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 71 IS - 12 SN - 1351-0711, 1351-0711 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - population-based studies KW - case-control studies KW - occupational exposure KW - occupational health KW - Risk assessment KW - Manufacturing industry KW - Inventories KW - Sex differences KW - Workers KW - Perception KW - Gender KW - Cleaning process KW - Occupational exposure KW - H 1000:Occupational Safety and Health KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808615939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=Identifying+gender+differences+in+reported+occupational+information+from+three+US+population-based+case-control+studies&rft.au=Locke%2C+Sarah+J%3BColt%2C+Joanne+S%3BStewart%2C+Patricia+A%3BArmenti%2C+Karla+R%3BBaris%2C+Dalsu%3BBlair%2C+Aaron%3BCerhan%2C+James+R%3BChow%2C+Wong-Ho%3BCozen%2C+Wendy%3BDavis%2C+Faith%3BDe+Roos%2C+Anneclaire+J%3BHartge%2C+Patricia%3BKaragas%2C+Margaret+R%3BJohnson%2C+Alison%3BPurdue%2C+Mark+P%3BRothman%2C+Nathaniel%3BSchwartz%2C+Kendra%3BSchwenn%2C+Molly%3BSeverson%2C+Richard%3BSilverman%2C+Debra+T%3BFriesen%2C+Melissa+C&rft.aulast=Locke&rft.aufirst=Sarah&rft.date=2014-12-28&rft.volume=71&rft.issue=12&rft.spage=855&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2013-101801 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Risk assessment; Workers; Inventories; Perception; Sex differences; Occupational exposure; Manufacturing industry; Gender; Cleaning process DO - http://dx.doi.org/10.1136/oemed-2013-101801 ER - TY - JOUR T1 - Work history and mortality risks in 90268 US radiological technologists AN - 1808717972; PQ0003453839 AB - ObjectivesThere have been few studies of work history and mortality risks in medical radiation workers. We expanded by 11years and more outcomes our previous study of mortality risks and work history, a proxy for radiation exposure.MethodsUsing Cox proportional hazards models, we estimated mortality risks according to questionnaire work history responses from 1983 to 1989 through 2008 by 90268 US radiological technologists. We controlled for potential confounding by age, birth year, smoking history, body mass index, race and gender.ResultsThere were 9566 deaths (3329 cancer and 3020 circulatory system diseases). Mortality risks increased significantly with earlier year began working for female breast (p trend=0.01) and stomach cancers (p trend=0.01), ischaemic heart (p trend=0.03) and cerebrovascular diseases (p trend=0.02). The significant trend with earlier year first worked was strongly apparent for breast cancer during baseline through 1997, but not 1998-2008. Risks were similar in the two periods for circulatory diseases. Radiological technologists working greater than or equal to 5years before 1950 had elevated mortality from breast cancer (HR=2.05, 95% CI 1.27 to 3.32), leukaemia (HR=2.57, 95% CI 0.96 to 6.68), ischaemic heart disease (HR=1.13, 95% CI 0.96 to 1.33) and cerebrovascular disease (HR=1.28, 95% CI 0.97 to 1.69). No other work history factors were consistently associated with mortality risks from specific cancers or circulatory diseases, or other conditions.ConclusionsRadiological technologists who began working in early periods and for more years before 1950 had increased mortality from a few cancers and some circulatory system diseases, likely reflecting higher occupational radiation exposures in the earlier years. JF - Occupational and Environmental Medicine AU - Liu, Jason J AU - Freedman, D Michal AU - Little, Mark P AU - Doody, Michele M AU - Alexander, Bruce H AU - Kitahara, Cari M AU - Lee, Terrence AU - Rajaraman, Preetha AU - Miller, Jeremy S AU - Kampa, Diane M AU - Simon, Steven L AU - Preston, Dale L AU - Linet, Martha S AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA Y1 - 2014/12/22/ PY - 2014 DA - 2014 Dec 22 SP - 819 EP - 835 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 71 IS - 12 SN - 1351-0711, 1351-0711 KW - Health & Safety Science Abstracts KW - mortality KW - neoplasms KW - circulatory system diseases KW - radiologic technologists KW - work history KW - Historical account KW - Mortality KW - Age KW - Body mass KW - Cancer KW - Smoking KW - Leukemia KW - Health risks KW - Radiation KW - Risk factors KW - Breast cancer KW - Occupational exposure KW - Heart diseases KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808717972?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=Work+history+and+mortality+risks+in+90268+US+radiological+technologists&rft.au=Liu%2C+Jason+J%3BFreedman%2C+D+Michal%3BLittle%2C+Mark+P%3BDoody%2C+Michele+M%3BAlexander%2C+Bruce+H%3BKitahara%2C+Cari+M%3BLee%2C+Terrence%3BRajaraman%2C+Preetha%3BMiller%2C+Jeremy+S%3BKampa%2C+Diane+M%3BSimon%2C+Steven+L%3BPreston%2C+Dale+L%3BLinet%2C+Martha+S&rft.aulast=Liu&rft.aufirst=Jason&rft.date=2014-12-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=47th+American+Geophysical+Union+Fall+Meeting&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Mortality; Historical account; Age; Body mass; Cancer; Health risks; Leukemia; Smoking; Radiation; Risk factors; Breast cancer; Occupational exposure; Heart diseases DO - http://dx.doi.org/10.1136/oemed-2013-101859 ER - TY - JOUR T1 - Photo activation of HPPH encapsulated in "Pocket" liposomes triggers multiple drug release and tumor cell killing in mouse breast cancer xenografts AN - 1647009351; 21327245 AB - We recently reported laser-triggered release of photosensitive compounds from liposomes containing dipalmitoylphosphatidylcholine (DPPC) and 1,2 bis(tricosa-10,12-diynoyl)-sn-glycero-3-phosphocholine (DC8,9PC). We hypothesized that the permeation of photoactivated compounds occurs through domains of enhanced fluidity in the liposome membrane and have thus called them "Pocket" liposomes. In this study we have encapsulated the red light activatable anticancer photodynamic therapy drug 2-(1-Hexyloxyethyl)-2-devinyl pyropheophorbide-a (HPPH) (Ex/Em410/670 nm) together with calcein (Ex/Em490/517 nm) as a marker for drug release in Pocket liposomes. A mole ratio of 7.6:1 lipid:HPPH was found to be optimal, with >80% of HPPH being included in the liposomes. Exposure of liposomes with a cw-diode 660 nm laser (90 mW, 0-5 minutes) resulted in calcein release only when HPPH was included in the liposomes. Further analysis of the quenching ratios of liposome-entrapped calcein in the laser treated samples indicated that the laser-triggered release occurred via the graded mechanism. In vitro studies with MDA-MB-231-LM2 breast cancer cell line showed significant cell killing upon treatment of cell-liposome suspensions with the laser. To assess in vivo efficacy, we implanted MDA-MB-231-LM2 cells containing the luciferase gene along the mammary fat pads on the ribcage of mice. For biodistribution experiments, trace amounts of a near infrared lipid probe DiR (Ex/Em745/840 nm) were included in the liposomes. Liposomes were injected intravenously and laser treatments (90 mW, 0.9 cm diameter, for an exposure duration ranging from 5-8 minutes) were done 4 hours postinjection (only one tumor per mouse was treated, keeping the second flank tumor as control). Calcein release occurred as indicated by an increase in calcein fluorescence from laser treated tumors only. The animals were observed for up to 15 days postinjection and tumor volume and luciferase expression was measured. A significant decrease in luciferase expression and reduction in tumor volume was observed only in laser treated animal groups injected with liposomes containing HPPH. Histopathological examination of tumor tissues indicated tumor necrosis resulting from laser treatment of the HPPH-encapsulated liposomes that were taken up into the tumor area. JF - International Journal of Nanomedicine AU - Sine, Jessica AU - Urban, Cordula AU - Thayer, Derek AU - Charron, Heather AU - Valim, Niksa AU - Tata, Darrell B AU - Schiff, Rachel AU - Blumenthal, Robert AU - Joshi, Amit AU - Puri, Anu AD - Membrane Structure and Function Section, Basic Research Laboratory, Center for Cancer Research, National Cancer Institute - Frederick, Frederick, MD, USA Y1 - 2014/12/19/ PY - 2014 DA - 2014 Dec 19 SP - 125 EP - 145 PB - Dove Medical Press Ltd, Beechfield House Macclesfield SK11 0JL United Kingdom VL - 10 SN - 1176-9114, 1176-9114 KW - Biotechnology and Bioengineering Abstracts KW - laser-triggered payload release KW - photo-agents KW - photopolymerizable phospholipids KW - tumor regression KW - phototriggering KW - Drug delivery KW - Fluorescence KW - Fluidity KW - Calcein KW - Lipids KW - photodynamic therapy KW - Tumors KW - Liposomes KW - Tumor cells KW - Light effects KW - Tumor cell lines KW - Necrosis KW - Fluorescent indicators KW - Breast cancer KW - Lasers KW - Xenografts KW - nanotechnology KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647009351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Nanomedicine&rft.atitle=Photo+activation+of+HPPH+encapsulated+in+%22Pocket%22+liposomes+triggers+multiple+drug+release+and+tumor+cell+killing+in+mouse+breast+cancer+xenografts&rft.au=Sine%2C+Jessica%3BUrban%2C+Cordula%3BThayer%2C+Derek%3BCharron%2C+Heather%3BValim%2C+Niksa%3BTata%2C+Darrell+B%3BSchiff%2C+Rachel%3BBlumenthal%2C+Robert%3BJoshi%2C+Amit%3BPuri%2C+Anu&rft.aulast=Sine&rft.aufirst=Jessica&rft.date=2014-12-19&rft.volume=10&rft.issue=&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Nanomedicine&rft.issn=11769114&rft_id=info:doi/10.2147%2FIJN.S72143 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Drug delivery; Fluidity; Fluorescence; Calcein; Lipids; photodynamic therapy; Tumors; Tumor cells; Liposomes; Light effects; Necrosis; Tumor cell lines; Breast cancer; Fluorescent indicators; Lasers; Xenografts; nanotechnology DO - http://dx.doi.org/10.2147/IJN.S72143 ER - TY - JOUR T1 - Pre-immature dendritic cells (PIDC) pulsed with HPV16 E6 or E7 peptide are capable of eliciting specific immune response in patients with advanced cervical cancer. AN - 1639972742; 25510844 AB - The protein products of the early genes E6 and E7 in high-risk HPV types 16 and 18 have been implicated in the oncogenic capability of these viruses. Therefore, these peptides represent attractive vaccine therapy targets. Thirty-two patients with advanced cervical cancer (HPV16 or 18 positive) were treated with HPV16 E6 (18-26) (Arm A) or HPV16 E7 (12-20) peptide (Arm B) pulsed on PBMCs in order to illicit immune response against the relevant peptide on both arms. These PBMCs were cultured for a short time (48 hours only) and in the presence of GM- CSF, accordingly, they were identified as "Pre-Immature Dentritic Cells". 51Cr release assay and ELISPOT demonstrated evidence of specific immune response against the relevant peptide in 10/16 (63%) evaluable patients in arm A and 7/12 (58%) in arm B. HPV16 E6 was found to be homologous to HPV18 E6 in both vivo and vitro. The median overall survival (OS) and progression free survival (PFS) for the full cohort was 10.0 and 3.5 months, respectively. There were no RECIST responses in any patient. The majority of toxicities were grade I and II. We demonstrated the feasibility and ability of Pre-Immature Dentritic Cells pulsed with HPV16 E6 (18-26) or HPV16 E7 (12-20) to induce a specific immune response against the relevant peptide despite the advanced disease of the cervical cancer patients treated on this trial. We believe that this observation deserves further investigations. JF - Journal of translational medicine AU - Rahma, Osama E AU - Herrin, Vincent E AU - Ibrahim, Rami A AU - Toubaji, Anton AU - Bernstein, Sarah AU - Dakheel, Omar AU - Steinberg, Seth M AU - Abu Eid, Rasha AU - Mkrtichyan, Mikayel AU - Berzofsky, Jay A AU - Khleif, Samir N AD - Cancer Vaccine Branch, CCR, NCI, 10 Center Drive, Bethesda 20892, MD, USA. skhleif@gru.edu. Y1 - 2014/12/16/ PY - 2014 DA - 2014 Dec 16 SP - 353 VL - 12 KW - Cancer Vaccines KW - 0 KW - E6 protein, Human papillomavirus type 16 KW - Oncogene Proteins, Viral KW - Papillomavirus E7 Proteins KW - Repressor Proteins KW - oncogene protein E7, Human papillomavirus type 16 KW - Index Medicus KW - Humans KW - Adult KW - Middle Aged KW - Female KW - Papillomavirus E7 Proteins -- administration & dosage KW - Uterine Cervical Neoplasms -- therapy KW - Dendritic Cells -- immunology KW - Cancer Vaccines -- immunology KW - Oncogene Proteins, Viral -- immunology KW - Repressor Proteins -- administration & dosage KW - Cancer Vaccines -- therapeutic use KW - Repressor Proteins -- immunology KW - Uterine Cervical Neoplasms -- immunology KW - Oncogene Proteins, Viral -- administration & dosage KW - Papillomavirus E7 Proteins -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639972742?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+translational+medicine&rft.atitle=Pre-immature+dendritic+cells+%28PIDC%29+pulsed+with+HPV16+E6+or+E7+peptide+are+capable+of+eliciting+specific+immune+response+in+patients+with+advanced+cervical+cancer.&rft.au=Rahma%2C+Osama+E%3BHerrin%2C+Vincent+E%3BIbrahim%2C+Rami+A%3BToubaji%2C+Anton%3BBernstein%2C+Sarah%3BDakheel%2C+Omar%3BSteinberg%2C+Seth+M%3BAbu+Eid%2C+Rasha%3BMkrtichyan%2C+Mikayel%3BBerzofsky%2C+Jay+A%3BKhleif%2C+Samir+N&rft.aulast=Rahma&rft.aufirst=Osama&rft.date=2014-12-16&rft.volume=12&rft.issue=&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Journal+of+translational+medicine&rft.issn=1479-5876&rft_id=info:doi/10.1186%2Fs12967-014-0353-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-15 N1 - Date created - 2014-12-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Oncol. 2001 Mar;18(3):475-8 [11179474] Cancer Immunol Immunother. 2012 Mar;61(3):373-84 [21927947] J Cancer Res Clin Oncol. 2003 Sep;129(9):521-30 [12898233] Ann Oncol. 2004 Feb;15(2):197-200 [14760108] J Clin Oncol. 2004 Aug 1;22(15):3113-9 [15284262] Hum Pathol. 2004 Aug;35(8):971-82 [15297964] J Virol. 2004 Nov;78(21):11451-60 [15479788] Lancet. 1996 Jun 1;347(9014):1523-7 [8684105] J Exp Med. 1997 Oct 20;186(8):1183-7 [9379142] Nature. 1998 Mar 19;392(6673):245-52 [9521319] J Pathol. 1999 Sep;189(1):12-9 [10451482] Lancet Oncol. 2005 May;6(5):271-8 [15863374] J Clin Oncol. 2005 Jul 20;23(21):4626-33 [15911865] Gynecol Oncol. 2006 Mar;100(3):469-78 [16249018] J Clin Virol. 2007 Mar;38(3):189-97 [17258503] Lung Cancer. 2007 Apr;56(1):135-7 [17157952] J Clin Invest. 2007 May;117(5):1195-203 [17476349] Int J Cancer. 2007 Aug 1;121(3):621-32 [17405118] Lancet. 2007 Jun 2;369(9576):1861-8 [17544766] Sex Health. 2007 Sep;4(3):147-63 [17931528] Curr Mol Med. 2009 Aug;9(6):766-73 [19689303] N Engl J Med. 2009 Nov 5;361(19):1838-47 [19890126] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Curr Opin Immunol. 2003 Apr;15(2):138-47 [12633662] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12967-014-0353-4 ER - TY - JOUR T1 - Reduced Prevalence of Vulvar HPV16/18 Infection Among Women Who Received the HPV16/18 Bivalent Vaccine: A Nested Analysis Within the Costa Rica Vaccine Trial AN - 1687671860; PQ0001542370 AB - Background Vaccine efficacy (VE) against vulvar human papillomavirus (HPV) infection has not been reported and data regarding its epidemiology are sparse. Methods Women (n = 5404) age 22-29 present at the 4-year study visit of the Costa Rica Vaccine Trial provided vulvar and cervical samples. A subset (n = 1044) was tested for HPV DNA (SPF sub(10)/LiPA sub(25) version 1). VE against 1-time detection of vulvar HPV16/18 among HPV vaccinated versus unvaccinated women was calculated and compared to the cervix. Prevalence of and risk factors for HPV were evaluated in the control arm (n = 536). Results Vulvar HPV16/18 VE (54.1%; 95% confidence interval [CI], 4.9%-79.1%) was comparable to cervix (45.8%; 95% CI, 6.4%-69.4%). Vulvar and cervical HPV16 prevalence within the control arm was 3.0% and 4.7%, respectively. Independent risk factors for vulvar HPV were similar to cervix and included: age (adjusted odds ratio [aOR] 0.5 [95% CI, .3-.9] > or =28 vs 22-23]); marital status (aOR 2.3 [95% CI, 1.5-3.5] single vs married/living-as-married); and number of sexual partners (aOR 3.6 [95% CI, 1.9-7.0] > or =6 vs 1). Conclusions In this intention-to-treat analysis, VE against vulvar and cervical HPV16/18 were comparable 4 years following vaccination. Risk factors for HPV were similar by anatomic site. JF - Journal of Infectious Diseases AU - Kuhs, Krystle A Lang AU - Gonzalez, Paula AU - Rodriguez, Ana Cecilia AU - van Doorn, Leen-Jan AU - Schiffman, Mark AU - Struijk, Linda AU - Chen, Sabrina AU - Quint, Wim AU - Lowy, Douglas R AU - Porras, Carolina AD - Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Dr, Rm 6-E210, Bethesda, MD 20892, krystle.kuhs@nih.gov Y1 - 2014/12/15/ PY - 2014 DA - 2014 Dec 15 SP - 1890 EP - 1899 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 210 IS - 12 SN - 0022-1899, 0022-1899 KW - Genetics Abstracts; Virology & AIDS Abstracts; Health & Safety Science Abstracts; Risk Abstracts KW - Costa Rica KW - HPV KW - HPV vaccine KW - vulvar human papillomavirus vaccine KW - Age KW - Data processing KW - Marriage KW - Infection KW - Clinical trials KW - Sexual behavior KW - Vaccination KW - Sexual partners KW - ASW, Costa Rica KW - Infectious diseases KW - Epidemiology KW - Human papillomavirus 16 KW - Risk factors KW - DNA KW - Females KW - Vaccines KW - Cervix KW - Human papillomavirus KW - G 07720:Immunogenetics KW - R2 23060:Medical and environmental health KW - H 4000:Food and Drugs KW - V 22400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687671860?accountid=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=Reduced+Prevalence+of+Vulvar+HPV16%2F18+Infection+Among+Women+Who+Received+the+HPV16%2F18+Bivalent+Vaccine%3A+A+Nested+Analysis+Within+the+Costa+Rica+Vaccine+Trial&rft.au=Kuhs%2C+Krystle+A+Lang%3BGonzalez%2C+Paula%3BRodriguez%2C+Ana+Cecilia%3Bvan+Doorn%2C+Leen-Jan%3BSchiffman%2C+Mark%3BStruijk%2C+Linda%3BChen%2C+Sabrina%3BQuint%2C+Wim%3BLowy%2C+Douglas+R%3BPorras%2C+Carolina&rft.aulast=Kuhs&rft.aufirst=Krystle+A&rft.date=2014-12-15&rft.volume=210&rft.issue=12&rft.spage=1890&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiu357 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-06-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Sexual partners; Age; Data processing; Epidemiology; Risk factors; DNA; Vaccines; Infection; Cervix; Vaccination; Infectious diseases; Marriage; Females; Sexual behavior; Clinical trials; Human papillomavirus 16; Human papillomavirus; ASW, Costa Rica DO - http://dx.doi.org/10.1093/infdis/jiu357 ER - TY - CPAPER T1 - Making the connection: Federal efforts on climate change and health T2 - 47th American Geophysical Union Fall Meeting AN - 1651740165; 6329742 JF - 47th American Geophysical Union Fall Meeting AU - Balbus, John Y1 - 2014/12/15/ PY - 2014 DA - 2014 Dec 15 KW - Climatic changes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1651740165?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=47th+American+Geophysical+Union+Fall+Meeting&rft.atitle=Making+the+connection%3A+Federal+efforts+on+climate+change+and+health&rft.au=Balbus%2C+John&rft.aulast=Balbus&rft.aufirst=John&rft.date=2014-12-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=47th+American+Geophysical+Union+Fall+Meeting&rft.issn=&rft_id=info:doi/ L2 - https://agu.confex.com/agu/fm14/meetingapp.cgi#ModuleSessionsByDay/0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-31 N1 - Last updated - 2015-02-06 ER - TY - CPAPER T1 - When the Well Runs Dry: Climate Change, Water and Human Health T2 - 47th American Geophysical Union Fall Meeting AN - 1651739632; 6330287 JF - 47th American Geophysical Union Fall Meeting AU - Balbus, John Y1 - 2014/12/15/ PY - 2014 DA - 2014 Dec 15 KW - Climatic changes KW - Water wells KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1651739632?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=47th+American+Geophysical+Union+Fall+Meeting&rft.atitle=When+the+Well+Runs+Dry%3A+Climate+Change%2C+Water+and+Human+Health&rft.au=Balbus%2C+John&rft.aulast=Balbus&rft.aufirst=John&rft.date=2014-12-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=47th+American+Geophysical+Union+Fall+Meeting&rft.issn=&rft_id=info:doi/ L2 - https://agu.confex.com/agu/fm14/meetingapp.cgi#ModuleSessionsByDay/0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-31 N1 - Last updated - 2015-02-06 ER - TY - JOUR T1 - Anthracycline-free neoadjuvant therapy induces pathological complete responses by exploiting immune proficiency in HER2+ breast cancer patients. AN - 1640327724; 25512030 AB - Neoadjuvant Chemotherapy (NC) including trastuzumab induces a high rate of pathological Complete Responses (pCR) in patients with locally advanced HER2-overexpressing Breast Cancer (BC), but is penalized by a severe cardiotoxicity when combined with anthracyclines. A phase II study was designed to assess whether an anthracycline-free NC regimen based on the early addition of trastuzumab to paclitaxel may increase the pCR rate without inducing severe cardiotoxicity in patients with locally advanced HER2-overexpressing BC. Immunomonitoring was performed to assess the contribution of patients' immunological background to the induction of clinical responses. Stage II-III HER2-positive BC patients received 24 weeks paclitaxel and trastuzumab NC, followed by 1 year adjuvant trastuzumab ± hormonal and/or radio-therapy. Assessment of pCR rate was the primary endpoint. A group of HER2-negative BC patients treated with neoadjuvant taxanes and anthracyclines was included. Serum levels of 10 cytokines and the efficiency of trastuzumab-mediated antibody-dependent cell cytotoxicity (ADCC) were monitored in vitro every 3 months. From July 2006 to February 2013, we enrolled 109 patients including 46 evaluable HER2-positive cases. A pCR rate of 50% was reached and no severe cardiotoxicity occurred. Serum cytokine profiling revealed only an IL-10 decrease (P = 0.02) in patients achieving a partial response, while HER2-negative patients disclosed marked cytokines changes. Compared to the unfavourable F/F genotype, patients carrying the V allele in the FcγRIIIa-158 polymorphism showed a higher efficacy of trastuzumab-ADCC throughout treatment (P ≤0.05). In the absence of anthracyclines, trastuzumab and paclitaxel induced a high rate of pCR, exploiting the synergy between the immunomodulating properties of these drugs and the retained immunological proficiency of patients with HER2-overexpressing BC. Trial registration number: NCT02307227, registered on ClinicalTrials.gov (http://www.clinicaltrials.gov, November 26, 2014). JF - BMC cancer AU - Miolo, Gianmaria AU - Muraro, Elena AU - Martorelli, Debora AU - Lombardi, Davide AU - Scalone, Simona AU - Spazzapan, Simon AU - Massarut, Samuele AU - Perin, Tiziana AU - Viel, Elda AU - Comaro, Elisa AU - Talamini, Renato AU - Bidoli, Ettore AU - Turchet, Elisa AU - Crivellari, Diana AU - Dolcetti, Riccardo AD - Cancer Bio-Immunotherapy Unit, Department of Medical Oncology, C,R,O, National Cancer Institute, Via F, Gallini 2, 33081 Aviano, PN, Italy. rdolcetti@cro.it. Y1 - 2014/12/15/ PY - 2014 DA - 2014 Dec 15 SP - 954 VL - 14 KW - Antibodies, Monoclonal, Humanized KW - 0 KW - Cytokines KW - FCGR3A protein, human KW - Receptors, IgG KW - Receptor, ErbB-2 KW - EC 2.7.10.1 KW - Trastuzumab KW - P188ANX8CK KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Cytokines -- blood KW - Paclitaxel -- administration & dosage KW - Young Adult KW - Neoplasm Staging KW - Receptor, ErbB-2 -- metabolism KW - Polymorphism, Genetic KW - Humans KW - Neoadjuvant Therapy KW - Aged KW - Antibodies, Monoclonal, Humanized -- administration & dosage KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Antibody-Dependent Cell Cytotoxicity -- immunology KW - Female KW - Receptors, IgG -- genetics KW - Breast Neoplasms -- immunology KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- mortality KW - Breast Neoplasms -- pathology KW - Breast Neoplasms -- metabolism KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1640327724?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+cancer&rft.atitle=Anthracycline-free+neoadjuvant+therapy+induces+pathological+complete+responses+by+exploiting+immune+proficiency+in+HER2%2B+breast+cancer+patients.&rft.au=Miolo%2C+Gianmaria%3BMuraro%2C+Elena%3BMartorelli%2C+Debora%3BLombardi%2C+Davide%3BScalone%2C+Simona%3BSpazzapan%2C+Simon%3BMassarut%2C+Samuele%3BPerin%2C+Tiziana%3BViel%2C+Elda%3BComaro%2C+Elisa%3BTalamini%2C+Renato%3BBidoli%2C+Ettore%3BTurchet%2C+Elisa%3BCrivellari%2C+Diana%3BDolcetti%2C+Riccardo&rft.aulast=Miolo&rft.aufirst=Gianmaria&rft.date=2014-12-15&rft.volume=14&rft.issue=&rft.spage=954&rft.isbn=&rft.btitle=&rft.title=BMC+cancer&rft.issn=1471-2407&rft_id=info:doi/10.1186%2F1471-2407-14-954 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-21 N1 - Date created - 2014-12-23 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT02307227; ClinicalTrials.gov N1 - SuppNotes - Cited By: Cell Immunol. 1997 Aug 25;180(1):55-61 [9316639] Blood. 1998 Jan 15;91(2):656-62 [9427722] J Clin Oncol. 2005 Jun 1;23(16):3676-85 [15738535] Br J Cancer. 2006 Jan 30;94(2):259-67 [16404427] Clin Cancer Res. 2007 Jan 1;13(1):228-33 [17200359] Cancer Res. 2007 Dec 15;67(24):11991-9 [18089830] J Clin Oncol. 2008 Apr 10;26(11):1778-80 [18347004] J Clin Oncol. 2008 Apr 10;26(11):1789-96 [18347005] Breast Cancer Res. 2008;10(3):R45 [18474099] Eur J Pharm Sci. 2009 Nov 5;38(4):283-90 [19733657] J Clin Oncol. 2009 Dec 1;27(34):5838-47 [19884552] Lancet. 2010 Jan 30;375(9712):377-84 [20113825] J Clin Oncol. 2010 Apr 10;28(11):1813-20 [20231686] Ann Oncol. 2011 Feb;22(2):321-8 [20693300] Ann Oncol. 2011 Jun;22(6):1302-7 [21109570] J Clin Oncol. 2011 Sep 1;29(25):3351-7 [21788566] N Engl J Med. 2011 Oct 6;365(14):1273-83 [21991949] Lancet Oncol. 2012 Jan;13(1):25-32 [22153890] Lancet. 2012 Feb 18;379(9816):633-40 [22257673] Breast Cancer Res. 2011;13(6):R117 [22112244] Breast Cancer Res Treat. 2012 May;133(1):11-21 [22057973] J Clin Oncol. 2012 May 20;30(15):1796-804 [22508812] Clin Cancer Res. 2012 Jun 15;18(12):3478-86 [22504044] BMC Cancer. 2012;12:165 [22559145] Ann Oncol. 2013 Aug;24(8):1999-2004 [23562929] Breast Cancer Res Treat. 2013 Dec;142(3):549-58 [24292815] Lancet Oncol. 2014 May;15(6):640-7 [24657003] N Engl J Med. 2015 Jan 8;372(2):134-41 [25564897] Br J Cancer. 2002 Jul 1;87(1):21-7 [12085250] Cancer. 2002 Aug 15;95(4):681-95 [12209710] J Clin Oncol. 2003 Jan 1;21(1):46-53 [12506169] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/1471-2407-14-954 ER - TY - JOUR T1 - Harnessing the fcμ receptor for potent and selective cytotoxic therapy of chronic lymphocytic leukemia. AN - 1637567101; 25344228 AB - Chronic lymphocytic leukemia (CLL) is a B-cell malignancy in need of new, effective, and safe therapies. The recently identified IgM receptor FcμR is overexpressed on malignant B cells in CLL and mediates the rapid internalization and lysosomal shuttling of IgM via its Fc fragment (Fcμ). To exploit this internalization and trafficking pathway for targeted drug delivery, we engineered an IgM-derived protein scaffold (Fcμ) and linked it with the cytotoxic agent monomethylauristatin F. This Fcμ-drug conjugate was selectively toxic for FcμR-expressing cell lines in vitro and for CLL cells but not autologous normal T cells ex vivo. Notably, the cytotoxic activity of the Fcμ-drug conjugate was maintained in CLL cells carrying a 17p deletion, which predicts resistance to standard chemotherapy. Next, we tested the possible therapeutic application of the Fcμ-drug conjugate in immunodeficient NOD/SCID/IL-2Rγ(null) (NSG) mice engrafted with peripheral blood cells from patients with leukemia. Three intravenous injections of the Fcμ-drug conjugate over a 10-day period were well tolerated and selectively killed the human CLL cells but not the coengrafted autologous human T cells. In summary, we developed a novel strategy for targeted cytotoxic therapy of CLL based on the unique properties of FcμR. FcμR-targeted drug delivery showed potent and specific therapeutic activity in CLL, thus providing proof of concept for FcμR as a valuable therapeutic target in CLL and for IgM-based antibody-drug conjugates as a new targeting platform. ©2014 American Association for Cancer Research. JF - Cancer research AU - Vire, Bérengère AU - Skarzynski, Martin AU - Thomas, Joshua D AU - Nelson, Christopher G AU - David, Alexandre AU - Aue, Georg AU - Burke, Terrence R AU - Rader, Christoph AU - Wiestner, Adrian AD - Hematology Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland. ; Chemical Biology Laboratory, Molecular Discovery Program, Center for Cancer Research, National Cancer Institute, NIH, Frederick, Maryland. ; Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland. ; Experimental Transplantation and Immunology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland. Department of Cancer Biology, The Scripps Research Institute, Scripps Florida, Jupiter, Florida. Department of Molecular Therapeutics, The Scripps Research Institute, Scripps Florida, Jupiter, Florida. wiestnera@mail.nih.gov crader@scripps.edu. ; Hematology Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland. wiestnera@mail.nih.gov crader@scripps.edu. Y1 - 2014/12/15/ PY - 2014 DA - 2014 Dec 15 SP - 7510 EP - 7520 VL - 74 IS - 24 KW - Immunoglobulin M KW - 0 KW - Receptors, Fc KW - immunoglobulin M receptor KW - Index Medicus KW - Drug Delivery Systems KW - Animals KW - Peripheral Blood Stem Cell Transplantation KW - Humans KW - Apoptosis -- immunology KW - Xenograft Model Antitumor Assays KW - Mice KW - Cell- and Tissue-Based Therapy KW - B-Lymphocytes -- immunology KW - Receptors, Fc -- immunology KW - Receptors, Fc -- therapeutic use KW - Leukemia, Lymphocytic, Chronic, B-Cell -- immunology KW - Immunoglobulin M -- immunology KW - Immunoglobulin M -- genetics KW - Leukemia, Lymphocytic, Chronic, B-Cell -- pathology KW - Cytotoxicity, Immunologic -- genetics KW - Leukemia, Lymphocytic, Chronic, B-Cell -- therapy KW - Receptors, Fc -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1637567101?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Harnessing+the+fc%CE%BC+receptor+for+potent+and+selective+cytotoxic+therapy+of+chronic+lymphocytic+leukemia.&rft.au=Vire%2C+B%C3%A9reng%C3%A8re%3BSkarzynski%2C+Martin%3BThomas%2C+Joshua+D%3BNelson%2C+Christopher+G%3BDavid%2C+Alexandre%3BAue%2C+Georg%3BBurke%2C+Terrence+R%3BRader%2C+Christoph%3BWiestner%2C+Adrian&rft.aulast=Vire&rft.aufirst=B%C3%A9reng%C3%A8re&rft.date=2014-12-15&rft.volume=74&rft.issue=24&rft.spage=7510&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-2030 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-10 N1 - Date created - 2014-12-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Biotechnol. 2012 Jul;30(7):631-7 [22781692] J Exp Med. 2009 Nov 23;206(12):2779-93 [19858324] Proc Natl Acad Sci U S A. 2012 Sep 25;109(39):15882-7 [22984178] Proc Natl Acad Sci U S A. 2012 Oct 2;109(40):E2699-706 [22988094] Clin Cancer Res. 2012 Nov 1;18(21):5845-9 [22962441] Blood. 2012 Dec 6;120(24):4684-91 [22875912] Leukemia. 2013 Dec;27(12):2311-21 [23619564] Methods. 2014 Jan 1;65(1):133-8 [23756202] N Engl J Med. 2014 Mar 13;370(11):997-1007 [24450857] N Engl J Med. 2014 Mar 20;370(12):1101-10 [24401022] J Oncol Pharm Pract. 2015 Apr;21(2):132-42 [24682654] Cancer Res. 1997 Nov 1;57(21):4940-7 [9354461] Nature. 2002 Apr 11;416(6881):603-7 [11948342] Lancet. 2010 Oct 2;376(9747):1164-74 [20888994] J Immunol. 1998 Oct 15;161(8):4091-7 [9780180] Leukemia. 1999 Oct;13(10):1501-5 [10516749] Int Immunol. 2005 May;17(5):539-47 [15778289] Immunol Rev. 2005 Aug;206:83-99 [16048543] Bioconjug Chem. 2006 Jan-Feb;17(1):114-24 [16417259] Clin Cancer Res. 2007 May 1;13(9):2745-50 [17473208] Biochemistry. 2009 Dec 22;48(50):12047-57 [19894757] MAbs. 2009 Mar-Apr;1(2):163-71 [20061826] Int Immunol. 2010 Mar;22(3):149-56 [20042454] Semin Hematol. 2010 Apr;47(2):115-23 [20350658] Semin Hematol. 2010 Apr;47(2):187-98 [20350666] Nat Rev Clin Oncol. 2010 Sep;7(9):521-32 [20603650] Clin Cancer Res. 2010 Oct 1;16(19):4769-78 [20805300] Blood. 2010 Nov 11;116(19):3705-14 [20610811] Blood. 2011 Jan 13;117(2):563-74 [20940416] J Clin Oncol. 2011 Feb 10;29(5):544-50 [21220603] Blood. 2011 May 19;117(20):5463-72 [21385850] Leuk Lymphoma. 2011 Sep;52(9):1641-54 [21619423] Mol Immunol. 2011 Sep;48(15-16):1818-26 [21632111] J Immunol. 2011 Oct 15;187(8):4040-50 [21908732] Methods Mol Biol. 2012;801:251-68 [21987258] Clin Cancer Res. 2011 Oct 15;17(20):6437-47 [22003071] J Clin Oncol. 2012 Jun 20;30(18):2183-9 [22454421] Blood. 2008 Jul 15;112(2):394-7 [18434611] Annu Rev Med. 2013;64:15-29 [23043493] J Immunol. 2013 Feb 1;190(3):987-96 [23267023] J Clin Oncol. 2013 Mar 20;31(9):1157-63 [23382472] N Engl J Med. 2013 Jul 4;369(1):32-42 [23782158] Am J Clin Pathol. 2013 Dec;140(6):813-8 [24225748] Nat Biotechnol. 2008 Aug;26(8):925-32 [18641636] Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12451-6 [18719095] Blood. 2008 Nov 15;112(10):4213-9 [18708628] Proc Natl Acad Sci U S A. 2009 Jul 7;106(27):11230-5 [19549827] Curr Opin Chem Biol. 2009 Jun;13(3):235-44 [19414278] J Clin Invest. 2009 Aug;119(8):2143-59 [19620786] Expert Opin Biol Ther. 2012 Sep;12(9):1191-206 [22650648] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-2030 ER - TY - JOUR T1 - A comprehensive evaluation of the efficacy of leading oxime therapies in guinea pigs exposed to organophosphorus chemical warfare agents or pesticides. AN - 1629962185; 25448441 AB - The currently fielded pre-hospital therapeutic regimen for the treatment of organophosphorus (OP) poisoning in the United States (U.S.) is the administration of atropine in combination with an oxime antidote (2-PAM Cl) to reactivate inhibited acetylcholinesterase (AChE). Depending on clinical symptoms, an anticonvulsant, e.g., diazepam, may also be administered. Unfortunately, 2-PAM Cl does not offer sufficient protection across the range of OP threat agents, and there is some question as to whether it is the most effective oxime compound available. The objective of the present study is to identify an oxime antidote, under standardized and comparable conditions, that offers protection at the FDA approved human equivalent dose (HED) of 2-PAM Cl against tabun (GA), sarin (GB), soman (GD), cyclosarin (GF), and VX, and the pesticides paraoxon, chlorpyrifos oxon, and phorate oxon. Male Hartley guinea pigs were subcutaneously challenged with a lethal level of OP and treated at approximately 1 min post challenge with atropine followed by equimolar oxime therapy (2-PAM Cl, HI-6 DMS, obidoxime Cl₂, TMB-4, MMB4-DMS, HLö-7 DMS, MINA, and RS194B) or therapeutic-index (TI) level therapy (HI-6 DMS, MMB4-DMS, MINA, and RS194B). Clinical signs of toxicity were observed for 24 h post challenge and blood cholinesterase [AChE and butyrylcholinesterase (BChE)] activity was analyzed utilizing a modified Ellman's method. When the oxime is standardized against the HED of 2-PAM Cl for guinea pigs, the evidence from clinical observations, lethality, quality of life (QOL) scores, and cholinesterase reactivation rates across all OPs indicated that MMB4 DMS and HLö-7 DMS were the two most consistently efficacious oximes. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved. JF - Toxicology and applied pharmacology AU - Wilhelm, Christina M AU - Snider, Thomas H AU - Babin, Michael C AU - Jett, David A AU - Platoff, Gennady E AU - Yeung, David T AD - Battelle, 505 King Avenue, JM-7, Columbus, OH 43201-2693, USA. Electronic address: wilhelmc@battelle.org. ; Battelle, 505 King Avenue, JM-7, Columbus, OH 43201-2693, USA. Electronic address: snidert@battelle.org. ; Battelle, 505 King Avenue, JM-7, Columbus, OH 43201-2693, USA. Electronic address: babinm@battelle.org. ; National Institutes of Health/National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA. Electronic address: jettd@ninds.nih.gov. ; National Institutes of Health/National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. Electronic address: platoffg@niaid.nih.gov. ; National Institutes of Health/National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA. Electronic address: dy70v@nih.gov. Y1 - 2014/12/15/ PY - 2014 DA - 2014 Dec 15 SP - 254 EP - 265 VL - 281 IS - 3 KW - Antidotes KW - 0 KW - Chemical Warfare Agents KW - Cholinesterase Inhibitors KW - Cholinesterase Reactivators KW - Muscarinic Antagonists KW - Oximes KW - Pesticides KW - Pyridinium Compounds KW - HLo 7 KW - 120103-35-7 KW - N,N'-monomethylenebis(pyridiniumaldoxime) KW - 61444-84-6 KW - Atropine KW - 7C0697DR9I KW - Cholinesterases KW - EC 3.1.1.8 KW - Index Medicus KW - Guinea pig KW - Intramuscular KW - Efficacy KW - Toxicity KW - Oxime KW - Pyridinium Compounds -- therapeutic use KW - Drug Therapy, Combination -- adverse effects KW - Animals KW - Pyridinium Compounds -- administration & dosage KW - Drug Administration Schedule KW - Muscarinic Antagonists -- adverse effects KW - Muscarinic Antagonists -- administration & dosage KW - Cholinesterases -- blood KW - Random Allocation KW - Guinea Pigs KW - Injections, Intramuscular KW - Atropine -- administration & dosage KW - Muscarinic Antagonists -- therapeutic use KW - Atropine -- adverse effects KW - Drug Monitoring KW - Injections, Subcutaneous KW - Pyridinium Compounds -- adverse effects KW - Male KW - Atropine -- therapeutic use KW - Cholinesterase Inhibitors -- administration & dosage KW - Antidotes -- administration & dosage KW - Oximes -- administration & dosage KW - Cholinesterase Inhibitors -- chemistry KW - Oximes -- therapeutic use KW - Antidotes -- therapeutic use KW - Chemical Warfare Agents -- chemistry KW - Cholinesterase Reactivators -- administration & dosage KW - Chemical Warfare Agents -- toxicity KW - Pesticides -- toxicity KW - Organophosphate Poisoning -- physiopathology KW - Organophosphate Poisoning -- drug therapy KW - Pesticides -- antagonists & inhibitors KW - Cholinesterase Inhibitors -- toxicity KW - Organophosphate Poisoning -- blood KW - Cholinesterase Reactivators -- therapeutic use KW - Antidotes -- adverse effects KW - Oximes -- adverse effects KW - Cholinesterase Reactivators -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629962185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+comprehensive+evaluation+of+the+efficacy+of+leading+oxime+therapies+in+guinea+pigs+exposed+to+organophosphorus+chemical+warfare+agents+or+pesticides.&rft.au=Wilhelm%2C+Christina+M%3BSnider%2C+Thomas+H%3BBabin%2C+Michael+C%3BJett%2C+David+A%3BPlatoff%2C+Gennady+E%3BYeung%2C+David+T&rft.aulast=Wilhelm&rft.aufirst=Christina&rft.date=2014-12-15&rft.volume=281&rft.issue=3&rft.spage=254&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2014.10.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-17 N1 - Date created - 2014-12-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2011 Jun 3;286(22):19422-30 [21464125] Acta Medica (Hradec Kralove). 2010;53(4):207-11 [21400978] J Pharm Sci. 2012 Oct;101(10):3979-88 [22833171] Expert Opin Drug Metab Toxicol. 2013 Jan;9(1):31-50 [23176543] Biochem J. 2013 Feb 15;450(1):231-42 [23216060] Basic Clin Pharmacol Toxicol. 2004 Aug;95(2):81-6 [15379785] J Toxicol Clin Toxicol. 2002;40(6):803-16 [12475193] Arch Toxicol. 2013 Apr;87(4):711-9 [23179755] Biochem Pharmacol. 2004 Dec 1;68(11):2237-48 [15498514] Toxicol Appl Pharmacol. 1970 Jan;16(1):40-7 [5416754] Arch Toxikol. 1970;26(4):293-305 [5501176] Arch Int Pharmacodyn Ther. 1973 Jul;204(1):110-23 [4746622] J Pharm Pharmacol. 1983 Jul;35(7):427-33 [6136583] Neurosci Biobehav Rev. 1991 Spring;15(1):135-9 [2052186] Toxicology. 1992;72(1):99-105 [1539175] Arch Toxicol. 1992;66(9):603-21 [1482283] J Appl Toxicol. 1994 Sep-Oct;14(5):317-31 [7822680] Hum Exp Toxicol. 1997 Aug;16(8):473-80 [9292288] Hum Exp Toxicol. 1998 Jun;17(6):331-5 [9688357] J Pharmacol Exp Ther. 1957 Apr;119(4):522-31 [13429460] Adv Clin Chem. 2004;38:151-216 [15521192] Biochem Pharmacol. 1961 Jul;7:88-95 [13726518] Biochim Biophys Acta. 1959 Aug;34:555-7 [14425589] Acta Medica (Hradec Kralove). 2005;48(2):87-90 [16259318] J Enzyme Inhib Med Chem. 2005 Oct;20(5):409-15 [16335048] Toxicology. 2006 Feb 15;219(1-3):85-96 [16332406] J Enzyme Inhib Med Chem. 2006 Dec;21(6):663-6 [17252938] Arh Hig Rada Toksikol. 2006 Dec;57(4):435-43 [17265683] Toxicol Rev. 2006;25(4):231-43 [17288495] Toxicol Appl Pharmacol. 2007 Mar;219(2-3):226-34 [17112559] Pharmacol Ther. 2013 Aug;139(2):249-59 [23603539] Int J Toxicol. 2013 Jul-Aug;32(4 Suppl):99S-107S [23929454] Nat Med. 2013 Oct;19(10):1194-5 [24100968] Chem Biol Interact. 2013 Dec 5;206(3):569-72 [23962483] Chem Res Toxicol. 2014 Jan 21;27(1):99-110 [24443939] Chem Biol Interact. 2013 Dec 5;206(3):435-43 [24091052] Clin Med Res. 2007 Mar;5(1):71-82 [17456837] Curr Pharm Des. 2007;13(33):3445-52 [18045198] Biochem Pharmacol. 2008 May 15;75(10):2045-53 [18384757] Toxicol Appl Pharmacol. 2008 Sep 1;231(2):157-64 [18508103] PLoS One. 2009;4(6):e5957 [19536291] Toxicol Mech Methods. 2009 Sep;19(6-7):386-400 [19778239] Am J Emerg Med. 2009 Nov;27(9):1117-24 [19931761] Chem Biol Interact. 2010 Sep 6;187(1-3):207-14 [20223229] Chem Biol Interact. 2010 Sep 6;187(1-3):318-24 [20230808] Fundam Appl Toxicol. 1992 Jan;18(1):102-6 [1601200] Arch Toxicol. 1992;66(3):216-9 [1497487] Chem Biol Interact. 2010 Sep 6;187(1-3):229-33 [20433814] J Biol Chem. 2012 Apr 6;287(15):11798-809 [22343626] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2014.10.009 ER - TY - JOUR T1 - Mass spectrometric analysis of rat cerebrospinal fluid proteins following exposure to the neurotoxicant carbonyl sulfide. AN - 1620587838; 25366400 AB - Using a proteomic-based approach we have investigated possible altered expression of a range of cerebral spinal fluid (CSF) proteins following exposure to the neurotoxicant carbonyl sulfide (COS). CSF is ideal for the investigation of markers of brain injury or disease since it is secreted from several central nervous system structures and changes in the CSF composition may reflect brain insult and many pathological processes. Animals were placed in exposure chambers and were exposed to 0 ppm or 500 ppm COS for 1, 2 or 3 days, 6 h per day. After the last inhalation exposure, 50-70 μL CSF sample was obtained by lumbar puncture. CSF samples were analyzed by electrospray ionization mass spectrometry (ESI-MS) on either a Premier quadrupole time-of-flight (QTOF) or an Agilent 6340 ion trap and by matrix-assisted laser desorption/ionization (MALDI)-MS on a 4800 MALDI-TOF/TOF analyzer. The dynamic range of abundance of the identified proteins spanned over more than three orders of magnitude. The four most abundant proteins identified (albumin, cystatin C, serotransferrin, transthyretin) are major proteins that are present in both CSF and blood at high levels but the fifth most abundant protein identified (prostaglandin H2D isomerase) is the second most abundant protein in human CSF and is secreted and synthesized in the rat central nervous system. No significant differences were observed between COS-treated CSF samples and the control CSF samples because of blood contamination. Quantitative MS protein analyses of rat CSF is limited by the low sample volumes that can practicably be obtained from rats and the low protein concentrations in rat CSF. Results of this work suggest a clear need for CSF collection that would minimize blood contamination. Published in 2014. This article is a U.S. Government work and is in the public domain in the USA. Published in 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - Rapid communications in mass spectrometry : RCM AU - Lardinois, O AU - Kirby, P J AU - Morgan, D L AU - Sills, R C AU - Tomer, K B AU - Deterding, L J AD - Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH/DHHS, 111 T.W. Alexander Drive, PO Box 12233, Research Triangle Park, NC, 27709, USA. Y1 - 2014/12/15/ PY - 2014 DA - 2014 Dec 15 SP - 2531 EP - 2538 VL - 28 IS - 23 KW - Cerebrospinal Fluid Proteins KW - 0 KW - Proteome KW - Sulfur Oxides KW - carbonyl sulfide KW - 871UI0ET21 KW - Index Medicus KW - Rats KW - Animals KW - Inhalation Exposure KW - Proteomics KW - Principal Component Analysis KW - Male KW - Cerebrospinal Fluid Proteins -- analysis KW - Neurotoxicity Syndromes -- etiology KW - Sulfur Oxides -- toxicity KW - Proteome -- analysis KW - Proteome -- chemistry KW - Neurotoxicity Syndromes -- cerebrospinal fluid KW - Spectrometry, Mass, Electrospray Ionization -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1620587838?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Rapid+communications+in+mass+spectrometry+%3A+RCM&rft.atitle=Mass+spectrometric+analysis+of+rat+cerebrospinal+fluid+proteins+following+exposure+to+the+neurotoxicant+carbonyl+sulfide.&rft.au=Lardinois%2C+O%3BKirby%2C+P+J%3BMorgan%2C+D+L%3BSills%2C+R+C%3BTomer%2C+K+B%3BDeterding%2C+L+J&rft.aulast=Lardinois&rft.aufirst=O&rft.date=2014-12-15&rft.volume=28&rft.issue=23&rft.spage=2531&rft.isbn=&rft.btitle=&rft.title=Rapid+communications+in+mass+spectrometry+%3A+RCM&rft.issn=1097-0231&rft_id=info:doi/10.1002%2Frcm.7046 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-17 N1 - Date created - 2014-11-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Electrophoresis. 2012 Dec;33(24):3617-30 [23160951] Neurochem Res. 2011 Mar;36(3):528-32 [21191652] Methods. 2013 Jun 15;61(3):186-218 [23623823] PLoS One. 2013;8(5):e64314 [23700471] Brain Res Brain Res Protoc. 2000 Feb;5(1):109-14 [10719272] Brain Res Bull. 2002 Nov 30;59(3):245-50 [12431755] Toxicol Appl Pharmacol. 2004 Oct 15;200(2):131-45 [15476866] Exp Neurol. 1976 Feb;50(2):330-6 [1248554] Eur J Biochem. 1989 Dec 8;186(1-2):35-42 [2689174] Appl Theor Electrophor. 1993;3(5):229-34 [7692978] Biochim Biophys Acta. 1996 Feb 29;1310(3):269-76 [8599604] Biopharm Drug Dispos. 1997 May;18(4):335-46 [9158881] Neurobiol Aging. 2005 Feb;26(2):207-27 [15582749] Toxicol Pathol. 2004 Sep-Oct;32(5):501-10 [15603534] J Chromatogr B Analyt Technol Biomed Life Sci. 2005 Feb 5;815(1-2):179-89 [15652808] Proteomics. 2005 Jan;5(1):290-6 [15672452] J Alzheimers Dis. 2005 Apr;7(2):125-33; discussion 173-80 [15851850] J Neurosci Methods. 2005 Jun 30;145(1-2):89-95 [15922028] Expert Rev Mol Diagn. 2005 Sep;5(5):661-72 [16149870] Curr Opin Mol Ther. 2005 Dec;7(6):557-64 [16372405] Dis Markers. 2006;22(1-2):3-26 [16410649] Mech Ageing Dev. 2006 Feb;127(2):133-7 [16293296] J Alzheimers Dis. 2005 Mar;8(4):377-86 [16556969] Toxicol Pathol. 2006;34(4):393-5 [16844667] J Proteome Res. 2008 Jan;7(1):386-99 [18052119] Methods Mol Biol. 2008;425:53-66 [18369886] Curr Med Chem. 2008;15(18):1788-801 [18691039] Proteomics. 2008 Oct;8(20):4357-66 [18814332] Clin Chim Acta. 2009 Feb;400(1-2):14-20 [18977210] Toxicol Pathol. 2009 Jun;37(4):502-11 [19395590] PLoS One. 2010;5(6):e10980 [20552007] Erratum In: Rapid Commun Mass Spectrom. 2015 Apr 30;29(8):782 [26406493] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/rcm.7046 ER - TY - JOUR T1 - An integrative approach to understanding bird origins AN - 1832582803; 722341-1 AB - Recent discoveries of spectacular dinosaur fossils overwhelmingly support the hypothesis that birds are descended from maniraptoran theropod dinosaurs, and furthermore, demonstrate that distinctive bird characteristics such as feathers, flight, endothermic physiology, unique strategies for reproduction and growth, and a novel pulmonary system originated among Mesozoic terrestrial dinosaurs. The transition from ground-living to flight-capable theropod dinosaurs now probably represents one of the best-documented major evolutionary transitions in life history. Recent studies in developmental biology and other disciplines provide additional insights into how bird characteristics originated and evolved. The iconic features of extant birds for the most part evolved in a gradual and stepwise fashion throughout archosaur evolution. However, new data also highlight occasional bursts of morphological novelty at certain stages particularly close to the origin of birds and an unavoidable complex, mosaic evolutionary distribution of major bird characteristics on the theropod tree. Research into bird origins provides a premier example of how paleontological and neontological data can interact to reveal the complexity of major innovations, to answer key evolutionary questions, and to lead to new research directions. A better understanding of bird origins requires multifaceted and integrative approaches, yet fossils necessarily provide the final test of any evolutionary model. JF - Science AU - Xu, Xing AU - Zhou, Zhonghe AU - Dudley, Robert AU - Mackem, Susan AU - Chuong, Cheng-Ming AU - Erickson, Gregory M AU - Varricchio, David J Y1 - 2014/12/12/ PY - 2014 DA - 2014 Dec 12 SP - 1341 PB - American Association for the Advancement of Science, Washington, DC VL - 346 IS - 6215 SN - 0036-8075, 0036-8075 KW - Archaeornithes KW - Diapsida KW - Chordata KW - phylogeny KW - biologic evolution KW - feathers KW - Reptilia KW - Aves KW - Archosauria KW - Theropoda KW - Saurischia KW - dinosaurs KW - Vertebrata KW - Tetrapoda KW - Archaeopteryx KW - 11:Vertebrate paleontology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1832582803?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ageorefinprocess&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science&rft.atitle=An+integrative+approach+to+understanding+bird+origins&rft.au=Xu%2C+Xing%3BZhou%2C+Zhonghe%3BDudley%2C+Robert%3BMackem%2C+Susan%3BChuong%2C+Cheng-Ming%3BErickson%2C+Gregory+M%3BVarricchio%2C+David+J&rft.aulast=Xu&rft.aufirst=Xing&rft.date=2014-12-12&rft.volume=346&rft.issue=6215&rft.spage=1341&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1253293 L2 - http://www.sciencemag.org/magazine LA - English DB - GeoRef N1 - Copyright - GeoRef in Process, Copyright 2017, American Geosciences Institute. After editing and indexing, this record will be added to Georef. N1 - PubXState - DC N1 - Document feature - illus. N1 - SuppNotes - Full text available only online N1 - Last updated - 2017-01-24 N1 - CODEN - SCIEAS N1 - SubjectsTermNotLitGenreText - Archaeopteryx; Archaeornithes; Archosauria; Aves; biologic evolution; Chordata; Diapsida; dinosaurs; feathers; phylogeny; Reptilia; Saurischia; Tetrapoda; Theropoda; Vertebrata DO - http://dx.doi.org/10.1126/science.1253293 ER - TY - JOUR T1 - Phase I study of the halichondrin B analogue eribulin mesylate in combination with cisplatin in advanced solid tumors. AN - 1635004048; 25349975 AB - Eribulin mesylate is a synthetic macrocyclic ketone analogue of Halichondrin B that has demonstrated high antitumor activity in preclinical and clinical settings. This phase I study aimed to determine the maximum tolerated dose (MTD), dose-limiting toxicities (DLTs), and pharmacokinetics in combination with cisplatin (CP) in patients with advanced solid tumours. Thirty-six patients with advanced solid tumours received eribulin mesylate 0.7-1.4 mg m(-2) and CP 60-75 mg m(-2). Eribulin mesylate was administered on days 1, 8, and 15 in combination with CP day 1 every 28-day cycle. The protocol was amended after dose level 4 (eribulin mesylate 1.4 mg m(-2), CP 60 mg m(-2)) when it was not feasible to administer eribulin mesylate on day 15 because of neutropenia; the treatment schedule was changed to eribulin mesylate on days 1 and 8 and CP on day 1 every 21 days. On the 28-day schedule, three patients had DLT during the first cycle: grade (G) 4 febrile neutropenia (1.0 mg m(-2), 60 mg m(-2)); G 3 anorexia/fatigue/hypokalemia (1.2 mg m(-2), 60 mg m(-2)); and G 3 stomatitis/nausea/vomiting/fatigue (1.4 mg m(-2), 60 mg m(-2)). On the 21-day schedule, three patients had DLT during the first cycle: G 3 hypokalemia/hyponatremia (1.4 mg m(-2), 60 mg m(-2)); G 4 mucositis (1.4 mg m(-2), 60 mg m(-2)); and G 3 hypokalemia (1.2 mg m(-2), 75 mg m(-2)). The MTD and recommended phase II dose was determined as eribulin mesylate 1.2 mg m(-2) (days 1, 8) and CP 75 mg m(-2) (day 1), on a 21-day cycle. Two patients had unconfirmed partial responses (PR) (pancreatic and breast cancers) and two had PR (oesophageal and bladder cancers). On the 21-day cycle, eribulin mesylate 1.2 mg m(-2), administered on days 1 and 8, in combination with CP 75 mg m(-2), administered on day 1 is well tolerated and showed preliminary anticancer activity. JF - British journal of cancer AU - Koczywas, M AU - Frankel, P H AU - Synold, T W AU - Lenz, H-J AU - Mortimer, J E AU - El-Khoueiry, A B AU - Gandara, D R AU - Cristea, M C AU - Chung, V M AU - Lim, D AU - Reckamp, K L AU - Lau, D H AU - Doyle, L A AU - Ruel, C AU - Carroll, M I AU - Newman, E M AD - Department of Medical Oncology, City of Hope, Duarte, CA, USA. ; Department of Information Sciences, City of Hope, Duarte, CA, USA. ; Department of Molecular Pharmacology, City of Hope National Medical Center, Duarte, CA, USA. ; Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA. ; Medical Center, UC Davis Comprehensive Cancer Center, Sacramento, CA, USA. ; Investigational Drug Research, National Cancer Institute, Rockville, MD, USA. ; Department of Research-RN, City of Hope, Duarte, CA, USA. Y1 - 2014/12/09/ PY - 2014 DA - 2014 Dec 09 SP - 2268 EP - 2274 VL - 111 IS - 12 KW - Ethers, Cyclic KW - 0 KW - Furans KW - Ketones KW - Macrolides KW - halichondrin B KW - 103614-76-2 KW - eribulin KW - LR24G6354G KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Furans -- administration & dosage KW - Young Adult KW - Ketones -- administration & dosage KW - Ketones -- adverse effects KW - Humans KW - Furans -- adverse effects KW - Adult KW - Aged KW - Middle Aged KW - Cisplatin -- adverse effects KW - Cisplatin -- administration & dosage KW - Neoplasms -- drug therapy KW - Macrolides -- therapeutic use KW - Ethers, Cyclic -- therapeutic use KW - Ethers, Cyclic -- adverse effects KW - Ethers, Cyclic -- administration & dosage KW - Macrolides -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Macrolides -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635004048?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+I+study+of+the+halichondrin+B+analogue+eribulin+mesylate+in+combination+with+cisplatin+in+advanced+solid+tumors.&rft.au=Koczywas%2C+M%3BFrankel%2C+P+H%3BSynold%2C+T+W%3BLenz%2C+H-J%3BMortimer%2C+J+E%3BEl-Khoueiry%2C+A+B%3BGandara%2C+D+R%3BCristea%2C+M+C%3BChung%2C+V+M%3BLim%2C+D%3BReckamp%2C+K+L%3BLau%2C+D+H%3BDoyle%2C+L+A%3BRuel%2C+C%3BCarroll%2C+M+I%3BNewman%2C+E+M&rft.aulast=Koczywas&rft.aufirst=M&rft.date=2014-12-09&rft.volume=111&rft.issue=12&rft.spage=2268&rft.isbn=&rft.btitle=&rft.title=British+journal+of+cancer&rft.issn=1532-1827&rft_id=info:doi/10.1038%2Fbjc.2014.554 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-16 N1 - Date created - 2014-12-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Pharmacol. 2006 Dec;70(6):1866-75 [16940412] Clin Cancer Res. 2007 Jun 15;13(12):3660-6 [17575231] Clin Cancer Res. 2009 Jun 15;15(12):4213-9 [19509146] Clin Cancer Res. 2009 Jun 15;15(12):4207-12 [19509177] Lancet. 2011 Mar 12;377(9769):914-23 [21376385] Anticancer Res. 2012 May;32(5):1611-9 [22593439] J Clin Oncol. 2006 Apr 1;24(10):1633-42 [16575015] Cancer Res. 2001 Feb 1;61(3):1013-21 [11221827] Cancer Res. 2004 Aug 15;64(16):5760-6 [15313917] Toxicol Lett. 1989 Mar;46(1-3):163-75 [2650023] J Biol Chem. 1991 Aug 25;266(24):15882-9 [1874739] J Natl Cancer Inst Monogr. 1993;(15):83-8 [7912534] Mol Cancer Ther. 2005 Jul;4(7):1086-95 [16020666] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/bjc.2014.554 ER - TY - CPAPER T1 - EHD proteins coordinate membrane reorganization and fusion to initiate early steps of ciliogenesis T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638908; 6328208 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Insinna, C AU - Lu, Q. AU - Ott, C AU - Baxa, U AU - Lopes, S AU - Lippincott- Schwartz, J AU - Caplan, S AU - Jackson, P AU - Westlake, C Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Membrane fusion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638908?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=EHD+proteins+coordinate+membrane+reorganization+and+fusion+to+initiate+early+steps+of+ciliogenesis&rft.au=Insinna%2C+C%3BLu%2C+Q.%3BOtt%2C+C%3BBaxa%2C+U%3BLopes%2C+S%3BLippincott-+Schwartz%2C+J%3BCaplan%2C+S%3BJackson%2C+P%3BWestlake%2C+C&rft.aulast=Insinna&rft.aufirst=C&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Neurogenetic insights into organelle biogenesis T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638875; 6328087 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Blackstone, Craig Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Biogenesis KW - Neurogenetics KW - Organelles UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638875?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Neurogenetic+insights+into+organelle+biogenesis&rft.au=Blackstone%2C+Craig&rft.aulast=Blackstone&rft.aufirst=Craig&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Light Sheet Fluorescence Microscopy (LSFM): Imaging Faster and Gentler T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638869; 6327982 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Kumar, Abhishek Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Imaging techniques KW - Fluorescence microscopy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638869?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Light+Sheet+Fluorescence+Microscopy+%28LSFM%29%3A+Imaging+Faster+and+Gentler&rft.au=Kumar%2C+Abhishek&rft.aulast=Kumar&rft.aufirst=Abhishek&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Myosin II pulls the nucleus forward to increase intracellular pressure and drive 3D cell movement T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638818; 6328120 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Petrie, R AU - Koo, H AU - Yamada, K Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Myosin KW - Cell migration KW - Pressure KW - Nuclei UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638818?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Myosin+II+pulls+the+nucleus+forward+to+increase+intracellular+pressure+and+drive+3D+cell+movement&rft.au=Petrie%2C+R%3BKoo%2C+H%3BYamada%2C+K&rft.aulast=Petrie&rft.aufirst=R&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Biomedical PhD career development trends: implications for workforce development and diversity T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638813; 6327718 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Gibbs Jr, Kenneth Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Species diversity KW - Careers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638813?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Biomedical+PhD+career+development+trends%3A+implications+for+workforce+development+and+diversity&rft.au=Gibbs+Jr%2C+Kenneth&rft.aulast=Gibbs+Jr&rft.aufirst=Kenneth&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - A novel actin-adhesion structure involved in nuclear positioning requires the formin FMN2 T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638805; 6327898 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Skau, C AU - Waterman, C Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638805?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=A+novel+actin-adhesion+structure+involved+in+nuclear+positioning+requires+the+formin+FMN2&rft.au=Skau%2C+C%3BWaterman%2C+C&rft.aulast=Skau&rft.aufirst=C&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Cytoskeletal dynamics, adhesion, and imaging T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638801; 6327888 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Waterman, Clare Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Cytoskeleton KW - Adhesion KW - Imaging techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638801?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Cytoskeletal+dynamics%2C+adhesion%2C+and+imaging&rft.au=Waterman%2C+Clare&rft.aulast=Waterman&rft.aufirst=Clare&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Your career: strategy or luck of the draw T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638778; 6327992 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Misteli, Tom Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Careers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638778?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Your+career%3A+strategy+or+luck+of+the+draw&rft.au=Misteli%2C+Tom&rft.aulast=Misteli&rft.aufirst=Tom&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - PINK1 is a ubiquitin kinase T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638763; 6328137 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Kane, L AU - Lazarou, M AU - Fogel, A AU - Li, Y. AU - Yamano, K AU - Sarraf, S AU - Banerjee, S AU - Youle, R Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - PTEN-induced putative kinase KW - Ubiquitin UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638763?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=PINK1+is+a+ubiquitin+kinase&rft.au=Kane%2C+L%3BLazarou%2C+M%3BFogel%2C+A%3BLi%2C+Y.%3BYamano%2C+K%3BSarraf%2C+S%3BBanerjee%2C+S%3BYoule%2C+R&rft.aulast=Kane&rft.aufirst=L&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Transcriptional regulation by noncoding RNA dissected with single-molecule observation in living cells T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638711; 6327809 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Larson, Daniel Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - RNA KW - Gene regulation KW - Transcription UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638711?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Transcriptional+regulation+by+noncoding+RNA+dissected+with+single-molecule+observation+in+living+cells&rft.au=Larson%2C+Daniel&rft.aulast=Larson&rft.aufirst=Daniel&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Organelle biogenesis: insights from the hereditary spastic paraplegias T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638686; 6328069 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Blackstone, Craig Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Hereditary spastic paraplegia KW - Biogenesis KW - Organelles UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638686?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Organelle+biogenesis%3A+insights+from+the+hereditary+spastic+paraplegias&rft.au=Blackstone%2C+Craig&rft.aulast=Blackstone&rft.aufirst=Craig&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Quality control of GPI-anchored proteins in the secretory pathway T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638628; 6328201 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Satpute-Krishnan, P AU - Lippincott-Schwartz, J Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Quality control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638628?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Quality+control+of+GPI-anchored+proteins+in+the+secretory+pathway&rft.au=Satpute-Krishnan%2C+P%3BLippincott-Schwartz%2C+J&rft.aulast=Satpute-Krishnan&rft.aufirst=P&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - The budding yeast polo kinase, Cdc5, regulates domain-specific expansion of the nuclear envelope T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638558; 6328032 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Cohen-Fix, O AU - Walters, A AU - May, C AU - Dauster, E AU - Cinquin, B AU - Smith, E AU - Larabell, C Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Nuclear membranes KW - Budding KW - Saccharomyces cerevisiae UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638558?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=The+budding+yeast+polo+kinase%2C+Cdc5%2C+regulates+domain-specific+expansion+of+the+nuclear+envelope&rft.au=Cohen-Fix%2C+O%3BWalters%2C+A%3BMay%2C+C%3BDauster%2C+E%3BCinquin%2C+B%3BSmith%2C+E%3BLarabell%2C+C&rft.aulast=Cohen-Fix&rft.aufirst=O&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - iPALM and FRET reveal the mechanism of vinculin activation and nano-scale spatial organization in focal adhesions T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638521; 6328016 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Case, L AU - Baird, M AU - Shtengel, G AU - Campbell, S AU - Hess, H AU - Davidson, M AU - Waterman, C Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - vinculin KW - fluorescence resonance energy transfer KW - Adhesion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638521?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=iPALM+and+FRET+reveal+the+mechanism+of+vinculin+activation+and+nano-scale+spatial+organization+in+focal+adhesions&rft.au=Case%2C+L%3BBaird%2C+M%3BShtengel%2C+G%3BCampbell%2C+S%3BHess%2C+H%3BDavidson%2C+M%3BWaterman%2C+C&rft.aulast=Case&rft.aufirst=L&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Finding treatments for mitochondrial diseases by stimulating quality control pathways T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638518; 6328072 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Youle, Richard Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Quality control KW - Disease control KW - Mitochondria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Finding+treatments+for+mitochondrial+diseases+by+stimulating+quality+control+pathways&rft.au=Youle%2C+Richard&rft.aulast=Youle&rft.aufirst=Richard&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Theory-experiment interface in biology T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638503; 6327827 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Lippincott-Schwartz, Jennifer AU - Phillips, Rob Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638503?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Theory-experiment+interface+in+biology&rft.au=Lippincott-Schwartz%2C+Jennifer%3BPhillips%2C+Rob&rft.aulast=Lippincott-Schwartz&rft.aufirst=Jennifer&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Two step model for centriole disengagement T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638434; 6327796 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Loncerak, Jadranka Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Centrioles KW - Models UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638434?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Two+step+model+for+centriole+disengagement&rft.au=Sine%2C+Jessica%3BUrban%2C+Cordula%3BThayer%2C+Derek%3BCharron%2C+Heather%3BValim%2C+Niksa%3BTata%2C+Darrell+B%3BSchiff%2C+Rachel%3BBlumenthal%2C+Robert%3BJoshi%2C+Amit%3BPuri%2C+Anu&rft.aulast=Sine&rft.aufirst=Jessica&rft.date=2014-12-19&rft.volume=10&rft.issue=&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Nanomedicine&rft.issn=11769114&rft_id=info:doi/10.2147%2FIJN.S72143 L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Nuclear keratin and the regulation of gene expression in tumor epithelial cells T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635697; 6327739 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Coulombe, Pierre Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Gene expression KW - Epithelial cells KW - Keratin KW - Tumors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635697?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Nuclear+keratin+and+the+regulation+of+gene+expression+in+tumor+epithelial+cells&rft.au=Coulombe%2C+Pierre&rft.aulast=Coulombe&rft.aufirst=Pierre&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Novel spectral imaging and analysis to unravel the organelle interactome T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635688; 6328022 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Valm, A AU - Cohen, S AU - Legant, W AU - Davidson, M AU - Betzig, E AU - Lippincott-Schwartz, J Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Organelles KW - Imaging techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635688?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Novel+spectral+imaging+and+analysis+to+unravel+the+organelle+interactome&rft.au=Valm%2C+A%3BCohen%2C+S%3BLegant%2C+W%3BDavidson%2C+M%3BBetzig%2C+E%3BLippincott-Schwartz%2C+J&rft.aulast=Valm&rft.aufirst=A&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Damage control: how PINK1 and Parkin survey mitochondrial fidelity and respond with selective autophagy T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635638; 6328078 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Youle, R Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - parkin protein KW - Fidelity KW - PTEN-induced putative kinase KW - Mitochondria KW - Phagocytosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635638?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Damage+control%3A+how+PINK1+and+Parkin+survey+mitochondrial+fidelity+and+respond+with+selective+autophagy&rft.au=Youle%2C+R&rft.aulast=Youle&rft.aufirst=R&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Current events at NIGMS T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635629; 6327719 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Lorsch, Jon Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Current+events+at+NIGMS&rft.au=Lorsch%2C+Jon&rft.aulast=Lorsch&rft.aufirst=Jon&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Novel ER shaping proteins Pex30 and Pex31 are involved in pre-peroxisome vesicle biogenesis T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635599; 6328135 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Joshi, A AU - Prinz, W Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Biogenesis KW - Vesicles UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635599?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Novel+ER+shaping+proteins+Pex30+and+Pex31+are+involved+in+pre-peroxisome+vesicle+biogenesis&rft.au=Joshi%2C+A%3BPrinz%2C+W&rft.aulast=Joshi&rft.aufirst=A&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Monitoring of Circulating Tumor DNA As Minimal Residual Disease in Diffuse Large B-Cell Lymphoma T2 - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AN - 1647635567; 6327559 JF - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AU - Roschewski, Mark AU - Dunleavy, Kieron AU - Fadle, Natalie AU - Regitz, Evi AU - Roth, Patrick AU - Monoranu, Camelia-Maria AU - Buslei, Rolf AU - Bohle, Rainer AU - Kim, Yoo-Jin AU - Preuss, Klaus-Dieter Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - minimal residual disease KW - B-cell lymphoma KW - Tumors KW - Lymphoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635567?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.atitle=Monitoring+of+Circulating+Tumor+DNA+As+Minimal+Residual+Disease+in+Diffuse+Large+B-Cell+Lymphoma&rft.au=Roschewski%2C+Mark%3BDunleavy%2C+Kieron%3BFadle%2C+Natalie%3BRegitz%2C+Evi%3BRoth%2C+Patrick%3BMonoranu%2C+Camelia-Maria%3BBuslei%2C+Rolf%3BBohle%2C+Rainer%3BKim%2C+Yoo-Jin%3BPreuss%2C+Klaus-Dieter&rft.aulast=Roschewski&rft.aufirst=Mark&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://ash.confex.com/ash/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - A mitochondria-specific isoform of the actin nucleating Spire protein regulates mitochondrial dynamics T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635546; 6327733 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Manor, Uri Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Mitochondria KW - Actin UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635546?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=A+mitochondria-specific+isoform+of+the+actin+nucleating+Spire+protein+regulates+mitochondrial+dynamics&rft.au=Manor%2C+Uri&rft.aulast=Manor&rft.aufirst=Uri&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Dynamic modulation of cortical actin at the immunological synapse controls cytotoxic granule secretion T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635513; 6327730 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Ritter, Alex Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Granules KW - Cytotoxicity KW - Cortex KW - Secretion KW - Actin KW - Immunological synapses UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635513?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Dynamic+modulation+of+cortical+actin+at+the+immunological+synapse+controls+cytotoxic+granule+secretion&rft.au=Ritter%2C+Alex&rft.aulast=Ritter&rft.aufirst=Alex&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Imaging the molecular architecture of the plasma membrane with correlative 3D super resolution light and electron microscopy T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635478; 6327816 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Taraska, Justin Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Plasma membranes KW - Imaging techniques KW - Electron microscopy KW - Light effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635478?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Imaging+the+molecular+architecture+of+the+plasma+membrane+with+correlative+3D+super+resolution+light+and+electron+microscopy&rft.au=Taraska%2C+Justin&rft.aulast=Taraska&rft.aufirst=Justin&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Lipid exhange at contact sites T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635454; 6327749 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Prinz, Will Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Lipids UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635454?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Lipid+exhange+at+contact+sites&rft.au=Prinz%2C+Will&rft.aulast=Prinz&rft.aufirst=Will&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Mechanism of protein incorporation into envelop of budding HIV particle T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635424; 6327936 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Sengupta, P AU - van Engelenburg, S. AU - Johnson, M AU - Lippincott-Schwartz, J Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Human immunodeficiency virus KW - Particulates KW - Budding UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635424?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Mechanism+of+protein+incorporation+into+envelop+of+budding+HIV+particle&rft.au=Sengupta%2C+P%3Bvan+Engelenburg%2C+S.%3BJohnson%2C+M%3BLippincott-Schwartz%2C+J&rft.aulast=Sengupta&rft.aufirst=P&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Coatopathies: genetic disorders of protein coats T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635413; 6328068 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Bonifacino, Juan Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635413?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Coatopathies%3A+genetic+disorders+of+protein+coats&rft.au=Bonifacino%2C+Juan&rft.aulast=Bonifacino&rft.aufirst=Juan&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Using Quantitative and Superresolution Microscopy to Visualize the Dynamic, 3D Molecular Clutch That Drives Cell Migration T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635322; 6327981 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Waterman, Clare Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Clutch KW - Microscopy KW - Cell migration KW - Migration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Using+Quantitative+and+Superresolution+Microscopy+to+Visualize+the+Dynamic%2C+3D+Molecular+Clutch+That+Drives+Cell+Migration&rft.au=Waterman%2C+Clare&rft.aulast=Waterman&rft.aufirst=Clare&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Microtubules and membrane-to-mitochondria connections: relationships between cell biology and targeted chemotherapeutics T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635321; 6327685 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Sackett, Dan Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Microtubules KW - Cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635321?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Microtubules+and+membrane-to-mitochondria+connections%3A+relationships+between+cell+biology+and+targeted+chemotherapeutics&rft.au=Sackett%2C+Dan&rft.aulast=Sackett&rft.aufirst=Dan&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Targeting the metabolic basis of Fumarate Hydratase-deficient kidney cancer T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635290; 6328070 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Linehan, W Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Kidneys KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635290?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Targeting+the+metabolic+basis+of+Fumarate+Hydratase-deficient+kidney+cancer&rft.au=Linehan%2C+W&rft.aulast=Linehan&rft.aufirst=W&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Technology development and biological discovery T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635237; 6327877 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Lippincott-Schwartz, Jennifer Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Technology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635237?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Technology+development+and+biological+discovery&rft.au=Lippincott-Schwartz%2C+Jennifer&rft.aulast=Lippincott-Schwartz&rft.aufirst=Jennifer&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - What's the 'Skinny' on Microbiome? Interplay of Immune Cells, Microbes, and Skin Barrier in Health and Disease T2 - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AN - 1647635227; 6327339 JF - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AU - Segre, Julie AU - Kong, Heidi AU - Candotti, Fabio AU - Holland, Steven AU - Freeman, Alexandra AU - Oh, Julia AU - Sokolic, Robert Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Barriers KW - Skin UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635227?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.atitle=What%27s+the+%27Skinny%27+on+Microbiome%3F+Interplay+of+Immune+Cells%2C+Microbes%2C+and+Skin+Barrier+in+Health+and+Disease&rft.au=Segre%2C+Julie%3BKong%2C+Heidi%3BCandotti%2C+Fabio%3BHolland%2C+Steven%3BFreeman%2C+Alexandra%3BOh%2C+Julia%3BSokolic%2C+Robert&rft.aulast=Segre&rft.aufirst=Julie&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://ash.confex.com/ash/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Functional specificity of integrin-based adhesions in cell function is defined by actin nucleators T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647635222; 6327842 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Waterman, C AU - Case, L AU - Swaminathan, V AU - Skau, C Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Specificity KW - Actin KW - Adhesion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.atitle=Functional+specificity+of+integrin-based+adhesions+in+cell+function+is+defined+by+actin+nucleators&rft.au=Waterman%2C+C%3BCase%2C+L%3BSwaminathan%2C+V%3BSkau%2C+C&rft.aulast=Waterman&rft.aufirst=C&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Cell+Biology+and+International+Federation+for+Cell+Biology+Meeting+%282014+ASCB%2FIFCB%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascb.org/2014meeting/program/files/assets/common/downloads/2014%20ASCB%20PROGRAM.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Treatment: Current Paradigms and Novel Targeted Approaches T2 - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AN - 1647635150; 6327308 JF - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AU - Dunleavy, Kieron Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Hematology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635150?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.atitle=Treatment%3A+Current+Paradigms+and+Novel+Targeted+Approaches&rft.au=Dunleavy%2C+Kieron&rft.aulast=Dunleavy&rft.aufirst=Kieron&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://ash.confex.com/ash/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - B-Cell Receptor Pathway Inhibition as Therapy for Chronic Lymphocytic Leukemia and Lymphoplasmacytic Lymphoma T2 - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AN - 1647634863; 6327362 JF - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AU - Wiestner, Adrian Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - B-cell receptor KW - Therapy KW - Chronic lymphatic leukemia KW - Lymphoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647634863?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.atitle=B-Cell+Receptor+Pathway+Inhibition+as+Therapy+for+Chronic+Lymphocytic+Leukemia+and+Lymphoplasmacytic+Lymphoma&rft.au=Wiestner%2C+Adrian&rft.aulast=Wiestner&rft.aufirst=Adrian&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://ash.confex.com/ash/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Acquired Aplastic Anemia: New Genetics, New Genomics T2 - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AN - 1647633728; 6327371 JF - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AU - Young, Neal AU - Dumitriu, Bogdan AU - Ogawa, Seishi Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Genetics KW - Anemia KW - genomics KW - Aplastic anemia UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647633728?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.atitle=Acquired+Aplastic+Anemia%3A+New+Genetics%2C+New+Genomics&rft.au=Young%2C+Neal%3BDumitriu%2C+Bogdan%3BOgawa%2C+Seishi&rft.aulast=Young&rft.aufirst=Neal&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://ash.confex.com/ash/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Erythroid-Specific Expression of LIN28A Is Sufficient for Robust Gamma-Globin Gene and Protein Expression in Adult Erythroblasts T2 - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AN - 1647633486; 6327465 JF - 56th Annual Meeting of the American Society of Hematology (ASH 2014) AU - Lee, Y AU - Byrnes, Colleen AU - de Vasconcellos, Jaira AU - Kaushal, Megha AU - Rabel, Antoinette AU - Tumburu, Laxminath AU - Allwardt, Joshua AU - Miller, Jeffery Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Erythroblasts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647633486?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.atitle=Erythroid-Specific+Expression+of+LIN28A+Is+Sufficient+for+Robust+Gamma-Globin+Gene+and+Protein+Expression+in+Adult+Erythroblasts&rft.au=Lee%2C+Y%3BByrnes%2C+Colleen%3Bde+Vasconcellos%2C+Jaira%3BKaushal%2C+Megha%3BRabel%2C+Antoinette%3BTumburu%2C+Laxminath%3BAllwardt%2C+Joshua%3BMiller%2C+Jeffery&rft.aulast=Lee&rft.aufirst=Y&rft.date=2014-12-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+of+Hematology+%28ASH+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://ash.confex.com/ash/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - JOUR T1 - p53 mutations and inflammation-associated cancer are linked through TNF signaling. AN - 1634277250; 25479634 AB - In this issue, Di Minin et al. (2014) link mutant p53 and chronic inflammation to tumorigenic progression via TNF signaling. Mutp53 interacts with the tumor suppressor DAB2IP in the cytoplasm, and induces a TNF-dependent transcriptional profile via NF-kB and JNK. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Molecular cell AU - Cooks, Tomer AU - Harris, Curtis C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, MD, 20892-4258, USA. Electronic address: tomer.cooks@nih.gov. ; Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, MD, 20892-4258, USA. Y1 - 2014/12/04/ PY - 2014 DA - 2014 Dec 04 SP - 611 EP - 612 VL - 56 IS - 5 KW - Tumor Necrosis Factor-alpha KW - 0 KW - Tumor Suppressor Protein p53 KW - ras GTPase-Activating Proteins KW - Index Medicus KW - Animals KW - Humans KW - Female KW - ras GTPase-Activating Proteins -- metabolism KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- pathology KW - Tumor Suppressor Protein p53 -- genetics KW - Tumor Necrosis Factor-alpha -- metabolism KW - Tumor Suppressor Protein p53 -- metabolism KW - Signal Transduction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1634277250?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cell&rft.atitle=p53+mutations+and+inflammation-associated+cancer+are+linked+through+TNF+signaling.&rft.au=Cooks%2C+Tomer%3BHarris%2C+Curtis+C&rft.aulast=Cooks&rft.aufirst=Tomer&rft.date=2014-12-04&rft.volume=56&rft.issue=5&rft.spage=611&rft.isbn=&rft.btitle=&rft.title=Molecular+cell&rft.issn=1097-4164&rft_id=info:doi/10.1016%2Fj.molcel.2014.11.018 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-05 N1 - Date created - 2014-12-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment On: Mol Cell. 2014 Dec 4;56(5):617-29 [25454946] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.molcel.2014.11.018 ER - TY - JOUR T1 - PET/CT imaging correlates with treatment outcome in patients with multidrug-resistant tuberculosis AN - 1709170903; PQ0001773266 AB - Definitive clinical trials of new chemotherapies for treating tuberculosis (TB) require following subjects until at least 6 months after treatment discontinuation to assess for durable cure, making these trials expensive and lengthy. Surrogate endpoints relating to treatment failure and relapse are currently limited to sputum microbiology, which has limited sensitivity and specificity. We prospectively assessed radiographic changes using 2-deoxy-2-[ super(18)F]-fluoro-Dglucose (FDG) positron emission tomography/computed tomography (PET/CT) at 2 and 6 months (CT only) in a cohort of subjects with multidrug-resistant TB, who were treated with second-line TB therapy for 2 years and then followed for an additional 6 months. CT scans were read semiquantitatively by radiologists and were computationally evaluated using custom software to provide volumetric assessment of TB-associated abnormalities. CT scans at 6 months (but not 2 months) assessed by radiologist readers were predictive of outcomes, and changes in computed abnormal volumes were predictive of drug response at both time points. Quantitative changes in FDG uptake 2 months after starting treatment were associated with long- term outcomes. In this cohort, some radiologic markers were more sensitive than conventional sputum microbiology in distinguishing successful from unsuccessful treatment. These results support the potential of imaging scans as possible surrogate endpoints in clinical trials of new TB drug regimens. Larger cohorts confirming these results are needed. JF - Science Translational Medicine AU - Chen, Ray Y AU - Dodd, Lori E AU - Lee, Myungsun AU - Paripati, Praveen AU - Hammoud, Dima A AU - Mountz, James M AU - Jeon, Doosoo AU - Zia, Nadeem AU - Zahiri, Homeira AU - Coleman, M Teresa AD - Tuberculosis Research Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD 20892, USA Y1 - 2014/12/03/ PY - 2014 DA - 2014 Dec 03 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 6 IS - 265 SN - 1946-6234, 1946-6234 KW - Microbiology Abstracts B: Bacteriology KW - Translation KW - Mycobacterium KW - Drug resistance KW - Chemotherapy KW - Clinical trials KW - Computer programs KW - software KW - Computed tomography KW - Positron emission tomography KW - Tuberculosis KW - Sputum KW - Drugs KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709170903?accountid=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=Science+Translational+Medicine&rft.atitle=PET%2FCT+imaging+correlates+with+treatment+outcome+in+patients+with+multidrug-resistant+tuberculosis&rft.au=Chen%2C+Ray+Y%3BDodd%2C+Lori+E%3BLee%2C+Myungsun%3BParipati%2C+Praveen%3BHammoud%2C+Dima+A%3BMountz%2C+James+M%3BJeon%2C+Doosoo%3BZia%2C+Nadeem%3BZahiri%2C+Homeira%3BColeman%2C+M+Teresa&rft.aulast=Chen&rft.aufirst=Ray&rft.date=2014-12-03&rft.volume=6&rft.issue=265&rft.spage=265ra166&rft.isbn=&rft.btitle=&rft.title=Science+Translational+Medicine&rft.issn=19466234&rft_id=info:doi/10.1126%2Fscitranslmed.3009501 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Computer programs; Translation; software; Chemotherapy; Drug resistance; Computed tomography; Positron emission tomography; Tuberculosis; Sputum; Drugs; Clinical trials; Mycobacterium DO - http://dx.doi.org/10.1126/scitranslmed.3009501 ER - TY - JOUR T1 - Simultaneous sequencing of oxidized methylcytosines produced by TET/JBP dioxygenases in Coprinopsis cinerea. AN - 1629955572; 25406324 AB - TET/JBP enzymes oxidize 5-methylpyrimidines in DNA. In mammals, the oxidized methylcytosines (oxi-mCs) function as epigenetic marks and likely intermediates in DNA demethylation. Here we present a method based on diglucosylation of 5-hydroxymethylcytosine (5hmC) to simultaneously map 5hmC, 5-formylcytosine, and 5-carboxylcytosine at near-base-pair resolution. We have used the method to map the distribution of oxi-mC across the genome of Coprinopsis cinerea, a basidiomycete that encodes 47 TET/JBP paralogs in a previously unidentified class of DNA transposons. Like 5-methylcytosine residues from which they are derived, oxi-mC modifications are enriched at centromeres, TET/JBP transposons, and multicopy paralogous genes that are not expressed, but rarely mark genes whose expression changes between two developmental stages. Our study provides evidence for the emergence of an epigenetic regulatory system through recruitment of selfish elements in a eukaryotic lineage, and describes a method to map all three different species of oxi-mCs simultaneously. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Chavez, Lukas AU - Huang, Yun AU - Luong, Khai AU - Agarwal, Suneet AU - Iyer, Lakshminarayan M AU - Pastor, William A AU - Hench, Virginia K AU - Frazier-Bowers, Sylvia A AU - Korol, Evgenia AU - Liu, Shuo AU - Tahiliani, Mamta AU - Wang, Yinsheng AU - Clark, Tyson A AU - Korlach, Jonas AU - Pukkila, Patricia J AU - Aravind, L AU - Rao, Anjana AD - Division of Signaling and Gene Expression, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037; Sanford Consortium for Regenerative Medicine, La Jolla, CA 92037; ; Pacific Biosciences, Menlo Park, CA 94025; ; Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA 02115; ; National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894; ; Division of Signaling and Gene Expression, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037; ; Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; ; Skirball Institute, NYU Langone Medical Center, New York University, New York, NY 10016; ; Environmental Toxicology Graduate Program and Department of Chemistry, University of California, Riverside, CA 92521; and. ; Division of Signaling and Gene Expression, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037; Department of Pharmacology and Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093 arao@liai.org. Y1 - 2014/12/02/ PY - 2014 DA - 2014 Dec 02 SP - E5149 EP - E5158 VL - 111 IS - 48 KW - DNA Transposable Elements KW - 0 KW - Fungal Proteins KW - 5-Methylcytosine KW - 6R795CQT4H KW - Dioxygenases KW - EC 1.13.11.- KW - Index Medicus KW - SMRT-seq KW - 5fC KW - 5mC KW - 5caC KW - TET KW - Gene Expression Regulation, Fungal KW - Genome, Fungal -- genetics KW - Hyphae -- growth & development KW - HEK293 Cells KW - Humans KW - Spores, Fungal -- growth & development KW - Sequence Analysis -- methods KW - Hyphae -- genetics KW - Chromosomes, Fungal -- genetics KW - Oxidation-Reduction KW - DNA Methylation KW - Spores, Fungal -- metabolism KW - DNA Transposable Elements -- genetics KW - Gene Expression Regulation, Developmental KW - Hyphae -- metabolism KW - Fungal Proteins -- metabolism KW - Dioxygenases -- genetics KW - 5-Methylcytosine -- metabolism KW - Basidiomycota -- growth & development KW - Basidiomycota -- genetics KW - Fungal Proteins -- genetics KW - Dioxygenases -- metabolism KW - Basidiomycota -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629955572?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Simultaneous+sequencing+of+oxidized+methylcytosines+produced+by+TET%2FJBP+dioxygenases+in+Coprinopsis+cinerea.&rft.au=Chavez%2C+Lukas%3BHuang%2C+Yun%3BLuong%2C+Khai%3BAgarwal%2C+Suneet%3BIyer%2C+Lakshminarayan+M%3BPastor%2C+William+A%3BHench%2C+Virginia+K%3BFrazier-Bowers%2C+Sylvia+A%3BKorol%2C+Evgenia%3BLiu%2C+Shuo%3BTahiliani%2C+Mamta%3BWang%2C+Yinsheng%3BClark%2C+Tyson+A%3BKorlach%2C+Jonas%3BPukkila%2C+Patricia+J%3BAravind%2C+L%3BRao%2C+Anjana&rft.aulast=Chavez&rft.aufirst=Lukas&rft.date=2014-12-02&rft.volume=111&rft.issue=48&rft.spage=E5149&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.1419513111 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-28 N1 - Date created - 2014-12-03 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - SRP041464; SRA; GSE46965; GEO N1 - SuppNotes - Cited By: Science. 2009 May 15;324(5929):930-5 [19372391] Nat Rev Mol Cell Biol. 2013 Jun;14(6):341-56 [23698584] Nature. 2009 Nov 19;462(7271):315-22 [19829295] PLoS One. 2010;5(1):e8888 [20126651] Science. 2010 May 14;328(5980):916-9 [20395474] Nucleic Acids Res. 2013 Jul;41(13):6421-9 [23658232] Nucleic Acids Res. 2013 Sep;41(16):7635-55 [23814188] Nature. 2013 Oct 24;502(7472):472-9 [24153300] Bioinformatics. 2014 Jan 15;30(2):284-6 [24227674] Cell. 2014 Jan 16;156(1-2):45-68 [24439369] Proc Natl Acad Sci U S A. 2014 Jan 28;111(4):1361-6 [24474761] Proc Natl Acad Sci U S A. 2014 Feb 4;111(5):1676-83 [24398522] Nature. 2014 Feb 20;506(7488):391-5 [24390346] J Am Chem Soc. 2014 Apr 2;136(13):4801-4 [24655109] Microbiol Mol Biol Rev. 2000 Jun;64(2):316-53 [10839819] Mol Cell Biol. 1986 Jan;6(1):195-200 [3785146] Genetics. 1993 Oct;135(2):357-66 [8244000] Genetics. 1994 May;137(1):87-94 [7914506] J Biol Chem. 1961 May;236:1487-93 [13753193] Science. 2009 Jan 2;323(5910):133-8 [19023044] Prog Mol Biol Transl Sci. 2011;101:25-104 [21507349] Nature. 2011 May 19;473(7347):394-7 [21552279] Angew Chem Int Ed Engl. 2011 Jul 25;50(31):7008-12 [21721093] Curr Biol. 2011 Aug 23;21(16):R616-7 [21854997] Science. 2011 Sep 2;333(6047):1300-3 [21778364] Science. 2011 Sep 2;333(6047):1303-7 [21817016] J Biol Chem. 2011 Oct 14;286(41):35334-8 [21862836] BMC Genomics. 2011;12:621 [22185659] Nucleic Acids Res. 2012 Feb;40(4):e29 [22156058] J Biol Chem. 2012 Jun 8;287(24):19886-95 [22514282] Front Cell Infect Microbiol. 2012;2:89 [22919680] Cell. 2012 Aug 31;150(5):909-21 [22939620] Nat Protoc. 2012 Oct;7(10):1897-908 [23018193] Nat Biotechnol. 2012 Dec;30(12):1232-9 [23138224] Cell. 2012 Dec 21;151(7):1417-30 [23260135] Biol Direct. 2012;7:39 [23146749] Cell. 2013 Feb 28;152(5):1146-59 [23434322] EMBO J. 2013 Mar 6;32(5):645-55 [23353889] BMC Biol. 2013;11:4 [23339471] Angew Chem Int Ed Engl. 2013 Apr 15;52(16):4350-5 [23559386] Cell. 2013 Apr 25;153(3):692-706 [23602152] Nat Methods. 2010 Jun;7(6):461-5 [20453866] Proc Natl Acad Sci U S A. 2010 Jun 29;107(26):11889-94 [20547848] Proc Natl Acad Sci U S A. 2010 Jun 29;107(26):11655-6 [20571118] PLoS Genet. 2010 Sep;6(9):e1001135 [20885784] Genome Res. 2010 Oct;20(10):1441-50 [20802089] Chem Commun (Camb). 2010 Nov 21;46(43):8195-7 [20927439] Nature. 2010 Dec 9;468(7325):839-43 [21057493] Nat Biotechnol. 2011 Jan;29(1):68-72 [21151123] Cell. 2013 Apr 25;153(3):678-91 [23602153] Cell Cycle. 2009 Jun 1;8(11):1698-710 [19411852] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1419513111 ER - TY - JOUR T1 - Spatiotemporal relationships among Late Pennsylvanian plant assemblages; palynological evidence from the Markley Formation, West Texas, U.S.A. AN - 1832611679; 716628-2 AB - The Pennsylvanian lowlands of western Pangea are best known for their diverse wetland floras of arborescent and herbaceous ferns, and arborescent horsetails and clubmosses. In apparent juxtaposition, a very different kind of flora, dominated by a xerophilous assemblage of conifers, taeniopterids and peltasperms, is occasionally glimpsed. Once believed to represent upland or extrabasinal floras from well-drained portions of the landscape, these dryland floras more recently have been interpreted as lowland assemblages growing during drier phases of glacial/interglacial cycles. Whether Pennsylvanian dryland and wetland floras were separated spatially or temporally remains an unsettled question, due in large part to taphonomic bias toward preservation of wetland plants. Previous paleobotanical and sedimentological analysis of the Markley Formation of latest Pennsylvanian (Gzhelian) age, from north central Texas, U.S.A, indicates close correlation between lithofacies and distinct dryland and wetland megaflora assemblages. Here we present a detailed analysis one of those localities, a section unusual in containing abundant palynomorphs, from the lower Markley Formation. Paleobotanical, palynological and lithological data from a section thought to represent a single interglacial/glacial phase are integrated and analyzed to create a complex picture of an evolving landscape. Megafloral data from throughout the Markley Formation show that conifer-dominated dryland floras occur exclusively in highly leached kaolinite beds, likely eroded from underlying soils, whereas a mosaic of wetland floras occupy histosols, ultisols, and fluvial overbank deposits. Palynological data largely conform to this pattern but reveal a more complex picture. An assemblage of mixed wetland and dryland palynofloral taxa is interpolated between a dryland assemblage and an overlying histosol containing wetland taxa. In this section, as well as elsewhere in the Markley Formation, kaolinite and overlying organic beds appear to have formed as a single genetic unit, with the kaolinite forming an impermeable aquiclude upon which a poorly drained wetland subsequently formed. Within a single inferred glacial/interglacial cycle, lithological data indicate significant fluctuations in water availability tracked by changes in palynofloral and megafloral taxa. Palynology reveals that elements of the dryland floras appear at low abundance even within wetland deposits. The combined data indicate a complex pattern of succession and suggest a mosaic of dryland and wetland plant communities in the Late Pennsylvanian. Our data alone cannot show whether dryland and wetland assemblages succeed one another temporally, or coexisted on the landscape. However, the combined evidence suggests relatively close spatial proximity within a fragmenting and increasingly arid environment. Abstract Copyright (2014) Elsevier, B.V. JF - Review of Palaeobotany and Palynology AU - Looy, Cindy V AU - Hotton, Carol L Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 10 EP - 27 PB - Elsevier, Amsterdam VL - 211 SN - 0034-6667, 0034-6667 KW - silicates KW - Spermatophyta KW - terrestrial environment KW - Cisuralian KW - Pennsylvanian KW - siliciclastics KW - Lower Permian KW - climate change KW - sedimentary rocks KW - Gzhelian KW - Markley Formation KW - Plantae KW - Paleozoic KW - Carboniferous KW - Texas KW - kaolinite KW - organic compounds KW - palynomorphs KW - trees KW - United States KW - Paleosols KW - stream sediments KW - Pteridophyta KW - drylands KW - pollen KW - Upper Pennsylvanian KW - coal KW - glacial environment KW - sediments KW - taphonomy KW - miospores KW - Midland Basin KW - soils KW - Coniferae KW - Pangaea KW - interglacial environment KW - assemblages KW - arid environment KW - Gymnospermae KW - cyclic processes KW - statistical analysis KW - Permian KW - Asselian KW - clay minerals KW - spores KW - peat KW - lithofacies KW - wetlands KW - classification KW - Lycopsida KW - sheet silicates KW - fluvial environment KW - microfossils KW - 09:Paleobotany UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1832611679?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ageorefinprocess&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Review+of+Palaeobotany+and+Palynology&rft.atitle=Spatiotemporal+relationships+among+Late+Pennsylvanian+plant+assemblages%3B+palynological+evidence+from+the+Markley+Formation%2C+West+Texas%2C+U.S.A.&rft.au=Looy%2C+Cindy+V%3BHotton%2C+Carol+L&rft.aulast=Looy&rft.aufirst=Cindy&rft.date=2014-12-01&rft.volume=211&rft.issue=&rft.spage=10&rft.isbn=&rft.btitle=&rft.title=Review+of+Palaeobotany+and+Palynology&rft.issn=00346667&rft_id=info:doi/10.1016%2Fj.revpalbo.2014.09.007 L2 - http://www.sciencedirect.com/science/journal/00346667 LA - English DB - GeoRef N1 - Copyright - GeoRef in Process, Copyright 2017, American Geosciences Institute. After editing and indexing, this record will be added to Georef. Reference includes data from CAPCAS, Elsevier Scientific Publishers, Amsterdam, Netherlands N1 - Number of references - 222 N1 - Document feature - illus. incl. 2 plates, 1 table, chart N1 - Last updated - 2017-01-24 N1 - CODEN - RPPYAX N1 - SubjectsTermNotLitGenreText - arid environment; Asselian; assemblages; Carboniferous; Cisuralian; classification; clay minerals; climate change; coal; Coniferae; cyclic processes; drylands; fluvial environment; glacial environment; Gymnospermae; Gzhelian; interglacial environment; kaolinite; lithofacies; Lower Permian; Lycopsida; Markley Formation; microfossils; Midland Basin; miospores; organic compounds; Paleosols; Paleozoic; palynomorphs; Pangaea; peat; Pennsylvanian; Permian; Plantae; pollen; Pteridophyta; sedimentary rocks; sediments; sheet silicates; silicates; siliciclastics; soils; Spermatophyta; spores; statistical analysis; stream sediments; taphonomy; terrestrial environment; Texas; trees; United States; Upper Pennsylvanian; wetlands DO - http://dx.doi.org/10.1016/j.revpalbo.2014.09.007 ER - TY - JOUR T1 - CD47 in the Tumor Microenvironment Limits Cooperation between Antitumor T-cell Immunity and Radiotherapy AN - 1811903696; PQ0003457542 AB - These findings establish that blocking the immunosuppressive molecule CD47 on cytotoxic T cells can enhance antitumor immunity in the context of radiotherapy, with the potential to increase curative radiation responses. Although significant advances in radiotherapy have increased its effectiveness in many cancer settings, general strategies to widen the therapeutic window between normal tissue toxicity and malignant tumor destruction would still offer great value. CD47 blockade has been found to confer radioprotection to normal tissues while enhancing tumor radiosensitivity. Here, we report that CD47 blockade directly enhances tumor immunosurveillance by CD8+ T cells. Combining CD47 blockade with irradiation did not affect fibrosarcoma growth in T cell-deficient mice, whereas adoptive transfer of tumor-specific CD8+ T cells restored combinatorial efficacy. Furthermore, ablation of CD8+ T cells abolished radiotherapeutic response in immunocompetent syngeneic hosts. CD47 blockade in either target cells or effector cells was sufficient to enhance antigen-dependent CD8+ CTL-mediated tumor cell killing in vitro. In CD47-deficient syngeneic hosts, engrafted B16 melanomas were 50% more sensitive to irradiation, establishing that CD47 expression in the microenvironment was sufficient to limit tumor radiosensitivity. Mechanistic investigations revealed increased tumor infiltration by cytotoxic CD8+ T cells in a CD47-deficient microenvironment, with an associated increase in T cell-dependent intratumoral expression of granzyme B. Correspondingly, an inverse correlation between CD8+ T-cell infiltration and CD47 expression was observed in human melanomas. Our findings establish that blocking CD47 in the context of radiotherapy enhances antitumor immunity by directly stimulating CD8+ cytotoxic T cells, with the potential to increase curative responses. Cancer Res; 74(23); 6771-83. copyright 2014 AACR. JF - Cancer Research AU - Soto-Pantoja, David R AU - Terabe, Masaki AU - Ghosh, Arunima AU - Ridnour, Lisa A AU - DeGraff, William G AU - Wink, David A AU - Berzofsky, Jay A AU - Roberts, David D AD - Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, dr9y@nih.gov Y1 - 2014/12/01/ PY - 2014 DA - 2014 Dec 01 SP - 6771 EP - 6783 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 74 IS - 23 SN - 0008-5472, 0008-5472 KW - Immunology Abstracts; Toxicology Abstracts KW - Fibrosarcoma KW - Radiotherapy KW - Toxicity KW - Tumors KW - CD8 antigen KW - Tumor cells KW - Cancer KW - Melanoma KW - Effector cells KW - Metastases KW - granzyme B KW - Cytotoxicity KW - Radiation KW - Immunosurveillance KW - Radioprotection KW - Lymphocytes T KW - Adoptive transfer KW - Radiosensitivity KW - Microenvironments KW - X 24390:Radioactive Materials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1811903696?accountid=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+Research&rft.atitle=CD47+in+the+Tumor+Microenvironment+Limits+Cooperation+between+Antitumor+T-cell+Immunity+and+Radiotherapy&rft.au=Soto-Pantoja%2C+David+R%3BTerabe%2C+Masaki%3BGhosh%2C+Arunima%3BRidnour%2C+Lisa+A%3BDeGraff%2C+William+G%3BWink%2C+David+A%3BBerzofsky%2C+Jay+A%3BRoberts%2C+David+D&rft.aulast=Soto-Pantoja&rft.aufirst=David&rft.date=2014-12-01&rft.volume=74&rft.issue=23&rft.spage=6771&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-0037-T LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-08-01 N1 - Last updated - 2016-10-26 N1 - SubjectsTermNotLitGenreText - Fibrosarcoma; Radiotherapy; CD8 antigen; Tumors; Toxicity; Tumor cells; Cancer; Effector cells; Melanoma; Metastases; granzyme B; Cytotoxicity; Radiation; Immunosurveillance; Radioprotection; Adoptive transfer; Lymphocytes T; Microenvironments; Radiosensitivity DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0037-T ER - TY - JOUR T1 - Phase II Clinical Trial of Amatuximab, a Chimeric Antimesothelin Antibody with Pemetrexed and Cisplatin in Advanced Unresectable Pleural Mesothelioma AN - 1808642784; PQ0003457449 AB - Purpose: Amatuximab is a chimeric monoclonal antibody to mesothelin, a cell surface glycoprotein highly expressed in malignant pleural mesothelioma (MPM). On the basis of its synergy with chemotherapy in preclinical studies, we evaluated the antitumor activity of amatuximab plus pemetrexed and cisplatin in patients with unresectable MPM.Experimental Design: In a single-arm phase II study, amatuximab (5 mg/kg) was administered on days 1 and 8 with pemetrexed (500 mg/m2) and cisplatin (75 mg/m2) on day 1 of 21-day cycles for up to six cycles. Patients with response or stable disease received amatuximab maintenance until disease progression. Primary endpoint was progression-free survival (PFS) at 6 months. Secondary endpoints were overall survival (OS), response rate, and safety.Results: Eighty-nine patients were enrolled at 26 centers. Median of five cycles (range, 1-6) of combination treatment was administered, and 56 (63%) patients received amatuximab maintenance. Combination therapy resulted in no overlapping toxicities. Eleven patients (12.4%) had amatuximab-related hypersensitivity reactions. Responses included partial responses in 33 (40%) and stable disease in 42 (51%). Six-month PFS rate was 51% [95% confidence interval (CI), 39.1-62.3)], median PFS was 6.1 months (95% CI, 5.8-6.4), and median OS was 14.8 months (95% CI, 12.4-18.5) with 29 patients alive at data cut-off.Conclusions: Amatuximab with pemetrexed and cisplatin was well tolerated with objective tumor response or stable disease rate of 90% by independent radiologic review. Although PFS was not significantly different from historical controls, the median OS was 14.8 months with a third of patients alive and 5 continuing to receive amatuximab at the time of analysis. Clin Cancer Res; 20(23); 5927-36. copyright 2014 AACR. JF - Clinical Cancer Research AU - Hassan, Raffit AU - Kindler, Hedy L AU - Jahan, Thierry AU - Bazhenova, Lyudmila AU - Reck, Martin AU - Thomas, Anish AU - Pastan, Ira AU - Parno, Jeff AU - O'Shannessy, Daniel J AU - Fatato, Penny AU - Maltzman, Julia D AU - Wallin, Bruce A AD - Thoracic and GI Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, hassanr@mail.nih.gov Y1 - 2014/12/01/ PY - 2014 DA - 2014 Dec 01 SP - 5927 EP - 5936 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 20 IS - 23 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Cell surface KW - Data processing KW - Monoclonal antibodies KW - Chemotherapy KW - Survival KW - Tumors KW - Toxicity KW - Clinical trials KW - Cancer KW - Hypersensitivity KW - Cisplatin KW - mesothelioma KW - Glycoproteins KW - Antitumor activity KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808642784?accountid=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=Phase+II+Clinical+Trial+of+Amatuximab%2C+a+Chimeric+Antimesothelin+Antibody+with+Pemetrexed+and+Cisplatin+in+Advanced+Unresectable+Pleural+Mesothelioma&rft.au=Hassan%2C+Raffit%3BKindler%2C+Hedy+L%3BJahan%2C+Thierry%3BBazhenova%2C+Lyudmila%3BReck%2C+Martin%3BThomas%2C+Anish%3BPastan%2C+Ira%3BParno%2C+Jeff%3BO%27Shannessy%2C+Daniel+J%3BFatato%2C+Penny%3BMaltzman%2C+Julia+D%3BWallin%2C+Bruce+A&rft.aulast=Hassan&rft.aufirst=Raffit&rft.date=2014-12-01&rft.volume=20&rft.issue=23&rft.spage=5927&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-0804 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Cell surface; Data processing; Monoclonal antibodies; Chemotherapy; Survival; Toxicity; Tumors; Clinical trials; Cancer; Hypersensitivity; Cisplatin; mesothelioma; Glycoproteins; Antitumor activity DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-0804 ER - TY - JOUR T1 - Perceptions of cancer as a death sentence: Prevalence and consequences AN - 1683509645 AB - Research suggests that perceiving cancer as a death sentence is a critical determinant of health care–seeking behaviors. However, there is limited information regarding the prevalence of this perception in the US population. Cross-sectional analysis of data (n = 7674 adults) from the 2007-2008 administration of the nationally representative Health Information National Trends Survey (HINTS 3) was performed. A majority (61.6%) of respondents perceived cancer as death sentence, and more than one-third (36%) of respondents reported that they avoid seeing their physicians. In the adult US population, perceiving cancer as a death sentence is common and is associated with education level and avoidance of physicians. JF - Journal of Health Psychology AU - Moser, Richard P AU - Arndt, Jamie AU - Han, Paul K AU - Waters, Erika A AU - Amsellem, Marni AU - Hesse, Bradford W AD - National Cancer Institute, USA ; University of Missouri, USA ; Maine Medical Center, USA ; Washington University School of Medicine, USA ; National Cancer Institute, SAIC-Frederick, USA ; National Cancer Institute, USA Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1518 EP - 1524 CY - London PB - SAGE PUBLICATIONS, INC. VL - 19 IS - 12 SN - 1359-1053 KW - Psychology KW - cancer KW - health behavior KW - health psychology KW - perception KW - public health psychology KW - Avoidance KW - Mental health services KW - Cancer KW - Death KW - Doctors KW - Health behaviour KW - Health care KW - Health information KW - Health psychology KW - Perceptions KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683509645?accountid=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+Health+Psychology&rft.atitle=Perceptions+of+cancer+as+a+death+sentence%3A+Prevalence+and+consequences&rft.au=Moser%2C+Richard+P%3BArndt%2C+Jamie%3BHan%2C+Paul+K%3BWaters%2C+Erika+A%3BAmsellem%2C+Marni%3BHesse%2C+Bradford+W&rft.aulast=Moser&rft.aufirst=Richard&rft.date=2014-12-01&rft.volume=19&rft.issue=12&rft.spage=1518&rft.isbn=&rft.btitle=&rft.title=Journal+of+Health+Psychology&rft.issn=13591053&rft_id=info:doi/10.1177%2F1359105313494924 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-05-19 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1177/1359105313494924 ER - TY - JOUR T1 - NAG-1/GDF-15 prevents obesity by increasing thermogenesis, lipolysis and oxidative metabolism AN - 1680442107; PQ0001187868 AB - Objective: Obesity is a major health problem associated with high morbidity and mortality. NSAID-activated gene (NAG-1) is a TGF- beta superfamily member reported to alter adipose tissue levels in mice. We investigated whether hNAG-1 acts as a regulator of adiposity and energy metabolism.Design/Subjects:hNAG-1 mice, ubiquitously expressing hNAG-1, were placed on a control or high-fat diet for 12 weeks. hNAG-1-expressing B16/F10 melanoma cells were used in a xenograft model to deliver hNAG-1 to obese C57BL/6 mice. Results: As compared with wild-type littermates, transgenic hNAG-1 mice have less white fat and brown fat despite equivalent food intake, improved glucose tolerance, lower insulin levels and are resistant to dietary- and genetic-induced obesity. hNAG-1 mice are more metabolically active with higher energy expenditure. Obese C57BL/6 mice treated with hNAG-1-expressing xenografts show decreases in adipose tissue and serum insulin levels. hNAG-1 mice and obese mice treated with hNAG-1-expressing xenografts show increased thermogenic gene expression (UCP1, PGC1 alpha , ECH1, Cox8b, Dio2, Cyc1, PGC1 beta , PPAR alpha , Elvol3) in brown adipose tissue (BAT) and increased expression of lipolytic genes (Adrb3, ATGL, HSL) in both white adipose tissue (WAT) and BAT, consistent with higher energy metabolism. Conclusion: hNAG-1 modulates metabolic activity by increasing the expression of key thermogenic and lipolytic genes in BAT and WAT. hNAG-1 appears to be a novel therapeutic target in preventing and treating obesity and insulin resistance. JF - International Journal of Obesity AU - Chrysovergis, K AU - Wang, X AU - Kosak, J AU - Lee, S-H AU - Kim, J S AU - Foley, J F AU - Travlos, G AU - Singh, S AU - Baek, S J AU - Eling, T E AD - Laboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC, USA Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1555 EP - 1564 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 38 IS - 12 SN - 0307-0565, 0307-0565 KW - Physical Education Index KW - Obesity KW - Animal subjects KW - Objectives KW - Fats KW - Football (American) KW - Diet KW - Hormones KW - Metabolism KW - Professional sports KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680442107?accountid=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=NAG-1%2FGDF-15+prevents+obesity+by+increasing+thermogenesis%2C+lipolysis+and+oxidative+metabolism&rft.au=Chrysovergis%2C+K%3BWang%2C+X%3BKosak%2C+J%3BLee%2C+S-H%3BKim%2C+J+S%3BFoley%2C+J+F%3BTravlos%2C+G%3BSingh%2C+S%3BBaek%2C+S+J%3BEling%2C+T+E&rft.aulast=Chrysovergis&rft.aufirst=K&rft.date=2014-12-01&rft.volume=38&rft.issue=12&rft.spage=1555&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2014.27 LA - English DB - Physical Education Index N1 - Date revised - 2015-05-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Obesity; Objectives; Animal subjects; Football (American); Fats; Diet; Hormones; Professional sports; Metabolism DO - http://dx.doi.org/10.1038/ijo.2014.27 ER - TY - JOUR T1 - Regulatory Forum Opinion Piece*: New Testing Paradigms for Reproductive and Developmental Toxicity-The NTP Modified One Generation Study and OECD 443 AN - 1680437041; PQ0001532683 AB - The National Toxicology Program (NTP) has developed a new flexible study design, termed the modified one generation (MOG) reproduction study. The MOG study will encompass measurements of developmental and reproductive toxicity parameters as well as enable the setting of appropriate dose levels for a cancer bioassay through evaluation of target organ toxicity that is based on test article exposure that starts during gestation. This study design is compared and contrasted with the new Organization for Economic Co-operation and Development (OECD) 443 test guideline, the extended one generation reproduction study. The MOG study has a number of advantages, with a focus on F1 animals, the generation of adequately powered, robust data sets that include both pre and postnatal developmental toxicity information, and the measurement of effects on reproductive structure and function in the same animals. This new study design does not employ the use of internal triggers in the design structure for the use of animals already on test and is also consistent with the principles of the 3R's. JF - Toxicologic Pathology AU - Foster, Paul MD AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA, foster2@niehs.nih.gov Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 1165 EP - 1167 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 42 IS - 8 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - developmental pathology KW - endocrine disrupters KW - female reproduction KW - male reproduction KW - reproductive system KW - safety assessment. KW - Data processing KW - Structure-function relationships KW - Economics KW - Gestation KW - Oligodendrocyte-myelin glycoprotein KW - Reproduction KW - Toxicity KW - Cancer KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680437041?accountid=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=Regulatory+Forum+Opinion+Piece*%3A+New+Testing+Paradigms+for+Reproductive+and+Developmental+Toxicity-The+NTP+Modified+One+Generation+Study+and+OECD+443&rft.au=Foster%2C+Paul+MD&rft.aulast=Foster&rft.aufirst=Paul&rft.date=2014-12-01&rft.volume=42&rft.issue=8&rft.spage=1165&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623314534920 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Number of references - 6 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Data processing; Structure-function relationships; Gestation; Economics; Reproduction; Oligodendrocyte-myelin glycoprotein; Toxicity; Cancer DO - http://dx.doi.org/10.1177/0192623314534920 ER - TY - JOUR T1 - Comparative Uterotrophic Effects of Endoxifen and Tamoxifen in Ovariectomized Sprague-Dawley Rats AN - 1680436314; PQ0001532676 AB - Endoxifen (4-hydroxy-N-desmethyl-tamoxifen), one of the major active metabolites of tamoxifen, has substantially greater estrogen antagonist properties and antiproliferative effects in breast tumor cells than tamoxifen, a mixed estrogen agonist/antagonist. An associated risk of endometrial cancer and hyperplasia has been linked to the estrogen agonist properties of tamoxifen. We evaluated endoxifen using a classic uterotrophic effects method. Rats were given endoxifen or tamoxifen orally for 3 days. Estradiol was the positive control. Endoxifen and tamoxifen plasma levels exceeded those previously observed clinically. Uterine weight was 3-fold higher in the estradiol group than in the tamoxifen or endoxifen groups, which did not differ from vehicle controls. Tamoxifen and endoxifen caused a greater increase in luminal epithelial cell height than estradiol. Both tamoxifen and endoxifen produced an increase in the stromal BrdU labeling index (LI) that was less than or equal to estradiol and inversely related to dose, but did not affect luminal epithelial cell BrdU LI. As expected, estradiol increased luminal epithelial cell proliferation. These results indicate that endoxifen induces uterotrophic effects, but is less potent than estradiol in eliciting these effects. Given prior preclinical observations that endoxifen has superior antitumor activity than tamoxifen, the observations of similar uterine effects suggest that the endoxifen risk/benefit ratio may be superior to tamoxifen. JF - Toxicologic Pathology AU - Schweikart, Karen M AU - Eldridge, Sandy R AU - Safgren, Stephanie L AU - Parman, Toufan AU - Reid, Joel M AU - Ames, Matthew M AU - Goetz, Matthew P AU - Davis, Myrtle A AD - Developmental Therapeutics Program, National Cancer Institute, Bethesda, Maryland, USA, schweikk@mail.nih.gov Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 1188 EP - 1196 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 42 IS - 8 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - endoxifen KW - tamoxifen KW - endometrial cell proliferation. KW - Epithelial cells KW - Endometrium KW - Uterus KW - Estrogens KW - Metabolites KW - Tumor cells KW - Tamoxifen KW - Cancer KW - Estradiol KW - Plasma levels KW - Hyperplasia KW - Ovariectomy KW - Menopause KW - Antitumor activity KW - X 24310:Pharmaceuticals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680436314?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Comparative+Uterotrophic+Effects+of+Endoxifen+and+Tamoxifen+in+Ovariectomized+Sprague-Dawley+Rats&rft.au=Schweikart%2C+Karen+M%3BEldridge%2C+Sandy+R%3BSafgren%2C+Stephanie+L%3BParman%2C+Toufan%3BReid%2C+Joel+M%3BAmes%2C+Matthew+M%3BGoetz%2C+Matthew+P%3BDavis%2C+Myrtle+A&rft.aulast=Schweikart&rft.aufirst=Karen&rft.date=2014-12-01&rft.volume=42&rft.issue=8&rft.spage=1188&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623314525688 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Number of references - 38 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Epithelial cells; Estrogens; Uterus; Endometrium; Metabolites; Tamoxifen; Tumor cells; Estradiol; Cancer; Hyperplasia; Plasma levels; Ovariectomy; Menopause; Antitumor activity DO - http://dx.doi.org/10.1177/0192623314525688 ER - TY - JOUR T1 - Cognitive problems among breast cancer survivors: loneliness enhances risk AN - 1665162336 AB - Background Cancer survivors often experience cognitive difficulties after treatment completion. Although chemotherapy enhances risk for cognitive problems, it is likely only one piece of a complex puzzle that explains survivorsʼ cognitive functioning. Loneliness may be one psychosocial risk factor. The current studies included both subjective and objective cognitive measures and tested whether lonelier breast cancer survivors would have more concentration and memory complaints and experience more concentration difficulties than their less lonely counterparts. Methods The relationship between loneliness and cognitive function was tested among three samples of breast cancer survivors. Study 1 was a sample of breast cancer survivors ( n=200) who reported their concentration and memory problems. Study 2a was a sample of breast cancer survivors ( n=185) and noncancer controls ( n=93) who reported their concentration and memory problems. Study 2b was a subsample of Study 2a breast cancer survivors ( n=22) and noncancer controls ( n=21) who completed a standardized neuropsychological test assessing concentration. Results Studies 1 and 2a revealed that lonelier women reported more concentration and memory problems than less lonely women. Study 2b utilized a standardized neuropsychological continuous performance test and demonstrated that lonelier women experienced more concentration problems than their less lonely counterparts. Conclusions These studies demonstrated that loneliness is linked to concentration and memory complaints and the experience of concentration problems among breast cancer survivors. The results were also highly consistent across three samples of breast cancer survivors. These data suggest that loneliness may be a risk factor for cognitive difficulties among cancer survivors. Copyright © 2014 John Wiley & Sons, Ltd. JF - Psycho-Oncology AU - Jaremka, Lisa M AU - Peng, Juan AU - Bornstein, Robert AU - Alfano, Catherine M AU - Andridge, Rebecca R AU - Povoski, Stephen P AU - Lipari, Adele M AU - Agnese, Doreen M AU - Farrar, William B AU - Yee, Lisa D AU - Carson, William E AU - Kiecolt-Glaser, Janice K AD - Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, OH, USA. ; Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, OH, USA., College of Public Health, The Ohio State University College of Medicine, Columbus, OH, USA. ; Department of Psychiatry, The Ohio State University College of Medicine, Columbus, OH, USA. ; National Cancer Institute, Bethesda, MD, USA. ; College of Public Health, The Ohio State University College of Medicine, Columbus, OH, USA. ; Comprehensive Cancer Center, The Ohio State University College of Medicine, Columbus, OH, USA., Department of Surgery, The Ohio State University College of Medicine, Columbus, OH, USA. ; Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, OH, USA., Department of Psychiatry, The Ohio State University College of Medicine, Columbus, OH, USA., Comprehensive Cancer Center, The Ohio State University College of Medicine, Columbus, OH, USA. ; Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, OH, USA. Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1356 EP - 1364 CY - Chichester PB - Wiley Subscription Services, Inc. VL - 23 IS - 12 SN - 1057-9249 KW - Medical Sciences--Psychiatry And Neurology KW - Breast cancer KW - Cancer KW - Chemotherapy KW - Clinical outcomes KW - Cognitive functioning KW - Complaints KW - Concentration KW - Continuous performance tasks KW - Loneliness KW - Memory KW - Psychosocial factors KW - Survivors KW - Women UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665162336?accountid=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=Cognitive+problems+among+breast+cancer+survivors%3A+loneliness+enhances+risk&rft.au=Jaremka%2C+Lisa+M%3BPeng%2C+Juan%3BBornstein%2C+Robert%3BAlfano%2C+Catherine+M%3BAndridge%2C+Rebecca+R%3BPovoski%2C+Stephen+P%3BLipari%2C+Adele+M%3BAgnese%2C+Doreen+M%3BFarrar%2C+William+B%3BYee%2C+Lisa+D%3BCarson%2C+William+E%3BKiecolt-Glaser%2C+Janice+K&rft.aulast=Jaremka&rft.aufirst=Lisa&rft.date=2014-12-01&rft.volume=23&rft.issue=12&rft.spage=1356&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3544 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/pon.3544 ER - TY - JOUR T1 - Disparities in Health Care Access and Receipt of Preventive Services by Disability Type: Analysis of the Medical Expenditure Panel Survey AN - 1665151201 AB - OBJECTIVE: To examine differences in access to health care and receipt of clinical preventive services by type of disability among working-age adults with disabilities. DATA SOURCE: Secondary analysis of Medical Expenditure Panel Survey (MEPS) data from 2002 to 2008. STUDY DESIGN: We conducted cross-sectional logistic regression analyses comparing people with different types of disabilities on health insurance status and type; presence of a usual source of health care; delayed or forgone care; and receipt of dental checkups and cancer screening. DATA COLLECTION: We pooled annualized MEPS data files across years. Our analytic sample consisted of adults (18-64 years) with physical, sensory, or cognitive disabilities and nonmissing data for all variables of interest. PRINCIPAL FINDINGS: Individuals with hearing impairment had better health care access and receipt than people with other disability types. People with multiple types of limitations were especially likely to have health care access problems and unmet health care needs. CONCLUSIONS: There are differences in health care access and receipt of preventive care depending on what type of disability people have. More in-depth research is needed to identify specific causes of these disparities and assess interventions to address health care barriers for particular disability groups. JF - Health Services Research AU - Horner‐Johnson, Willi AU - Dobbertin, Konrad AU - Lee, Jae Chul AU - Andresen, Elena M AD - Institute on Development and Disability. Oregon Health and Science University ; Rehabilitation Medicine Department, Clinical Research Center. National Institutes of Health ; Institute on Development and Disability. Oregon Health and Science University Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1980 EP - 1999 CY - Chicago PB - Wiley Subscription Services, Inc. VL - 49 IS - 6 SN - 0017-9124 KW - Medical Sciences KW - Disability KW - Analysis KW - Cancer KW - Delayed KW - Health costs KW - Health insurance KW - Health status KW - Hearing KW - Hearing impairment KW - Insurance KW - Interventions KW - Learning disabled people KW - Screening KW - Service provision KW - Unmet needs KW - Expenditure KW - Health care KW - Health inequalities KW - Preventive health care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665151201?accountid=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+Services+Research&rft.atitle=Disparities+in+Health+Care+Access+and+Receipt+of+Preventive+Services+by+Disability+Type%3A+Analysis+of+the+Medical+Expenditure+Panel+Survey&rft.au=Horner%E2%80%90Johnson%2C+Willi%3BDobbertin%2C+Konrad%3BLee%2C+Jae+Chul%3BAndresen%2C+Elena+M&rft.aulast=Horner%E2%80%90Johnson&rft.aufirst=Willi&rft.date=2014-12-01&rft.volume=49&rft.issue=6&rft.spage=1980&rft.isbn=&rft.btitle=&rft.title=Health+Services+Research&rft.issn=00179124&rft_id=info:doi/10.1111%2F1475-6773.12195 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-25 DO - http://dx.doi.org/10.1111/1475-6773.12195 ER - TY - JOUR T1 - Characterizing the Factor Structure of Parent Reported Executive Function in Autism Spectrum Disorders: The Impact of Cognitive Inflexibility AN - 1665151191 AB - Parents of children with autism spectrum disorders (ASD) consistently report executive functioning (EF) deficits. This study investigates the factor structure of the Behavior Rating Inventory of Executive Function (BRIEF) as reported by parents of children with ASD and typically developing children (TDC). BRIEFs for 411 children with ASD and 467 TDC were examined. Confirmatory factor analysis of a nine-factor model met thresholds for goodness-of-fit in TDC, but not in the ASD sample. We found globally elevated EF problems in the ASD sample, especially on the Shift scale. These findings confirm that children with ASD exhibit significant EF deficits. Further investigation is needed to understand the pervasive nature of cognitive inflexibility in children with ASD. JF - Journal of Autism and Developmental Disorders AU - Granader, Yael AU - Wallace, Gregory L AU - Hardy, Kristina K AU - Yerys, Benjamin E AU - Lawson, Rachel A AU - Rosenthal, Michael AU - Wills, Meagan C AU - Dixon, Eunice AU - Pandey, Juhi AU - Penna, Rebecca AU - Schultz, Robert T AU - Kenworthy, Lauren AD - Children’s National Medical Center, 15245 Shady Grove Road, Suite 350, Rockville, MD, 20850, USA ygranade@childrensnational.org ygranade@childrensnational.org ygranade@childrensnational.org ygranade@childrensnational.org ygranade@childrensnational.org; Laboratory of Brain and Cognition, National Institute of Mental Health, Bethesda, MD, USA, Department of Speech and Hearing Sciences, George Washington University, Washington, DC, USA ; Center for Autism Research, Children’s Hospital of Philadelphia and the University of Pennsylvania, Philadelphia, PA, USA ; Children’s National Medical Center, 15245 Shady Grove Road, Suite 350, Rockville, MD, 20850, USA, Loyola University Maryland, Baltimore, MD, USA ; Laboratory of Brain and Cognition, National Institute of Mental Health, Bethesda, MD, USA ; Children’s National Medical Center, 15245 Shady Grove Road, Suite 350, Rockville, MD, 20850, USA Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 3056 EP - 3062 CY - New York PB - Springer Science & Business Media VL - 44 IS - 12 SN - 0162-3257 KW - Children And Youth - About KW - Autism KW - Autistic children KW - Autistic spectrum disorders KW - Children KW - Confirmatory factor analysis KW - Executive function KW - Factor analysis KW - Parents KW - Thresholds UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665151191?accountid=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=Characterizing+the+Factor+Structure+of+Parent+Reported+Executive+Function+in+Autism+Spectrum+Disorders%3A+The+Impact+of+Cognitive+Inflexibility&rft.au=Granader%2C+Yael%3BWallace%2C+Gregory+L%3BHardy%2C+Kristina+K%3BYerys%2C+Benjamin+E%3BLawson%2C+Rachel+A%3BRosenthal%2C+Michael%3BWills%2C+Meagan+C%3BDixon%2C+Eunice%3BPandey%2C+Juhi%3BPenna%2C+Rebecca%3BSchultz%2C+Robert+T%3BKenworthy%2C+Lauren&rft.aulast=Granader&rft.aufirst=Yael&rft.date=2014-12-01&rft.volume=44&rft.issue=12&rft.spage=3056&rft.isbn=&rft.btitle=&rft.title=Journal+of+Autism+and+Developmental+Disorders&rft.issn=01623257&rft_id=info:doi/10.1007%2Fs10803-014-2169-8 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1007/s10803-014-2169-8 ER - TY - JOUR T1 - Pathways between acculturation and health behaviors among residents of low-income housing: the mediating role of social and contextual factors AN - 1660032497; 4650083 AB - Acculturation may influence health behaviors, yet mechanisms underlying its effect are not well understood. In this study, we describe relationships between acculturation and health behaviors among low-income housing residents, and examine whether these relationships are mediated by social and contextual factors. Residents of 20 low-income housing sites in the Boston metropolitan area completed surveys that assessed acculturative characteristics, social/contextual factors, and health behaviors. A composite acculturation scale was developed using latent class analysis, resulting in four distinct acculturative groups. Path analysis was used to examine interrelationships between acculturation, health behaviors, and social/contextual factors, specifically self-reported social ties, social support, stress, material hardship, and discrimination. Of the 828 respondents, 69% were born outside of the U.S. Less acculturated groups exhibited healthier dietary practices and were less likely to smoke than more acculturated groups. Acculturation had a direct effect on diet and smoking, but not physical activity. Acculturation also showed an indirect effect on diet through its relationship with material hardship. Our finding that material hardship mediated the relationship between acculturation and diet suggests the need to explicate the significant role of financial resources in interventions seeking to promote healthy diets among low-income immigrant groups. Future research should examine these social and contextual mediators using larger, population-based samples, preferably with longitudinal data. All rights reserved, Elsevier JF - Social science and medicine AU - Stoddard, Anne M AU - Tamers, Sara AU - Tucker-Seeley, Reginald D AU - Sorensen, Glorian C AU - Allen, Jennifer Dacey AU - Caspi, Caitlin AU - Yang, May AU - Leyva, Bryan AD - DanaFarber Cancer Institute ; University of Minnesota ; New England Research Institutes ; National Cancer Institute Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 26 EP - 36 VL - 123 SN - 0277-9536, 0277-9536 KW - Sociology KW - Smoking KW - Acculturation KW - Social support KW - Immigrants KW - Social housing KW - U.S.A. KW - Low income UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660032497?accountid=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=Pathways+between+acculturation+and+health+behaviors+among+residents+of+low-income+housing%3A+the+mediating+role+of+social+and+contextual+factors&rft.au=Stoddard%2C+Anne+M%3BTamers%2C+Sara%3BTucker-Seeley%2C+Reginald+D%3BSorensen%2C+Glorian+C%3BAllen%2C+Jennifer+Dacey%3BCaspi%2C+Caitlin%3BYang%2C+May%3BLeyva%2C+Bryan&rft.aulast=Stoddard&rft.aufirst=Anne&rft.date=2014-12-01&rft.volume=123&rft.issue=&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Social+science+and+medicine&rft.issn=02779536&rft_id=info:doi/10.1016%2Fj.socscimed.2014.10.034 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-03-02 N1 - Last updated - 2015-03-03 N1 - SubjectsTermNotLitGenreText - 539 3105 3198; 6232 8037; 11847 6045 5706; 11755 5707 6071 1542 11325; 7553 6271; 11938 11949 13521; 433 293 14 DO - http://dx.doi.org/10.1016/j.socscimed.2014.10.034 ER - TY - JOUR T1 - Beyond cry and laugh: Toward a multilevel model of language production AN - 1660012673; 201501622 AB - Language production is a multilevel phenomenon, and human capacities to communicate vocally progress from early forms, based on projections of motor cortex to brainstem nuclei, to complex elaborations, mediated by high-order cognition and fostered by socially mediated feedback. Adapted from the source document JF - Behavioral and Brain Sciences AU - Bornstein, Marc H AU - Esposito, Gianluca AD - Child and Family Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Rockledge I, Bethesda, MD 20892-7971, USA. Marc_H_Bornstein@nih.gov Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 548 EP - 549 VL - 37 IS - 6 SN - 0140-525X, 0140-525X KW - Cognitive Processes (12950) KW - Humans (32796) KW - Communication (13600) KW - Neurolinguistics (57250) KW - Brain (09350) KW - Social Factors (79910) KW - article KW - 4018: psycholinguistics; neurolinguistics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660012673?accountid=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=Behavioral+and+Brain+Sciences&rft.atitle=Beyond+cry+and+laugh%3A+Toward+a+multilevel+model+of+language+production&rft.au=Bornstein%2C+Marc+H%3BEsposito%2C+Gianluca&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2014-12-01&rft.volume=37&rft.issue=6&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=Behavioral+and+Brain+Sciences&rft.issn=0140525X&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-09-27 N1 - CODEN - BBSCDH N1 - SubjectsTermNotLitGenreText - Brain (09350); Cognitive Processes (12950); Neurolinguistics (57250); Social Factors (79910); Communication (13600); Humans (32796) ER - TY - JOUR T1 - Safety and tolerability of chikungunya virus-like particle vaccine in healthy adults: a phase 1 dose-escalation trial AN - 1654693536; 21143840 AB - Background Chikungunya virus-a mosquito-borne alphavirus-is endemic in Africa and south and southeast Asia and has recently emerged in the Caribbean. No drugs or vaccines are available for treatment or prevention. We aimed to assess the safety, tolerability, and immunogenicity of a new candidate vaccine. Methods VRC 311 was a phase 1, dose-escalation, open-label clinical trial of a virus-like particle (VLP) chikungunya virus vaccine, VRC-CHKVLP059-00-VP, in healthy adults aged 18-50 years who were enrolled at the National Institutes of Health Clinical Center (Bethesda, MD, USA). Participants were assigned to sequential dose level groups to receive vaccinations at 10 mu g, 20 mu g, or 40 mu g on weeks 0, 4, and 20, with follow-up for 44 weeks after enrolment. The primary endpoints were safety and tolerability of the vaccine. Secondary endpoints were chikungunya virus-specific immune responses assessed by ELISA and neutralising antibody assays. This trial is registered with ClinicalTrials.gov, NCT01489358. Findings 25 participants were enrolled from Dec 12, 2011, to March 22, 2012, into the three dosage groups: 10 mu g (n=5), 20 mu g (n=10), and 40 mu g (n=10). The protocol was completed by all five participants at the 10 mu g dose, all ten participants at the 20 mu g dose, and eight of ten participants at the 40 mu g dose; non-completions were for personal circumstances unrelated to adverse events. 73 vaccinations were administered. All injections were well tolerated, with no serious adverse events reported. Neutralising antibodies were detected in all dose groups after the second vaccination (geometric mean titres of the half maximum inhibitory concentration: 2688 in the 10 mu g group, 1775 in the 20 mu g group, and 7246 in the 40 mu g group), and a significant boost occurred after the third vaccination in all dose groups (10 mu g group p=0.0197, 20 mu g group p<0.0001, and 40 mu g group p<0.0001). 4 weeks after the third vaccination, the geometric mean titres of the half maximum inhibitory concentration were 8745 for the 10 mu g group, 4525 for the 20 mu g group, and 5390 for the 40 mu g group. Interpretation The chikungunya VLP vaccine was immunogenic, safe, and well tolerated. This study represents an important step in vaccine development to combat this rapidly emerging pathogen. Further studies should be done in a larger number of participants and in more diverse populations. Funding Intramural Research Program of the Vaccine Research Center, National Institute of Allergy and Infectious Diseases, and National Institutes of Health. JF - Lancet AU - Chang, Lee-Jah AU - Dowd, Kimberly A AU - Mendoza, Floreliz H AU - Saunders, Jamie G AU - Sitar, Sandra AU - Plummer, Sarah H AU - Yamshchikov, Galina AU - Sarwar, Uzma N AU - Hu, Zonghui AU - Enama, Mary E AU - Bailer, Robert T AU - Koup, Richard A AU - Schwartz, Richard M AU - Akahata, Wataru AU - Nabel, Gary J AU - Mascola, John R AU - Pierson, Theodore C AU - Graham, Barney S AU - Ledgerwood, Julie E AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 2046 EP - 2052 PB - Elsevier B.V., Radarweg 29 Amsterdam 1043 NX Netherlands VL - 384 IS - 9959 SN - 0140-6736, 0140-6736 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Virology & AIDS Abstracts KW - Virus-like particles KW - Disease control KW - Clinical trials KW - Public health KW - Hypersensitivity KW - Endemic species KW - ASW, Caribbean Sea KW - Infectious diseases KW - ELISA KW - Drugs KW - Enzyme-linked immunosorbent assay KW - Chikungunya virus KW - Pathogens KW - Vaccination KW - USA KW - Antibodies KW - Immunogenicity KW - Africa KW - Immune response KW - Vaccines KW - ISEW, Southeast Asia KW - Research programs KW - V 22350:Immunology KW - Q1 08604:Stock assessment and management KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654693536?accountid=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=Lancet&rft.atitle=Safety+and+tolerability+of+chikungunya+virus-like+particle+vaccine+in+healthy+adults%3A+a+phase+1+dose-escalation+trial&rft.au=Chang%2C+Lee-Jah%3BDowd%2C+Kimberly+A%3BMendoza%2C+Floreliz+H%3BSaunders%2C+Jamie+G%3BSitar%2C+Sandra%3BPlummer%2C+Sarah+H%3BYamshchikov%2C+Galina%3BSarwar%2C+Uzma+N%3BHu%2C+Zonghui%3BEnama%2C+Mary+E%3BBailer%2C+Robert+T%3BKoup%2C+Richard+A%3BSchwartz%2C+Richard+M%3BAkahata%2C+Wataru%3BNabel%2C+Gary+J%3BMascola%2C+John+R%3BPierson%2C+Theodore+C%3BGraham%2C+Barney+S%3BLedgerwood%2C+Julie+E&rft.aulast=Chang&rft.aufirst=Lee-Jah&rft.date=2014-12-01&rft.volume=384&rft.issue=9959&rft.spage=2046&rft.isbn=&rft.btitle=&rft.title=Lancet&rft.issn=01406736&rft_id=info:doi/10.1016%2FS0140-6736%2814%2961185-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Endemic species; Antibodies; Infectious diseases; Disease control; ELISA; Pathogens; Vaccines; Vaccination; Public health; Enzyme-linked immunosorbent assay; Virus-like particles; Clinical trials; Hypersensitivity; Immunogenicity; Immune response; Drugs; Research programs; Chikungunya virus; USA; ASW, Caribbean Sea; Africa; ISEW, Southeast Asia DO - http://dx.doi.org/10.1016/S0140-6736(14)61185-5 ER - TY - JOUR T1 - Neural Correlates of Auditory Short-Term Memory in Rostral Superior Temporal Cortex AN - 1647020733; 21221519 AB - Background: Auditory short-term memory (STM) in the monkey is less robust than visual STM and may depend on a retained sensory trace, which is likely to reside in the higherorder cortical areas of the auditory ventral stream. Results: We recorded from the rostral superior temporal cortex as monkeys performed serial auditory delayed match-tosample (DMS). A subset of neurons exhibited modulations of their firing rate during the delay between sounds, during the sensory response, or during both. This distributed subpopulation carried a predominantly sensory signal modulated by the mnemonic context of the stimulus. Excitatory and suppressive effects on match responses were dissociable in their timing and in their resistance to sounds intervening between the sample and match. Conclusions: Like the monkeys' behavioral performance, these neuronal effects differ from those reported in the same species during visual DMS, suggesting different neural mechanisms for retaining dynamic sounds and static images in STM. JF - Current Biology AU - Scott, Brian H AU - Mortimer, Mishkin AU - Pingbo, Yin AD - Laboratory of Neuropsychology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA, brianscott@mail.nih.gov Y1 - 2014/12/01/ PY - 2014 DA - 2014 Dec 01 SP - 2767 EP - 2775 PB - Cell Press, 1100 Massachusetts Avenue Cambridge MA 02138 United States VL - 24 IS - 23 SN - 0960-9822, 0960-9822 KW - CSA Neurosciences Abstracts; Ecology Abstracts KW - Firing rate KW - Neuromodulation KW - Memory KW - Cortex (visual) KW - Neurons KW - Subpopulations KW - Cortex (temporal) KW - Cortex (auditory) KW - Short term memory KW - Cortex (somatosensory) KW - N3 11007:Neurobiology KW - D 04040:Ecosystem and Ecology Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647020733?accountid=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=Current+Biology&rft.atitle=Neural+Correlates+of+Auditory+Short-Term+Memory+in+Rostral+Superior+Temporal+Cortex&rft.au=Scott%2C+Brian+H%3BMortimer%2C+Mishkin%3BPingbo%2C+Yin&rft.aulast=Scott&rft.aufirst=Brian&rft.date=2014-12-01&rft.volume=24&rft.issue=23&rft.spage=2767&rft.isbn=&rft.btitle=&rft.title=Current+Biology&rft.issn=09609822&rft_id=info:doi/10.1016%2Fj.cub.2014.10.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Memory; Neuromodulation; Firing rate; Cortex (visual); Subpopulations; Neurons; Cortex (temporal); Cortex (auditory); Short term memory; Cortex (somatosensory) DO - http://dx.doi.org/10.1016/j.cub.2014.10.004 ER - TY - JOUR T1 - Compounds with species and cell type specific toxicity identified in a 2000 compound drug screen of neural stem cells and rat mixed cortical neurons AN - 1647009959; 21321507 AB - Human primary neural tissue is a vital component for the quick and simple determination of chemical compound neurotoxicity in vitro. In particular, such tissue would be ideal for high-throughput screens that can be used to identify novel neurotoxic or neurotherapeutic compounds. We have previously established a high-throughput screening platform using human induced pluripotent stem cell (iPSC)-derived neural stem cells (NSCs) and neurons. In this study, we conducted a 2000 compound screen with human NSCs and rat cortical cells to identify compounds that are selectively toxic to each group. Approximately 100 of the tested compounds showed specific toxicity to human NSCs. A secondary screen of a small subset of compounds from the primary screen on human iPSCs, NSC-derived neurons, and fetal astrocytes validated the results from >80% of these compounds with some showing cell specific toxicity. Amongst those compounds were several cardiac glycosides, all of which were selectively toxic to the human cells. As the screen was able to reliably identify neurotoxicants, many with species and cell-type specificity, this study demonstrates the feasibility of this NSC-driven platform for higher-throughput neurotoxicity screens. JF - Neurotoxicology AU - Malik, Nasir AU - Efthymiou, Anastasia G AU - Mather, Karly AU - Chester, Nathaniel AU - Wang, Xiantao AU - Nath, Avindra AU - Rao, Mahendra S AU - Steiner, Joseph P AD - National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, United States Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 192 EP - 200 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 45 SN - 0161-813X, 0161-813X KW - CSA Neurosciences Abstracts; Toxicology Abstracts KW - Neurotoxicity screening KW - Neural stem cells KW - Cardiac glycosides KW - Cortex KW - Astrocytes KW - Neurons KW - Neurotoxicity KW - Inhibitory postsynaptic potentials KW - high-throughput screening KW - Drugs KW - Fetuses KW - N3 11028:Neuropharmacology & toxicology KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647009959?accountid=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=Compounds+with+species+and+cell+type+specific+toxicity+identified+in+a+2000+compound+drug+screen+of+neural+stem+cells+and+rat+mixed+cortical+neurons&rft.au=Malik%2C+Nasir%3BEfthymiou%2C+Anastasia+G%3BMather%2C+Karly%3BChester%2C+Nathaniel%3BWang%2C+Xiantao%3BNath%2C+Avindra%3BRao%2C+Mahendra+S%3BSteiner%2C+Joseph+P&rft.aulast=Malik&rft.aufirst=Nasir&rft.date=2014-12-01&rft.volume=45&rft.issue=&rft.spage=192&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/10.1016%2Fj.neuro.2014.10.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Cortex; Astrocytes; Neurons; Inhibitory postsynaptic potentials; Neurotoxicity; high-throughput screening; Drugs; Neural stem cells; Cardiac glycosides; Fetuses DO - http://dx.doi.org/10.1016/j.neuro.2014.10.007 ER - TY - JOUR T1 - Meeting the healthy people 2020 goals: using the health information national trends survey to monitor progress on health communication objectives AN - 1646694103; 4635615 AB - The Healthy People initiative outlines a comprehensive set of goals aimed at improving the nation's health and reducing health disparities. Health communication has been included as an explicit goal since the launch of Healthy People 2010. The Health Information National Trends Survey (HINTS) was established as a means of exploring how the changing information environment was affecting the public's health, and is therefore an ideal tool for monitoring key health communication objectives included in the Healthy People agenda. In this article, the authors apply an integrative data analysis strategy to more than 10 years of HINTS data to demonstrate how public health surveillance can be used to evaluate broad national health goals, like those set forth under the Healthy People initiative. The authors analyzed just one item from the HINTS survey regarding Internet access in order to illustrate what public health surveillance tools, like HINTS, can reveal about important indicators that are of interest to all those who work to improve the health of the public. Results show that reported Internet penetration has exceeded the Healthy People 2020 target of 75.4%. HINTS data also allowed modeling of the effects of various sociodemographic factors, which revealed persistent differences on the basis of age and education, with the oldest age groups and those with less than a college education falling short of the Healthy People 2020 target as of 2013. Furthermore, although differences by race/ethnicity were observed, the analyses suggest that race in itself accounts for very little of the variance in Internet access. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Hesse, Bradford W AU - Gaysynsky, Anna AU - Ottenbacher, Allison AU - Moser, Richard P AU - Blake, Kelly D AU - Chou, Wen-Ying Sylvia AU - Vieux, Sana AU - Beckjord, Ellen AD - National Cancer Institute ; Patient-Centered Outcomes Research Institute ; University of Pittsburgh Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1497 EP - 1509 VL - 19 IS - 12 SN - 1081-0730, 1081-0730 KW - Sociology KW - Information KW - Objectivity KW - Communication KW - Surveillance KW - Internet KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1646694103?accountid=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=Meeting+the+healthy+people+2020+goals%3A+using+the+health+information+national+trends+survey+to+monitor+progress+on+health+communication+objectives&rft.au=Hesse%2C+Bradford+W%3BGaysynsky%2C+Anna%3BOttenbacher%2C+Allison%3BMoser%2C+Richard+P%3BBlake%2C+Kelly+D%3BChou%2C+Wen-Ying+Sylvia%3BVieux%2C+Sana%3BBeckjord%2C+Ellen&rft.aulast=Hesse&rft.aufirst=Bradford&rft.date=2014-12-01&rft.volume=19&rft.issue=12&rft.spage=1497&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2014.954084 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-01-20 N1 - Last updated - 2015-01-20 N1 - SubjectsTermNotLitGenreText - 10449 5772; 2572; 6813 6518; 12424 6608 6085; 6515; 8826 DO - http://dx.doi.org/10.1080/10810730.2014.954084 ER - TY - JOUR T1 - Immune-based therapies for childhood cancer. AN - 1645780841; 25348789 AB - After decades of research, immunotherapies for cancer are demonstrating increasing success. These agents can amplify existent antitumour immunity or induce durable antitumour immune responses in a wide array of cancers. The spectrum of immunotherapeutics is broad, spanning monoclonal antibodies and their derivatives, tumour vaccines, and adoptive therapies using T cells and natural killer cells. Only a small number of immunotherapies have been tested in paediatric cancers, but impressive antitumour effects have already been observed. Mononclonal antibodies targeting GD2 that induce antibody-dependent cell-mediated cytotoxicity improve survival in high-risk neuroblastoma. Bi-specific monoclonal antibodies that simultaneously target CD19 and activate T cells can induce remission in acute B-cell lymphoblastic leukaemia (B-ALL) and adoptive immunotherapy using T cells genetically engineered to express chimeric antigen receptors targeting CD19 induce impressive responses in B-ALL. Efforts are underway to generate and test new immunotherapies in a wider array of paediatric cancers. Major challenges include a need to identify immunotherapy targets on the most lethal childhood cancers, to expand availability of technology-intense platforms, such as adoptive cell therapy, to optimize management of novel toxicities associated with this new class of cancer therapies and to determine how best to incorporate these therapies into standard treatment paradigms. JF - Nature reviews. Clinical oncology AU - Mackall, Crystal L AU - Merchant, Melinda S AU - Fry, Terry J AD - Paediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, 10 Center Drive, MSC 1104, Bethesda, MD 20892, USA. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 693 EP - 703 VL - 11 IS - 12 KW - Index Medicus KW - Humans KW - Immunotherapy, Adoptive KW - Child KW - Neoplasms -- drug therapy KW - Immunotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645780841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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.+Clinical+oncology&rft.atitle=Immune-based+therapies+for+childhood+cancer.&rft.au=Mackall%2C+Crystal+L%3BMerchant%2C+Melinda+S%3BFry%2C+Terry+J&rft.aulast=Mackall&rft.aufirst=Crystal&rft.date=2014-12-01&rft.volume=11&rft.issue=12&rft.spage=693&rft.isbn=&rft.btitle=&rft.title=Nature+reviews.+Clinical+oncology&rft.issn=1759-4782&rft_id=info:doi/10.1038%2Fnrclinonc.2014.177 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-09 N1 - Date created - 2014-11-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nrclinonc.2014.177 ER - TY - JOUR T1 - Base excision repair capacity in informing healthspan. AN - 1645228453; 25355293 AB - Base excision repair (BER) is a frontline defense mechanism for dealing with many common forms of endogenous DNA damage, several of which can drive mutagenic or cell death outcomes. The pathway engages proteins such as glycosylases, abasic endonucleases, polymerases and ligases to remove substrate modifications from DNA and restore the genome back to its original state. Inherited mutations in genes related to BER can give rise to disorders involving cancer, immunodeficiency and neurodegeneration. Studies employing genetically defined heterozygous (haploinsufficient) mouse models indicate that partial reduction in BER capacity can increase vulnerability to both spontaneous and exposure-dependent pathologies. In humans, measurement of BER variation has been imperfect to this point, yet tools to assess BER in epidemiological surveys are steadily evolving. We provide herein an overview of the BER pathway and discuss the current efforts toward defining the relationship of BER defects with disease susceptibility. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Brenerman, Boris M AU - Illuzzi, Jennifer L AU - Wilson, David M AD - Laboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA. ; Laboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA wilsonda@mail.nih.gov. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 2643 EP - 2652 VL - 35 IS - 12 KW - Index Medicus KW - Animals KW - Humans KW - Mice KW - DNA Repair -- genetics KW - Disease Susceptibility KW - DNA Damage -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645228453?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Base+excision+repair+capacity+in+informing+healthspan.&rft.au=Brenerman%2C+Boris+M%3BIlluzzi%2C+Jennifer+L%3BWilson%2C+David+M&rft.aulast=Brenerman&rft.aufirst=Boris&rft.date=2014-12-01&rft.volume=35&rft.issue=12&rft.spage=2643&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu225 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-14 N1 - Date created - 2014-12-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1999 Nov 9;96(23):13300-5 [10557315] Int J Cancer. 2000 Jan 1;85(1):21-6 [10585577] Biochemistry. 1999 Dec 14;38(50):16553-60 [10600117] Environ Mol Mutagen. 1999;34(4):256-9 [10618173] Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):686-91 [10639140] EMBO J. 2000 Mar 15;19(6):1397-404 [10716939] Nature. 2000 Jun 15;405(6788):807-10 [10866204] Carcinogenesis. 2000 Jul;21(7):1329-34 [10874010] J Biol Chem. 2000 Jul 28;275(30):23234-9 [10930429] Cancer Res. 2001 Jul 15;61(14):5552-7 [11454706] Carcinogenesis. 2001 Sep;22(9):1335-41 [11532852] Nat Genet. 2001 Oct;29(2):189-93 [11586300] Mutagenesis. 2002 Jan;17(1):37-43 [11752232] Nat Genet. 2002 Feb;30(2):227-32 [11818965] Free Radic Biol Med. 2002 Apr 15;32(8):678-82 [11937293] Nucleic Acids Res. 2002 Apr 15;30(8):1817-25 [11937636] Carcinogenesis. 2002 Sep;23(9):1419-25 [12189182] Nat Genet. 2002 Oct;32(2):267-72 [12244316] Mutat Res. 2002 Oct 31;508(1-2):1-19 [12379456] J Natl Cancer Inst. 2003 Sep 3;95(17):1312-9 [12953085] Trends Mol Med. 2006 Sep;12(9):440-50 [16899408] DNA Repair (Amst). 2007 Apr 1;6(4):544-59 [17112792] Cell Res. 2008 Jan;18(1):27-47 [18166975] Cell Res. 2008 Jan;18(1):48-63 [18166976] Mech Ageing Dev. 2008 Jul-Aug;129(7-8):366-82 [18423806] J Clin Invest. 2008 Jul;118(7):2516-25 [18521188] Nat Rev Genet. 2008 Aug;9(8):619-31 [18626472] Mol Carcinog. 2008 Aug;47(8):638-46 [18300266] Biol Reprod. 2008 Nov;79(5):824-31 [18650495] Proc Natl Acad Sci U S A. 2009 Jan 20;106(3):888-93 [19139400] Free Radic Biol Med. 2009 Jun 1;46(11):1488-99 [19268524] BMC Biotechnol. 2009;9:39 [19389244] DNA Repair (Amst). 2010 Feb 4;9(2):144-52 [20042377] Nat Genet. 2010 Mar;42(3):245-9 [20118933] Nature. 2010 May 27;465(7297):473-7 [20505728] J Biol Chem. 2010 Jun 18;285(25):19246-58 [20404327] Carcinogenesis. 2010 Dec;31(12):2111-7 [20732909] Mech Ageing Dev. 2010 Nov-Dec;131(11-12):661-5 [20854835] Nature. 2011 Feb 17;470(7334):419-23 [21278727] DNA Repair (Amst). 2011 Apr 3;10(4):390-7 [21333614] Antioxid Redox Signal. 2011 Jun 15;14(12):2491-507 [20649466] Mutat Res. 2011 Jun 3;711(1-2):100-12 [21167187] Nucleic Acids Res. 2011 Sep 1;39(17):7487-98 [21666255] Nat Immunol. 2003 Oct;4(10):1023-8 [12958596] Cancer Res. 2003 Sep 15;63(18):5799-807 [14522902] Annu Rev Microbiol. 2003;57:395-418 [14527285] Mutat Res. 2003 Oct 29;531(1-2):37-80 [14637246] DNA Repair (Amst). 2003 Dec 9;2(12):1405-17 [14642568] DNA Repair (Amst). 2004 Jan 5;3(1):1-12 [14697754] Nat Rev Cancer. 2003 Dec;3(12):952-9 [14737125] Curr Opin Struct Biol. 2004 Feb;14(1):43-9 [15102448] Mutagenesis. 2004 May;19(3):169-85 [15123782] Biochem Biophys Res Commun. 2004 Jun 18;319(1):240-6 [15158468] Free Radic Biol Med. 2004 Aug 1;37(3):422-7 [15223076] Cancer Res. 2004 Jul 1;64(13):4411-4 [15231648] Mol Cell. 2004 Jul 23;15(2):209-20 [15260972] J Biol Chem. 2004 Aug 27;279(35):36504-13 [15218023] Mol Cell Biol. 2004 Sep;24(18):8145-53 [15340075] Circ Res. 2004 Oct 29;95(9):902-10 [15472121] Nature. 1968 May 18;218(5142):652-6 [5655953] Biochemistry. 1972 Jan 4;11(1):23-9 [5009434] Biochemistry. 1973 Dec 4;12(25):5151-4 [4600811] Carcinogenesis. 1983 Dec;4(12):1565-8 [6652869] EMBO J. 1982;1(2):211-6 [7188181] Biochemistry. 1990 Mar 13;29(10):2532-7 [2185829] Mol Cell Biol. 1992 Apr;12(4):1605-12 [1549115] EMBO J. 1992 Sep;11(9):3323-35 [1380454] Cancer Res. 1992 Oct 1;52(19):5307-12 [1394135] Nature. 1993 Apr 22;362(6422):709-15 [8469282] Trends Genet. 1993 Jul;9(7):246-9 [8379000] Science. 1994 Jul 1;265(5168):103-6 [8016642] Methods Enzymol. 1994;234:16-33 [7808289] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7166-9 [9207062] Nucleic Acids Res. 1998 Mar 1;26(5):1276-81 [9469837] Teratog Carcinog Mutagen. 1998;18(1):17-26 [9586767] J Biol Chem. 1998 Aug 14;273(33):21203-9 [9694877] Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):9997-10002 [9707589] Dev Biol. 1999 Apr 15;208(2):513-29 [10191063] J Pathol. 1999 Jan;187(1):8-18 [10341702] Cancer Res. 1999 Jun 1;59(11):2522-6 [10363965] Oncogene. 2006 Mar 13;25(11):1612-9 [16550161] FEBS J. 2006 Apr;273(8):1620-9 [16623699] DNA Repair (Amst). 2006 May 10;5(5):544-55 [16442856] Cancer Res. 2006 Aug 1;66(15):7460-5 [16885342] Nucleic Acids Res. 2011 Oct;39(18):7992-8004 [21737425] J Exp Med. 2011 Oct 24;208(11):2209-16 [21967769] Mol Reprod Dev. 2011 Dec;78(12):906-19 [21919107] Nat Rev Cancer. 2012 Feb;12(2):104-20 [22237395] Cell Mol Life Sci. 2012 Mar;69(5):727-40 [21952828] Free Radic Res. 2012 Apr;46(4):460-78 [22300253] J Hypertens. 2012 May;30(5):917-25 [22441348] J Clin Invest. 2012 Jul;122(7):2680-9 [22684101] Mutat Res. 2012 Aug 1;736(1-2):122-9 [21459100] J Vis Exp. 2012;(66):e4168 [22895410] Cancer Lett. 2012 Dec 31;327(1-2):26-47 [22293091] Cancer Lett. 2012 Dec 31;327(1-2):61-72 [22353689] Cold Spring Harb Perspect Biol. 2013 Apr;5(4):a012583 [23545420] Nucleic Acids Res. 2013 Apr 1;41(6):3483-90 [23408852] PLoS Genet. 2013 Apr;9(4):e1003413 [23593019] Mo Med. 2013 Jul-Aug;110(4):314-9 [24003649] Cold Spring Harb Perspect Biol. 2013 Oct;5(10):a012609 [24086042] Mech Ageing Dev. 2013 Oct;134(10):440-8 [23643943] Cell Rep. 2014 Jan 16;6(1):1-8 [24388753] Mutat Res Rev Mutat Res. 2014 Jan-Mar;759:27-39 [24184488] Nat Cell Biol. 2014 Apr;16(4):293-300 [24691255] Proc Natl Acad Sci U S A. 2014 May 6;111(18):E1823-32 [24757057] DNA Repair (Amst). 2014 Jul;19:27-37 [24794402] Environ Mol Mutagen. 2014 Dec;55(9):689-703 [25044514] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu225 ER - TY - JOUR T1 - Perceptions of cancer as a death sentence: prevalence and consequences AN - 1642623125; 4630232 AB - Research suggests that perceiving cancer as a death sentence is a critical determinant of health care-seeking behaviors. However, there is limited information regarding the prevalence of this perception in the US population. Cross-sectional analysis of data (n = 7674 adults) from the 2007-2008 administration of the nationally representative Health Information National Trends Survey (HINTS 3) was performed. A majority (61.6%) of respondents perceived cancer as death sentence, and more than one-third (36%) of respondents reported that they avoid seeing their physicians. In the adult US population, perceiving cancer as a death sentence is common and is associated with education level and avoidance of physicians. Reprinted by permission of Sage Publications Ltd JF - Journal of health psychology AU - Moser, Richard AU - Arndt, Jamie AU - Han, Paul AU - Waters, Erika AU - Amsellem, Marni AU - Hesse, Bradford AD - National Cancer Institute, USA ; University of Missouri ; Maine Medical Center ; Washington University in St. Louis Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1518 EP - 1524 VL - 19 IS - 12 SN - 1359-1053, 1359-1053 KW - Sociology KW - Doctors KW - Health care KW - Perception KW - U.S.A. KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1642623125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+psychology&rft.atitle=Perceptions+of+cancer+as+a+death+sentence%3A+prevalence+and+consequences&rft.au=Moser%2C+Richard%3BArndt%2C+Jamie%3BHan%2C+Paul%3BWaters%2C+Erika%3BAmsellem%2C+Marni%3BHesse%2C+Bradford&rft.aulast=Moser&rft.aufirst=Richard&rft.date=2014-12-01&rft.volume=19&rft.issue=12&rft.spage=1518&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+psychology&rft.issn=13591053&rft_id=info:doi/10.1177%2F1359105313494924 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-01-07 N1 - Last updated - 2015-01-07 N1 - SubjectsTermNotLitGenreText - 1939 3617 6220; 9382; 5775 13521; 3675 10299 13682 7883 8864; 433 293 14 DO - http://dx.doi.org/10.1177/1359105313494924 ER - TY - JOUR T1 - Genomic predictors for recurrence patterns of hepatocellular carcinoma: model derivation and validation. AN - 1640479642; 25536056 AB - Typically observed at 2 y after surgical resection, late recurrence is a major challenge in the management of hepatocellular carcinoma (HCC). We aimed to develop a genomic predictor that can identify patients at high risk for late recurrence and assess its clinical implications. Systematic analysis of gene expression data from human liver undergoing hepatic injury and regeneration revealed a 233-gene signature that was significantly associated with late recurrence of HCC. Using this signature, we developed a prognostic predictor that can identify patients at high risk of late recurrence, and tested and validated the robustness of the predictor in patients (n = 396) who underwent surgery between 1990 and 2011 at four centers (210 recurrences during a median of 3.7 y of follow-up). In multivariate analysis, this signature was the strongest risk factor for late recurrence (hazard ratio, 2.2; 95% confidence interval, 1.3-3.7; p = 0.002). In contrast, our previously developed tumor-derived 65-gene risk score was significantly associated with early recurrence (p = 0.005) but not with late recurrence (p = 0.7). In multivariate analysis, the 65-gene risk score was the strongest risk factor for very early recurrence (<1 y after surgical resection) (hazard ratio, 1.7; 95% confidence interval, 1.1-2.6; p = 0.01). The potential significance of STAT3 activation in late recurrence was predicted by gene network analysis and validated later. We also developed and validated 4- and 20-gene predictors from the full 233-gene predictor. The main limitation of the study is that most of the patients in our study were hepatitis B virus-positive. Further investigations are needed to test our prediction models in patients with different etiologies of HCC, such as hepatitis C virus. Two independently developed predictors reflected well the differences between early and late recurrence of HCC at the molecular level and provided new biomarkers for risk stratification. Please see later in the article for the Editors' Summary. JF - PLoS medicine AU - Kim, Ji Hoon AU - Sohn, Bo Hwa AU - Lee, Hyun-Sung AU - Kim, Sang-Bae AU - Yoo, Jeong Eun AU - Park, Yun-Yong AU - Jeong, Woojin AU - Lee, Sung Sook AU - Park, Eun Sung AU - Kaseb, Ahmed AU - Kim, Baek Hui AU - Kim, Wan Bae AU - Yeon, Jong Eun AU - Byun, Kwan Soo AU - Chu, In-Sun AU - Kim, Sung Soo AU - Wang, Xin Wei AU - Thorgeirsson, Snorri S AU - Luk, John M AU - Kang, Koo Jeong AU - Heo, Jeonghoon AU - Park, Young Nyun AU - Lee, Ju-Seog AD - Department of Systems Biology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America; Kleberg Center for Molecular Markers, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America; Division of Gastroenterology and Hepatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea. ; Department of Systems Biology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America; Kleberg Center for Molecular Markers, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America. ; Department of Pathology and Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea. ; ASAN Institute for Life Sciences, Asan Medical Center, Department of Medicine, University of Ulsan College of Medicine, Seoul, Korea. ; Department of Life Sciences, Division of Life and Pharmaceutical Sciences, Center for Cell Signaling and Drug Discovery Research, Ewha Womans University, Seoul, Korea. ; Department of Hematology-Oncology, Inje University Haeundae Paik Hospital, Busan, Korea. ; Institute for Medical Convergence, Yonsei University College of Medicine, Seoul, Korea. ; Department of GI Medical Oncology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America. ; Department of Pathology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea. ; Department of Surgery, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea. ; Division of Gastroenterology and Hepatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea. ; Korean Bioinformation Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea. ; Department of Biochemistry and Molecular Biology, Medical Research Center and Biomedical Science Institute, School of Medicine, Kyung Hee University, Seoul, Korea. ; Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Pharmacology, National University of Singapore, Singapore. ; Department of Surgery, Keimyung University School of Medicine, Daegu, Korea. ; Departments of Molecular Biology and Immunology, Kosin University College of Medicine, Busan, Korea. ; Department of Systems Biology, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America; Kleberg Center for Molecular Markers, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America; Department of Biochemistry and Molecular Biology, Medical Research Center and Biomedical Science Institute, School of Medicine, Kyung Hee University, Seoul, Korea. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 1 VL - 11 IS - 12 KW - STAT3 Transcription Factor KW - 0 KW - Index Medicus KW - Young Adult KW - Risk Factors KW - Humans KW - Adult KW - Aged KW - STAT3 Transcription Factor -- genetics KW - Middle Aged KW - Neoplasm Recurrence, Local -- genetics KW - Male KW - Female KW - Multivariate Analysis KW - Carcinoma, Hepatocellular -- genetics KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1640479642?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+medicine&rft.atitle=Genomic+predictors+for+recurrence+patterns+of+hepatocellular+carcinoma%3A+model+derivation+and+validation.&rft.au=Kim%2C+Ji+Hoon%3BSohn%2C+Bo+Hwa%3BLee%2C+Hyun-Sung%3BKim%2C+Sang-Bae%3BYoo%2C+Jeong+Eun%3BPark%2C+Yun-Yong%3BJeong%2C+Woojin%3BLee%2C+Sung+Sook%3BPark%2C+Eun+Sung%3BKaseb%2C+Ahmed%3BKim%2C+Baek+Hui%3BKim%2C+Wan+Bae%3BYeon%2C+Jong+Eun%3BByun%2C+Kwan+Soo%3BChu%2C+In-Sun%3BKim%2C+Sung+Soo%3BWang%2C+Xin+Wei%3BThorgeirsson%2C+Snorri+S%3BLuk%2C+John+M%3BKang%2C+Koo+Jeong%3BHeo%2C+Jeonghoon%3BPark%2C+Young+Nyun%3BLee%2C+Ju-Seog&rft.aulast=Kim&rft.aufirst=Ji&rft.date=2014-12-01&rft.volume=11&rft.issue=12&rft.spage=e1001770&rft.isbn=&rft.btitle=&rft.title=PLoS+medicine&rft.issn=1549-1676&rft_id=info:doi/10.1371%2Fjournal.pmed.1001770 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-01 N1 - Date created - 2014-12-24 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE39791; GEO; GSE22058; GSE15239; GSE14520; GSE12720 N1 - SuppNotes - Cited By: Hepatology. 1999 Dec;30(6):1434-40 [10573522] Bioinformatics. 2014 Feb 15;30(4):523-30 [24336805] Science. 2001 Aug 3;293(5531):853-7 [11387442] Hepatology. 2002 Mar;35(3):519-24 [11870363] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6567-72 [12011421] J Comput Biol. 2002;9(3):505-11 [12162889] Bioinformatics. 2003 Jan 22;19(2):185-93 [12538238] J Hepatol. 2003 Feb;38(2):200-7 [12547409] Lancet. 2003 Mar 15;361(9361):923-9 [12648972] Nat Med. 2003 Apr;9(4):416-23 [12640447] Bioinformatics. 2003 Dec 12;19(18):2448-55 [14668230] J Surg Oncol. 2004 Jan;85(1):36-41 [14696085] Hepatology. 2004 May;39(5):1332-42 [15122762] Hepatology. 2004 Sep;40(3):667-76 [15349906] Gastroenterology. 2004 Nov;127(5 Suppl 1):S27-34 [15508094] Adv Cancer Res. 1972;16:181-234 [4563044] N Engl J Med. 1986 Dec 25;315(26):1650-9 [3537791] Gastroenterology. 1996 Sep;111(3):720-6 [8780578] N Engl J Med. 1999 Mar 11;340(10):745-50 [10072408] Gastroenterology. 2004 Nov;127(5):1372-80 [15521006] Clin Liver Dis. 2005 May;9(2):191-211, v [15831268] Hepatology. 2005 Jul;42(1):165-75 [15962318] Hepatology. 2005 Nov;42(5):1208-36 [16250051] J Am Coll Surg. 2006 Feb;202(2):275-83 [16427553] Cancer Cell. 2006 Aug;10(2):99-111 [16904609] Cancer Res. 2007 Mar 15;67(6):2497-507 [17363567] Gastroenterology. 2007 Jun;132(7):2557-76 [17570226] Science. 2007 Jul 6;317(5834):121-4 [17615358] Clin Cancer Res. 2007 Nov 1;13(21):6275-83 [17975138] Mol Oncol. 2014 Jul;8(5):1043-53 [24785097] Liver Transpl. 2007 Dec;13(12):1669-77 [18044786] Ann Surg Oncol. 2008 May;15(5):1392-8 [18335279] Clin Cancer Res. 2008 Apr 1;14(7):2056-64 [18381945] Ann Surg. 2008 Jun;247(6):1049-57 [18520234] Nature. 2008 Jul 24;454(7203):436-44 [18650914] Pathology. 2008 Oct;40(6):558-63 [18752121] N Engl J Med. 2008 Nov 6;359(19):1995-2004 [18923165] Am J Transplant. 2009 Apr;9(4):758-72 [19353763] Nat Rev Cancer. 2009 Nov;9(11):798-809 [19851315] Cancer Cell. 2010 Mar 16;17(3):286-97 [20227042] Mol Syst Biol. 2010 Aug 24;6:402 [20739924] Curr Top Dev Biol. 2010;92:367-409 [20816402] Mol Cancer Ther. 2011 Jan;10(1):9-15 [20971825] Liver Transpl. 2011 Jul;17(7):866-74 [21542129] Clin Cancer Res. 2011 Sep 15;17(18):6040-51 [21825042] J Clin Oncol. 2012 Mar 20;30(9):1005-14 [22355058] J Gastrointest Surg. 2012 Apr;16(4):828-36 [22072303] Gastroenterology. 2012 Apr;142(4):957-966.e12 [22202459] Hepatology. 2012 May;55(5):1443-52 [22105560] Front Med. 2013 Jun;7(2):242-54 [23681888] Cancer. 2000 Aug 1;89(3):500-7 [10931448] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pmed.1001770 ER - TY - JOUR T1 - Nuclear imaging: A powerful novel approach for tuberculosis AN - 1639993500; 21005737 AB - Nearly 20 years after the World Health Organization declared tuberculosis (TB) a global public health emergency, TB still remains a major global threat with 8.6 million new cases and 1.3 million deaths annually. Mycobacterium tuberculosis adapts to a quiescent physiological state, and is notable for complex interaction with the host, producing poorly-understood disease states ranging from latent infection to fully active disease. Of the approximately 2.5 billion people latently infected with M. tuberculosis, many will develop reactivation disease (relapse), years after the initial infection. In this review, we discuss the application of nuclear bioimaging to TB, including the current state of the field, considerations for radioprobe development, study of TB drug pharmacokinetics in infected tissues, and areas of research and clinical needs that could be addressed by nuclear bioimaging. Finally, since molecular imaging is readily available for humans, validated tracers will become valuable tools for clinical applications. JF - Nuclear Medicine and Biology AU - Johnson, Daniel H AU - Via, Laura E AU - Kim, Peter AU - Laddy, Dominick AU - Lau, Chuen-Yen AU - Weinstein, Edward A AU - Jain, Sanjay AD - NIAID/NIH, Bethesda, MD; DAIDS/NIAID/NIH, 5601 Fisher Lane, Rm 9E39 MSC 9830, Rockville MD 20852, daniel.johnson@nih.gov Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 777 EP - 784 PB - Elsevier B.V., Box 882 New York NY 10159 United States VL - 41 IS - 10 SN - 0969-8051, 0969-8051 KW - Microbiology Abstracts B: Bacteriology KW - Drug-resistance KW - PET KW - SPECT KW - Probe-design KW - Pharmacokinetics KW - Latent infection KW - Tracers KW - Computed tomography KW - Nuclear medicine KW - Therapeutic applications KW - Tuberculosis KW - Drug development KW - Mycobacterium tuberculosis KW - Public health KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639993500?accountid=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=Nuclear+Medicine+and+Biology&rft.atitle=Nuclear+imaging%3A+A+powerful+novel+approach+for+tuberculosis&rft.au=Johnson%2C+Daniel+H%3BVia%2C+Laura+E%3BKim%2C+Peter%3BLaddy%2C+Dominick%3BLau%2C+Chuen-Yen%3BWeinstein%2C+Edward+A%3BJain%2C+Sanjay&rft.aulast=Johnson&rft.aufirst=Daniel&rft.date=2014-12-01&rft.volume=41&rft.issue=10&rft.spage=777&rft.isbn=&rft.btitle=&rft.title=Nuclear+Medicine+and+Biology&rft.issn=09698051&rft_id=info:doi/10.1016%2Fj.nucmedbio.2014.08.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2015-04-16 N1 - SubjectsTermNotLitGenreText - Tracers; Latent infection; Computed tomography; Therapeutic applications; Nuclear medicine; Drug development; Tuberculosis; Pharmacokinetics; Public health; Mycobacterium tuberculosis DO - http://dx.doi.org/10.1016/j.nucmedbio.2014.08.005 ER - TY - JOUR T1 - endocrine-modulating effects on the ovarian steroidogenic pathway ex vivo independent of oxidative stress AN - 1639992015; 21120955 AB - Gold nanoparticles (GNPs) have gained considerable attention for application in science and industry. However, the untoward effects of such particles on female fertility remain unclear. The objectives of this study were to (1) examine the effects of 10-nm GNPs on progesterone and estradiol-17 beta accumulation by rat ovaries ex vivo and (2) to identify the locus/loci whereby GNPs modulate steroidogenesis via multiple-reference gene quantitative real-time RT-PCR. Regression analyses indicated a positive relationship between both Star (p < 0.05, r super(2) = 0.278) and Cyp11a1 (p < 0.001, r super(2) = 0.366) expression and P4 accumulation upon exposure to 1.43 106 GNPs/mL. Additional analyses showed that E2 accumulation was positively associated with Hsd3b1 (p < 0.05, r super(2) = 0.181) and Cyp17a1 (p < 0.01, r super(2) = 0.301) expression upon exposure to 1.43 1 super(3) and 1.43 10 super(9) GNPs/mL, respectively. These results suggest a subtle treatment-dependent impact of low-dose GNPs on the relationship between progesterone or estradiol-17 beta and specific steroidogenic target genes, independent of oxidative stress or inhibin. JF - Nanotoxicology AU - Larson, Jeremy K AU - Carvan, Michael J, III AU - Teeguarden, Justin G AU - Watanabe, Gen AU - Taya, Kazuyoshi AU - Krystofiak, Evan AU - Hutz, Reinhold J AD - University of Wisconsin-Milwaukee, Biological Sciences, Milwaukee, WI, USA; University of Wisconsin-Milwaukee and Children's Research Institute, NIEHS Children's Environmental Health Sciences Core Center, Milwaukee, WI, USA, rjhutz@uwm.edu Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 856 EP - 866 PB - Informa Healthcare, 52 Vanderbilt Ave. New York New York 10017 USA VL - 8 IS - 8 SN - 1743-5390, 1743-5390 KW - Toxicology Abstracts KW - nanotoxicology KW - genomics KW - Fertility KW - Progesterone KW - Oxidative stress KW - Inhibin KW - Regression analysis KW - Gold KW - Polymerase chain reaction KW - Ovaries KW - nanoparticles KW - Steroidogenesis KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639992015?accountid=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=Nanotoxicology&rft.atitle=endocrine-modulating+effects+on+the+ovarian+steroidogenic+pathway+ex+vivo+independent+of+oxidative+stress&rft.au=Larson%2C+Jeremy+K%3BCarvan%2C+Michael+J%2C+III%3BTeeguarden%2C+Justin+G%3BWatanabe%2C+Gen%3BTaya%2C+Kazuyoshi%3BKrystofiak%2C+Evan%3BHutz%2C+Reinhold+J&rft.aulast=Larson&rft.aufirst=Jeremy&rft.date=2014-12-01&rft.volume=8&rft.issue=8&rft.spage=856&rft.isbn=&rft.btitle=&rft.title=Nanotoxicology&rft.issn=17435390&rft_id=info:doi/10.3109%2F17435390.2013.837208 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Fertility; Progesterone; Inhibin; Oxidative stress; Regression analysis; Polymerase chain reaction; Gold; Ovaries; Steroidogenesis; nanoparticles DO - http://dx.doi.org/10.3109/17435390.2013.837208 ER - TY - JOUR T1 - A Generic Approach to Pathological Lung Segmentation AN - 1639980148; 21125565 AB - In this study, we propose a novel pathological lung segmentation method that takes into account neighbor prior constraints and a novel pathology recognition system. Our proposed framework has two stages; during stage one, we adapted the fuzzy connectedness (FC) image segmentation algorithm to perform initial lung parenchyma extraction. In parallel, we estimate the lung volume using rib-cage information without explicitly delineating lungs. This rudimentary, but intelligent lung volume estimation system allows comparison of volume differences between rib cage and FC based lung volume measurements. Significant volume difference indicates the presence of pathology, which invokes the second stage of the proposed framework for the refinement of segmented lung. In stage two, texture-based features are utilized to detect abnormal imaging patterns (consolidations, ground glass, interstitial thickening, tree-inbud, honeycombing, nodules, and micro-nodules) that might have been missed during the first stage of the algorithm. This refinement stage is further completed by a novel neighboring anatomy-guided segmentation approach to include abnormalities with weak textures, and pleura regions. We evaluated the accuracy and efficiency of the proposed method on more than 400 CT scans with the presence of a wide spectrum of abnormalities. To our best of knowledge, this is the first study to evaluate all abnormal imaging patterns in a single segmentation framework. The quantitative results show that our pathological lung segmentation method improves on current standards because of its high sensitivity and specificity and may have considerable potential to enhance the performance of routine clinical tasks. JF - IEEE Transactions on Medical Imaging AU - Mansoor, Awais AU - Bagci, Ulas AU - Xu, Ziyue AU - Foster, Brent AU - Olivier, Kenneth N AU - Elinoff, Jason M AU - Suffredini, Anthony F AU - Udupa, Jayaram K AU - Mollura, Daniel J AD - Department of Radiology and Imaging Sciences, National Institutes of Health (NIH), Bethesda, Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 2293 EP - 2310 PB - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States VL - 33 IS - 12 SN - 0278-0062, 0278-0062 KW - Biotechnology and Bioengineering Abstracts KW - Parenchyma KW - Rib KW - Pleura KW - Lung KW - Computed tomography KW - Segmentation KW - Algorithms KW - Image processing KW - Nodules KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639980148?accountid=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=A+Generic+Approach+to+Pathological+Lung+Segmentation&rft.au=Mansoor%2C+Awais%3BBagci%2C+Ulas%3BXu%2C+Ziyue%3BFoster%2C+Brent%3BOlivier%2C+Kenneth+N%3BElinoff%2C+Jason+M%3BSuffredini%2C+Anthony+F%3BUdupa%2C+Jayaram+K%3BMollura%2C+Daniel+J&rft.aulast=Mansoor&rft.aufirst=Awais&rft.date=2014-12-01&rft.volume=33&rft.issue=12&rft.spage=2293&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Medical+Imaging&rft.issn=02780062&rft_id=info:doi/10.1109%2FTMI.2014.2337057 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Parenchyma; Pleura; Rib; Lung; Computed tomography; Algorithms; Segmentation; Image processing; Nodules DO - http://dx.doi.org/10.1109/TMI.2014.2337057 ER - TY - JOUR T1 - Reporter mice express green fluorescent protein at initiation of meiosis in spermatocytes. AN - 1639493430; 25293348 AB - Transgenic mice were generated using a heat shock protein 2 (Hspa2) gene promoter to express green fluorescent protein (GFP) at the beginning of meiotic prophase I in spermatocytes. Expression was confirmed in four lines by in situ fluorescence, immunohistochemistry, western blotting, and PCR assays. The expression and distribution of the GFP and HSPA2 proteins co-localized in spermatocytes and spermatids in three lines, but GFP expression was variegated in one line (F46), being present in some clones of meiotic and post-meiotic germ cells and not in others. Fluorescence activated cell sorting (FACS) was used to isolate purified populations of spermatocytes and spermatids. Although bisulfite sequencing revealed differences in the DNA methylation patterns in the promoter regions of the transgene of the variegated expressing GFP line, a uniformly expressing GFP reporter line, and the Hspa2 gene, these differences did not correlate with variegated expression. The Hspa2-GFP reporter mice provide a novel tool for studies of meiosis by allowing detection of GFP in situ and in isolated spermatogenic cells. They will allow sorting of meiotic and post-meiotic germ cells for characterization of molecular features and correlation of expression of GFP with stage-specific spermatogenic cell proteins and developmental events. © 2014 Wiley Periodicals, Inc. JF - Genesis (New York, N.Y. : 2000) AU - Brown, Paula R AU - Odet, Fanny AU - Bortner, Carl D AU - Eddy, Edward M AD - Gamete Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 976 EP - 984 VL - 52 IS - 12 KW - HSP70 Heat-Shock Proteins KW - 0 KW - Hspa2 protein, mouse KW - Recombinant Proteins KW - Green Fluorescent Proteins KW - 147336-22-9 KW - Index Medicus KW - variegated gene expression KW - spermatogenesis KW - heat shock protein KW - fluorescence activated cell sorting KW - Animals KW - Promoter Regions, Genetic KW - Spermatids -- cytology KW - DNA Methylation KW - Recombinant Proteins -- metabolism KW - Spermatids -- metabolism KW - Mice KW - Recombinant Proteins -- genetics KW - Mice, Transgenic KW - Male KW - Female KW - Spermatocytes -- cytology KW - HSP70 Heat-Shock Proteins -- metabolism KW - HSP70 Heat-Shock Proteins -- genetics KW - Meiosis KW - Spermatocytes -- metabolism KW - Green Fluorescent Proteins -- metabolism KW - Green Fluorescent Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639493430?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genesis+%28New+York%2C+N.Y.+%3A+2000%29&rft.atitle=Reporter+mice+express+green+fluorescent+protein+at+initiation+of+meiosis+in+spermatocytes.&rft.au=Brown%2C+Paula+R%3BOdet%2C+Fanny%3BBortner%2C+Carl+D%3BEddy%2C+Edward+M&rft.aulast=Brown&rft.aufirst=Paula&rft.date=2014-12-01&rft.volume=52&rft.issue=12&rft.spage=976&rft.isbn=&rft.btitle=&rft.title=Genesis+%28New+York%2C+N.Y.+%3A+2000%29&rft.issn=1526-968X&rft_id=info:doi/10.1002%2Fdvg.22830 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-14 N1 - Date created - 2014-12-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cell. 1991 Jul 12;66(1):77-83 [1649008] Cold Spring Harb Perspect Biol. 2013 Aug;5(8):a017780 [23906716] Proc Natl Acad Sci U S A. 1996 Apr 16;93(8):3264-8 [8622925] Nat Genet. 1998 Jan;18(1):56-9 [9425901] Biol Reprod. 1999 Nov;61(5):1256-66 [10529272] J Biol Chem. 2007 Dec 14;282(50):36143-54 [17932037] Mol Cell Biol. 2008 Mar;28(5):1770-82 [18172011] Nucleic Acids Res. 2008 Apr;36(7):2320-9 [18296483] Genetics. 2009 Apr;181(4):1687-91 [19204377] Methods Mol Biol. 2009;558:279-97 [19685331] Methods Mol Biol. 2009;558:299-321 [19685332] Genesis. 2010 Feb;48(2):114-20 [20027617] Cytogenet Genome Res. 2010;128(1-3):46-56 [20389037] Nucleic Acids Res. 2000 Sep 1;28(17):3301-9 [10954598] Proc Natl Acad Sci U S A. 2003 May 27;100(11):6487-92 [12738887] Methods Enzymol. 1999;302:272-84 [12876779] Dev Biol. 2003 Oct 1;262(1):173-82 [14512027] Biol Reprod. 2004 Jul;71(1):319-30 [15028632] Biol Reprod. 2004 Sep;71(3):722-31 [15115718] J Cell Physiol. 1975 Aug;86(1):177-89 [1236854] J Histochem Cytochem. 1977 Jul;25(7):480-94 [893996] EMBO J. 1985 Sep;4(9):2225-30 [3935430] Mol Cell Biol. 1988 Feb;8(2):828-32 [3352605] Mol Cell Biol. 1988 Aug;8(8):3260-6 [3211143] Methods Mol Biol. 2012;825:31-44 [22144234] Curr Opin Endocrinol Diabetes Obes. 2013 Jun;20(3):217-23 [23511242] Dev Biol. 1992 Mar;150(1):1-11 [1537426] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/dvg.22830 ER - TY - JOUR T1 - Linking cancer genome to proteome: NCI's investment into proteogenomics AN - 1639473894; 21123868 AB - Advances in both targeted and unbiased MS-based proteomics are now at a mature stage for comprehensively and reproducibly characterizing a large part of the cancer proteome. These developments combined with the extensive genomic characterization of several cancer types by large-scale initiatives such as the International Cancer Genome Consortium and Cancer Genome Atlas Project have paved the way for proteogenomic analysis of omics datasets and integration methods. The advances serve as the basis for the National Cancer Institute's Clinical Proteomic Tumor Analysis Consortium and this article highlights its current work and future steps in the area of proteogenomics. JF - Proteomics AU - Rivers, Robert C AU - Kinsinger, Christopher AU - Boja, Emily S AU - Hiltke, Tara AU - Mesri, Mehdi AU - Rodriguez, Henry AD - Office of Cancer Clinical Proteomics Research, National Cancer Institute, Bethesda, MD, USA. Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 2633 EP - 2636 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 14 IS - 23-24 SN - 1615-9853, 1615-9853 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Genomes KW - Integration KW - Atlases KW - proteomics KW - Tumors KW - genomics KW - Cancer KW - G 07880:Human Genetics KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639473894?accountid=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=Linking+cancer+genome+to+proteome%3A+NCI%27s+investment+into+proteogenomics&rft.au=Rivers%2C+Robert+C%3BKinsinger%2C+Christopher%3BBoja%2C+Emily+S%3BHiltke%2C+Tara%3BMesri%2C+Mehdi%3BRodriguez%2C+Henry&rft.aulast=Rivers&rft.aufirst=Robert&rft.date=2014-12-01&rft.volume=14&rft.issue=23-24&rft.spage=2633&rft.isbn=&rft.btitle=&rft.title=Proteomics&rft.issn=16159853&rft_id=info:doi/10.1002%2Fpmic.201400193 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2015-02-12 N1 - SubjectsTermNotLitGenreText - Genomes; Integration; Atlases; genomics; Tumors; proteomics; Cancer DO - http://dx.doi.org/10.1002/pmic.201400193 ER - TY - JOUR T1 - Delayed uric Acid accumulation in plasma provides additional anti-oxidant protection against iron-triggered oxidative stress after a wingate test. AN - 1637562479; 25435669 AB - Reactive oxygen species are produced during anaerobic exercise mostly by Fe ions released into plasma and endothelial/muscle xanthine oxidase activation that generates uric acid (UA) as the endpoint metabolite. Paradoxically, UA is considered a major antioxidant by virtue of being able to chelate pro-oxidative iron ions. This work aimed to evaluate the relationship between UA and plasma markers of oxidative stress following the exhaustive Wingate test. Plasma samples of 17 male undergraduate students were collected before, 5 and 60 min after maximal anaerobic effort for the measurement of total iron, haem iron, UA, ferric-reducing antioxidant activity in plasma (FRAP), and malondialdehyde (MDA, biomarker of lipoperoxidation). Iron and FRAP showed similar kinetics in plasma, demonstrating an adequate pro-/antioxidant balance immediately after exercise and during the recovery period (5-60 min). Slight variations of haem iron concentrations did not support a relevant contribution of rhabdomyolysis or haemolysis for iron overload following exercise. UA concentration did not vary immediately after exercise but rather increased 29% during the recovery period. Unaltered MDA levels were concomitantly measured. We propose that delayed UA accumulation in plasma is an auxiliary antioxidant response to post-exercise (iron-mediated) oxidative stress, and the high correlation between total UA and FRAP in plasma (R-Square = 0.636; p = 0.00582) supports this hypothesis. JF - Biology of sport AU - Souza-Junior, Tp AU - Lorenço-Lima, L AU - Ganini, D AU - Vardaris, Cv AU - Polotow, Tg AU - Barros, Mp AD - Department of Physical Education, Federal University of Parana (UFPR), Curitiba, PR, Brazil. ; Postgraduate program in Human Movement Sciences, Institute of Physical Activity and Sports Sciences (ICAFE), Cruzeiro do Sul University, Sao Paulo, SP, Brazil. ; Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, NIEHS, Research Triangle Park, USA. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 271 EP - 276 VL - 31 IS - 4 SN - 0860-021X, 0860-021X KW - anaerobic metabolism KW - haemoglobin KW - exercise KW - xanthine oxidase KW - lipid peroxidation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1637562479?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+sport&rft.atitle=Delayed+uric+Acid+accumulation+in+plasma+provides+additional+anti-oxidant+protection+against+iron-triggered+oxidative+stress+after+a+wingate+test.&rft.au=Souza-Junior%2C+Tp%3BLoren%C3%A7o-Lima%2C+L%3BGanini%2C+D%3BVardaris%2C+Cv%3BPolotow%2C+Tg%3BBarros%2C+Mp&rft.aulast=Souza-Junior&rft.aufirst=Tp&rft.date=2014-12-01&rft.volume=31&rft.issue=4&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Biology+of+sport&rft.issn=0860021X&rft_id=info:doi/10.5604%2F20831862.1120934 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-01 N1 - Date created - 2014-12-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.5604/20831862.1120934 ER - TY - JOUR T1 - Stochastic dynamic models and Chebyshev splines AN - 1636460761; 4625632 AB - In this article, we establish a connection between a stochastic dynamic model (SDM) driven by a linear stochastic differential equation (SDE) and a Chebyshev spline, which enables researchers to borrow strength across fields both theoretically and numerically. We construct a differential operator for the penalty function and develop a reproducing kernel Hilbert space (RKHS) induced by the SDM and the Chebyshev spline. The general form of the linear SDE allows us to extend the well-known connection between an integrated Brownian motion and a polynomial spline to a connection between more complex diffusion processes and Chebyshev splines. One interesting special case is connection between an integrated Ornstein-Uhlenbeck process and an exponential spline. We use two real data sets to illustrate the integrated Ornstein– ;Uhlenbeck process model and exponential spline model and show their estimates are almost identical. The Canadian Journal of Statistics 42: 610-634; 2014 © 2014 Statistical Society of Canada // ABSTRACT IN : Les auteurs établissent un lien entre un modèle stochastique dynamique basé sur une équation différentielle stochastique linéaire et une spline de Chebyshev, permettant aux chercheurs de transférer des connaissances dans ces champs respectifs, autant d'un point de vue théorique que numé ;rique. Ils construisent un opérateur différentiel pour la fonction de pénalité et développent un espace de Hilbert à noyau reproduisant découlant du modèle stochastique dynamique et de la spline de Chebyshev. La forme générale de l'équation différentielle stochastique linéaire permet de généraliser le lien bien connu entre un mouvement brownien intégré et une spline polynomiale à un lien entre des processus de diffusion plus complexes et les splines de Chebyshev. Un cas particulier d'intérêt lie un processus d'Ornstein-Uhlenbeck intégré et une spline exponentielle. Les auteurs utilisent deux jeux de données réelles pour illustrer le processus d'Ornstein-Uhlenbeck intégré et un modèle de spline exponentielle. Ils montrent que les estimés obtenus sont presque identiques. La revue canadienne de statistique xx: 1-25; 2014 © 2014 Société statistique du Canada JF - Canadian journal of statistics AU - Fan, Ruzong AU - Zhu, Bin AU - Wang, Yuedong AD - National Institutes of Health ; University of California, Santa Barbara Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 610 EP - 634 VL - 42 IS - 4 SN - 0319-5724, 0319-5724 KW - Economics KW - Stochastic processes KW - Statistics KW - Dynamic models KW - Canada KW - Economic models KW - Diffusionism KW - Functional analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1636460761?accountid=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=Stochastic+dynamic+models+and+Chebyshev+splines&rft.au=Fan%2C+Ruzong%3BZhu%2C+Bin%3BWang%2C+Yuedong&rft.aulast=Fan&rft.aufirst=Ruzong&rft.date=2014-12-01&rft.volume=42&rft.issue=3&rft.spage=883&rft.isbn=&rft.btitle=&rft.title=Analytical+and+bioanalytical+chemistry&rft.issn=1618-2650&rft_id=info:doi/10.1007%2Fs00216-014-8118-8 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-12-16 N1 - Last updated - 2014-12-16 N1 - SubjectsTermNotLitGenreText - 12265 3865 4025 10214 12224 971 12228 10919; 3786 8163; 3555 1073; 5345 971; 12233; 3969 8163; 75 293 14 DO - http://dx.doi.org/10.1002/cjs.11233 ER - TY - JOUR T1 - Association of seropositivity to Helicobacter species and biliary tract cancer in the ATBC study AN - 1635032490; 21045942 AB - Helicobacter have been detected in human bile and hepatobiliary tissue. Despite evidence that Helicobacter species promote gallstone formation and hepatobiliary tumors in laboratory studies, it remains unclear whether Helicobacter species contribute to these cancers in humans. We used a multiplex panel to assess whether seropositivity to 15 Helicobacter pylori proteins was associated with subsequent incidence of hepatobiliary cancers in the Finnish Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study. We included 64 biliary cancers, 122 liver cancers, and 224 age-matched controls which occurred over the course of 22 years. Helicobacter pylori seropositivity was defined as those positive to greater than or equal to 4 antigens. Odds ratios (OR) and 95% confidence intervals were adjusted for major hepatobiliary cancer risk factors. Among the controls, 88% were seropositive to H. pylori at baseline. Among those who subsequently developed hepatobiliary cancer, the prevalence of seropositivity was higher: 100% for gallbladder cancer, 97% of extrahepatic bile duct cancer, 91% of ampula of Vater cancer, 96% of intrahepatic bile duct cancer, and 94% of hepatocellular carcinoma. Although the OR for gallbladder cancer could not be calculated, the OR for the other sites were 7.01 (95% confidence interval [CI]: 0.79-62.33), 2.21 (0.19-25.52), 10.67 (0.76-150.08), and 1.20 (0.42-3.45), respectively, with an OR of 5.47 (95% CI: 1.17-25.65) observed for the biliary tract cancers combined. ORs above 1 were observed for many of the investigated antigens, although most of these associations were not statistically significant. Conclusion: Seropositivity to H. pylori proteins was associated with an increased risk of biliary tract cancers in ATBC. Further studies are needed to confirm our findings and to determine how H. pylori might influence the risk of biliary tract cancer. (Hepatology 2014; 60:1962-1970) JF - Hepatology AU - Murphy, Gwen AU - Michel, Angelika AU - Taylor, Philip R AU - Albanes, Demetrius AU - Weinstein, Stephanie J AU - Virtamo, Jarmo AU - Parisi, Dominick AU - Snyder, Kirk AU - Butt, Julia AU - McGlynn, Katherine A AU - Koshiol, Jill AU - Pawlita, Michael AU - Lai, Gabriel Y AU - Abnet, Christian C AU - Dawsey, Sanford M AU - Freedman, Neal D AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1963 EP - 1971 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 60 IS - 6 SN - 0270-9139, 0270-9139 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Helicobacter pylori KW - Gallbladder KW - Bile duct KW - Liver cancer KW - Risk factors KW - Statistical analysis KW - Tumors KW - Biliary tract KW - Hepatocellular carcinoma KW - J 02400:Human Diseases KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635032490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology&rft.atitle=Association+of+seropositivity+to+Helicobacter+species+and+biliary+tract+cancer+in+the+ATBC+study&rft.au=Murphy%2C+Gwen%3BMichel%2C+Angelika%3BTaylor%2C+Philip+R%3BAlbanes%2C+Demetrius%3BWeinstein%2C+Stephanie+J%3BVirtamo%2C+Jarmo%3BParisi%2C+Dominick%3BSnyder%2C+Kirk%3BButt%2C+Julia%3BMcGlynn%2C+Katherine+A%3BKoshiol%2C+Jill%3BPawlita%2C+Michael%3BLai%2C+Gabriel+Y%3BAbnet%2C+Christian+C%3BDawsey%2C+Sanford+M%3BFreedman%2C+Neal+D&rft.aulast=Murphy&rft.aufirst=Gwen&rft.date=2014-12-01&rft.volume=60&rft.issue=6&rft.spage=1963&rft.isbn=&rft.btitle=&rft.title=Hepatology&rft.issn=02709139&rft_id=info:doi/10.1002%2Fhep.27193 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2015-03-04 N1 - SubjectsTermNotLitGenreText - Gallbladder; Bile duct; Risk factors; Liver cancer; Statistical analysis; Tumors; Biliary tract; Hepatocellular carcinoma; Helicobacter pylori DO - http://dx.doi.org/10.1002/hep.27193 ER - TY - JOUR T1 - Wistar rats acquire and maintain self-administration of 20 % ethanol without water deprivation, saccharin/sucrose fading, or extended access training AN - 1635028166; 21030598 AB - Rationale: Operant self-administration (SA) is an important model of motivation to consume ethanol (EtOH), but low rates of voluntary consumption in rats are thought to necessitate water deprivation and saccharin/sucrose fading for acquisition of responding. Objectives: Here, we sought to devise an effective model of SA that does not use water deprivation or saccharin/sucrose fading. Methods: First, we tested if Wistar rats would acquire and maintain SA behavior of 20 % EtOH under two conditions, water deprivation (WD) and non-water deprivation (NWD). Second, we tested the efficacy of our SA procedure by confirming a prior study which found that the NK1 antagonist L822429 specifically blocked stress-induced reinstatement of EtOH seeking but not SA. Finally, we assessed the effect of naltrexone, an FDA-approved medication for alcohol dependence that has been shown to suppress EtOH SA in rodents. Results: Lever presses (LPs) and rewards were consistent with previous reports that utilized WD and saccharin/sucrose fading. Similar to previous findings, we found that L822429 blocked stress-induced reinstatement but not baseline SA of 20 % EtOH. Moreover, naltrexone dose-dependently decreased alcohol intake and motivation to consume alcohol for rats that are self-administering 20 % EtOH. Conclusions: Our findings provide a method for voluntary oral EtOH SA in rats that is convenient for experimenters and eliminates the potential confound of sweeteners in EtOH-operant SA studies. Unlike models that use intermittent access to 20 % EtOH, this method does not induce escalation, and based on pharmacological experiments, it appears to be driven by the positive reinforcing effects of EtOH. JF - Psychopharmacology AU - Augier, E AU - Flanigan, M AU - Dulman, R S AU - Pincus, A AU - Schank, J R AU - Rice, K C AU - Kejun, C AU - Heilig, M AU - Tapocik, J D AD - Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, 20892, USA, eric.augier@nih.gov Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 4561 EP - 4568 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 231 IS - 23 SN - 0033-3158, 0033-3158 KW - Physical Education Index; Animal Behavior Abstracts; CSA Neurosciences Abstracts KW - Alcohol KW - Saccharin KW - Alcoholic beverages KW - Operant conditioning KW - Sweeteners KW - Motivation KW - Animal subjects KW - Medications KW - Reinstatement KW - Water KW - Models KW - Drug dependence KW - Reward KW - Behavior KW - Sucrose KW - Naltrexone KW - Reinforcement KW - Lipopolysaccharides KW - Drug self-administration KW - Ethanol KW - Self efficacy KW - N3 11001:Behavioral and Cognitive Neuroscience KW - Y 25130:Methodology KW - PE 090:Sports Medicine & Exercise Sport Science UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635028166?accountid=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=Psychopharmacology&rft.atitle=Wistar+rats+acquire+and+maintain+self-administration+of+20+%25+ethanol+without+water+deprivation%2C+saccharin%2Fsucrose+fading%2C+or+extended+access+training&rft.au=Augier%2C+E%3BFlanigan%2C+M%3BDulman%2C+R+S%3BPincus%2C+A%3BSchank%2C+J+R%3BRice%2C+K+C%3BKejun%2C+C%3BHeilig%2C+M%3BTapocik%2C+J+D&rft.aulast=Augier&rft.aufirst=E&rft.date=2014-12-01&rft.volume=231&rft.issue=23&rft.spage=4561&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/10.1007%2Fs00213-014-3605-3 LA - English DB - Physical Education Index N1 - Date revised - 2014-12-01 N1 - Number of references - 24 N1 - Last updated - 2015-03-04 N1 - SubjectsTermNotLitGenreText - Alcohol; Behavior; Reward; Motivation; Animal subjects; Medications; Water; Self efficacy; Saccharin; Alcoholic beverages; Sweeteners; Operant conditioning; Reinstatement; Models; Drug dependence; Sucrose; Naltrexone; Reinforcement; Lipopolysaccharides; Ethanol; Drug self-administration DO - http://dx.doi.org/10.1007/s00213-014-3605-3 ER - TY - JOUR T1 - Q and B values are critical measurements required for inter-instrument standardization and development of multicolor flow cytometry staining panels AN - 1635027765; 21033485 AB - Much of the complexity of multicolor flow cytometry experiments lies within the development of antibody staining panels and the standardization of instruments. In this article, we propose a theoretical metric and describe how measurements of sensitivity and resolution can be used to predict the success of panels, and ensure that performance across instruments is standardized (i.e., inter-instrument standardization). Sensitivity can be determined by summing two major contributors of background, background originating from the instrument (optical noise and electronic noise) and background due to the experimental conditions (i.e., Raman scatter, and spillover spreading arising from other fluorochromes in the panel). The former we define as B sub(cal) and the latter we define as B sub(sos). The combination of instrument and experiment background is defined as B sub(tot). Importantly, the B sub(tot) will affect the degree of panel separation, therefore the greater the degree of B sub(tot) the lower the separation potential. In contrast, resolution is a measure of separation between populations. Resolution is directly proportional to the number of photoelectrons generated per molecule of excited fluorochrome and is known as the "Q" value. Q and B sub(tot) values can be used to define the performance of each detector on an instrument and together they can be used to calculate a separation index. Hence, detectors with known Q and B sub(tot) values can be used to evaluate panel success based on the detector specific separation index. However, the current technologies do not enable measurements of Q and B sub(tot) values for all parameters, but new technology to allow these measurements will likely be introduced in the near future. Nonetheless, Q and B sub(tot) measurements can aid in panel development, and reveal sources of instrument-to-instrument variation in panel performance. In addition, Q and B values can form the basis for a comprehensive and versatile quality assurance program. Published 2014 Wiley Periodicals Inc. JF - Cytometry Part A AU - Perfetto, Stephen P AU - Chattopadhyay, Pratip K AU - Wood, James AU - Nguyen, Richard AU - Ambrozak, David AU - Hill, Juliane P AU - Roederer, Mario AD - Vaccine Research Center, NIAID, NIH, Bethesda, Maryland, 20724. Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1037 EP - 1048 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 85 IS - 12 SN - 1552-4922, 1552-4922 KW - Biotechnology and Bioengineering Abstracts KW - Flow cytometry KW - Standardization KW - Antibodies KW - Spreading KW - Quality control KW - fluorochromes KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635027765?accountid=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=Q+and+B+values+are+critical+measurements+required+for+inter-instrument+standardization+and+development+of+multicolor+flow+cytometry+staining+panels&rft.au=Perfetto%2C+Stephen+P%3BChattopadhyay%2C+Pratip+K%3BWood%2C+James%3BNguyen%2C+Richard%3BAmbrozak%2C+David%3BHill%2C+Juliane+P%3BRoederer%2C+Mario&rft.aulast=Perfetto&rft.aufirst=Stephen&rft.date=2014-12-01&rft.volume=85&rft.issue=12&rft.spage=1037&rft.isbn=&rft.btitle=&rft.title=Cytometry+Part+A&rft.issn=15524922&rft_id=info:doi/10.1002%2Fcyto.a.22579 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2014-12-11 N1 - SubjectsTermNotLitGenreText - Flow cytometry; Standardization; Antibodies; Spreading; Quality control; fluorochromes DO - http://dx.doi.org/10.1002/cyto.a.22579 ER - TY - JOUR T1 - Urinary bisphenol A-glucuronide and postmenopausal breast cancer in Poland AN - 1635026371; 21029934 AB - Purpose : Concerns regarding a possible link between bisphenol A (BPA) and breast cancer have been mounting, but studies in human populations are lacking. We evaluated the association between the major urinary BPA metabolite [BPA-glucuronide (BPA-G)] and postmenopausal breast cancer risk in a large population-based case-control study conducted in two cities in Poland (2000-2003); we further explored the association of BPA-G levels with known postmenopausal breast cancer risk factors in our control population. Methods: We analyzed creatinine-adjusted urinary BPA-G levels among 575 postmenopausal cases matched on age and study site to 575 controls without breast cancer using a recently developed assay. Odds ratios and 95 % confidence intervals were used to estimate the association between urinary BPA-G level and breast cancer using conditional logistic regression. Among controls, geometric mean BPA-G levels were compared across categories of breast cancer risk factors using linear regression models. Results: There was no indication that increased BPA-G was associated with postmenopausal breast cancer (p-trend = 0.59). Among controls, mean BPA-G was higher among women reporting extended use of menopausal hormones, a prior screening mammogram, and residence in Warsaw. Other comparisons across strata of postmenopausal breast cancer risk factors were not related to differences in BPA-G. Conclusions: Urinary BPA-G, measured at the time of diagnosis, is not linked to postmenopausal breast cancer. JF - Cancer Causes & Control AU - Trabert, Britton AU - Falk, Roni T AU - Figueroa, Jonine D AU - Graubard, Barry I AU - Garcia-Closas, Montserrat AU - Lissowska, Jolanta AU - Peplonska, Beata AU - Fox, Stephen D AU - Brinton, Louise A AD - Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, 9609 Medical Center Drive, Room 7E-228, Bethesda, MD, 20892-9774, USA, britton.trabert@nih.gov Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1587 EP - 1593 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 25 IS - 12 SN - 0957-5243, 0957-5243 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Bisphenol A KW - Health risks KW - Cities KW - Age KW - Post-menopause KW - Urine KW - Poland KW - Human populations KW - Breast cancer KW - Metabolites KW - Hormones KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635026371?accountid=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=Urinary+bisphenol+A-glucuronide+and+postmenopausal+breast+cancer+in+Poland&rft.au=Trabert%2C+Britton%3BFalk%2C+Roni+T%3BFigueroa%2C+Jonine+D%3BGraubard%2C+Barry+I%3BGarcia-Closas%2C+Montserrat%3BLissowska%2C+Jolanta%3BPeplonska%2C+Beata%3BFox%2C+Stephen+D%3BBrinton%2C+Louise+A&rft.aulast=Trabert&rft.aufirst=Britton&rft.date=2014-12-01&rft.volume=25&rft.issue=12&rft.spage=1587&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-014-0461-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Number of references - 27 N1 - Last updated - 2015-02-12 N1 - SubjectsTermNotLitGenreText - Bisphenol A; Cities; Health risks; Age; Urine; Post-menopause; Human populations; Breast cancer; Metabolites; Hormones; Poland DO - http://dx.doi.org/10.1007/s10552-014-0461-8 ER - TY - JOUR T1 - Role of nucleotide excision repair and p53 in zidovudine (AZT)-induced centrosomal deregulation. AN - 1634498926; 25073973 AB - The nucleoside reverse transcriptase inhibitor zidovudine (AZT) induces genotoxic damage that includes centrosomal amplification (CA > 2 centrosomes/cell) and micronucleus (MN) formation. Here we explored these end points in mice deficient in DNA repair and tumor suppressor function to evaluate their effect on AZT-induced DNA damage. We used mesenchymal-derived fibroblasts cultured from C57BL/6J mice that were null and wild type (WT) for Xpa, and WT, haploinsufficient and null for p53 (6 different genotypes). Dose-responses for CA formation, in cells exposed to 0, 10, and 100 μM AZT for 24 hr, were observed in all genotypes except the Xpa((+/+)) p53((+/-)) cells, which had very low levels of CA, and the Xpa((-/-)) p53((-/-)) cells, which had very high levels of CA. For CA there was a significant three-way interaction between Xpa, p53, and AZT concentration, and Xpa((-/-)) cells had significantly higher levels of CA than Xpa((+/+)) cells, only for p53((+/-)) cells. In contrast, the MN and MN + chromosomes (MN + C) data showed a lack of AZT dose response. The Xpa((-/-)) cells, with p53((+/+)) or ((+/-)) genotypes, had levels of MN and MN + C higher than the corresponding Xpa((+/+)) cells. The data show that CA is a major event induced by exposure to AZT in these cells, and that there is a complicated relationship between AZT and CA formation with respect to gene dosage of Xpa and p53. The loss of both genes resulted in high levels of damage, and p53 haploinsufficicency strongly protected Xpa((+/+)) cells from AZT-induced CA damage. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - Environmental and molecular mutagenesis AU - Momot, Dariya AU - Nostrand, Terri A AU - John, Kaarthik AU - Ward, Yvona AU - Steinberg, Seth M AU - Liewehr, David J AU - Poirier, Miriam C AU - Olivero, Ofelia A AD - Carcinogen-DNA Interactions Section, LCBG, National Cancer Institute, NIH, Bethesda, Maryland. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 719 EP - 726 VL - 55 IS - 9 KW - Tumor Suppressor Protein p53 KW - 0 KW - Xeroderma Pigmentosum Group A Protein KW - Xpa protein, mouse KW - Zidovudine KW - 4B9XT59T7S KW - Index Medicus KW - micronuclei with whole chromosomes KW - centrosomal amplification KW - Xpa KW - zidovudine KW - micronuclei KW - Cell Proliferation -- drug effects KW - Bone Marrow Cells -- drug effects KW - Animals KW - Micronucleus Tests KW - Cell Survival -- drug effects KW - Dose-Response Relationship, Drug KW - Mice, Inbred C57BL KW - Mice, Transgenic KW - Xeroderma Pigmentosum Group A Protein -- genetics KW - DNA Repair -- genetics KW - Zidovudine -- toxicity KW - Centrosome -- drug effects KW - Tumor Suppressor Protein p53 -- genetics KW - DNA Repair -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1634498926?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+nucleotide+excision+repair+and+p53+in+zidovudine+%28AZT%29-induced+centrosomal+deregulation.&rft.au=Momot%2C+Dariya%3BNostrand%2C+Terri+A%3BJohn%2C+Kaarthik%3BWard%2C+Yvona%3BSteinberg%2C+Seth+M%3BLiewehr%2C+David+J%3BPoirier%2C+Miriam+C%3BOlivero%2C+Ofelia+A&rft.aulast=Momot&rft.aufirst=Dariya&rft.date=2014-12-01&rft.volume=55&rft.issue=9&rft.spage=719&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21889 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-28 N1 - Date created - 2014-11-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/em.21889 ER - TY - JOUR T1 - A DRD1 polymorphism predisposes to lung cancer among those exposed to secondhand smoke during childhood. AN - 1629965619; 25281486 AB - Lung cancer has a familial component which suggests a genetic contribution to its etiology. Given the strong evidence linking smoking with lung cancer, we studied miRNA-related loci in genes associated with smoking behavior. CHRNA, CHRNB gene families, CYP2A6, and DRD1 (dopamine receptor D1) were mined for SNPs that fell within the seed region of miRNA binding sites and then tested for associations with risk in a three-stage validation approach. A 3'UTR (untranslated region) SNP in DRD1 was associated with a lower risk of lung cancer among individuals exposed to secondhand smoke during childhood [OR, 0.69; 95% confidence interval (CI), 0.60-0.79; P < 0.0001]. This relationship was evident in both ever (OR, 0.74; 95% CI, 0.62-0.88; P = 0.001) and never smokers (OR, 0.61; 95% CI, 0.47-0.79; P < 0.0001), European American (OR, 0.65; 95% CI, 0.53-0.80; P < 0.0001), and African American (OR, 0.73; 95% CI, 0.62-0.88; P = 0.001) populations. Although much remains undefined about the long-term risks associated with exposure to secondhand smoke and heterogeneity between individuals in regard to their susceptibility to the effects of secondhand smoke, our data show an interaction between an SNP in the 3'UTR of DRD1 and exposure to secondhand smoke during childhood. Further work is needed to explore the mechanistic underpinnings of this SNP and the nature of the interaction between DRD1 and exposure to secondhand smoke during childhood. ©2014 American Association for Cancer Research. JF - Cancer prevention research (Philadelphia, Pa.) AU - Robles, Ana I AU - Yang, Ping AU - Jen, Jin AU - McClary, Andrew C AU - Calhoun, Kara AU - Bowman, Elise D AU - Vähäkangas, Kirsi AU - Greathouse, K Leigh AU - Wang, Yi AU - Olivo-Marston, Susan AU - Wenzlaff, Angela S AU - Deng, Bo AU - Schwartz, Ann G AU - Ryan, Bríd M AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Mayo Clinic, Department of Health Sciences Research, Rochester, Minnesota. ; Department of Laboratory Medicine and Pathology and Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, Minnesota. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Department of Pathology, Stanford University Hospital and Clinics, Stanford, California. ; School of Pharmacy/Toxicology, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland. ; Division of Preventive Medicine, School of Environmental Science and Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, China. Division of Epidemiology, Health Sciences Research, Mayo Clinic, Rochester, Minnesota. ; Division of Epidemiology, College of Public Health, Ohio State University, Columbus, Ohio. ; Karmanos Cancer Institute, Department of Oncology, Wayne State University School of Medicine, Detroit, Michigan. ; Division of Epidemiology, Health Sciences Research, Mayo Clinic, Rochester, Minnesota. Thoracic Surgery Department, Institute of Surgery Research, Daping Hospital, The Third Military Medical University, Chongqing, China. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ryanb@mail.nih.gov. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 1210 EP - 1218 VL - 7 IS - 12 KW - 3' Untranslated Regions KW - 0 KW - CHRNA1 protein, human KW - CHRNA2 protein, human KW - DRD1 protein, human KW - MicroRNAs KW - Receptors, Dopamine D1 KW - Receptors, Nicotinic KW - Tobacco Smoke Pollution KW - CYP2A6 protein, human KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP2A6 KW - Index Medicus KW - Neoplasm Staging KW - MicroRNAs -- genetics KW - Humans KW - Prognosis KW - Aged KW - Child KW - Receptors, Nicotinic -- genetics KW - Cytochrome P-450 CYP2A6 -- genetics KW - Risk Factors KW - Case-Control Studies KW - Follow-Up Studies KW - Middle Aged KW - 3' Untranslated Regions -- genetics KW - Female KW - Male KW - Lung Neoplasms -- etiology KW - Receptors, Dopamine D1 -- genetics KW - Disease Susceptibility KW - Polymorphism, Genetic -- genetics KW - Tobacco Smoke Pollution -- adverse effects KW - Smoking -- genetics KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629965619?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.atitle=A+DRD1+polymorphism+predisposes+to+lung+cancer+among+those+exposed+to+secondhand+smoke+during+childhood.&rft.au=Robles%2C+Ana+I%3BYang%2C+Ping%3BJen%2C+Jin%3BMcClary%2C+Andrew+C%3BCalhoun%2C+Kara%3BBowman%2C+Elise+D%3BV%C3%A4h%C3%A4kangas%2C+Kirsi%3BGreathouse%2C+K+Leigh%3BWang%2C+Yi%3BOlivo-Marston%2C+Susan%3BWenzlaff%2C+Angela+S%3BDeng%2C+Bo%3BSchwartz%2C+Ann+G%3BRyan%2C+Br%C3%ADd+M&rft.aulast=Robles&rft.aufirst=Ana&rft.date=2014-12-01&rft.volume=7&rft.issue=12&rft.spage=1210&rft.isbn=&rft.btitle=&rft.title=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.issn=1940-6215&rft_id=info:doi/10.1158%2F1940-6207.CAPR-14-0158 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-30 N1 - Date created - 2014-12-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Neuroimmunomodulation. 2001;9(1):23-33 [11435749] Neurosci Lett. 2014 Jan 13;558:20-5 [24095672] Am J Psychiatry. 2002 May;159(5):761-7 [11986129] Carcinogenesis. 2003 Feb;24(2):269-74 [12584177] Am J Epidemiol. 2003 Aug 1;158(3):251-8 [12882947] Cancer Epidemiol Biomarkers Prev. 2003 Dec;12(12):1389-94 [14693727] Natl Cancer Inst Monogr. 1966 Jan;19:127-204 [5905667] Br Med J. 1976 Dec 25;2(6051):1525-36 [1009386] Med Pediatr Oncol. 1984;12(3):224-7 [6727779] IARC Sci Publ. 1984;(57):627-65 [6533057] Neurology. 1986 Nov;36(11):1490-6 [3531917] N Engl J Med. 1990 Sep 6;323(10):632-6 [2385268] Adv Data. 1991 Jun 18;(202):1-11 [10111692] Psychopharmacology (Berl). 1992;107(2-3):285-9 [1615127] Life Sci. 1993;53(5):415-24 [8336520] Hum Mol Genet. 1994 Jan;3(1):209 [8162032] Proc Natl Acad Sci U S A. 1994 Dec 20;91(26):12912-6 [7809145] Am J Med Genet. 1994 Sep 1;52(3):308-14 [7810562] J Neuroimmunol. 1995 Jul;60(1-2):1-8 [7642739] JAMA. 2004 Dec 22;292(24):2977-83 [15613665] BMJ. 2005 Feb 5;330(7486):277 [15681570] Chest. 2005 Jul;128(1):452-62 [16002972] Environ Health Perspect. 2006 Aug;114(8):1293-6 [16882542] Am J Prev Med. 2007 Jun;32(6):542-3 [17533072] Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1260-5 [17548694] Cancer Causes Control. 2007 Sep;18(7):705-11 [17562193] Behav Brain Res. 2014 May 15;265:163-70 [24583058] Int J Cancer. 2007 Dec 1;121(11):2373-80 [17893866] Hum Genet. 2008 Mar;123(2):133-40 [18092181] PLoS Genet. 2007 Nov;3(11):e207 [18039032] Nature. 2008 Apr 3;452(7187):633-7 [18385738] Nature. 2008 Apr 3;452(7187):638-42 [18385739] Nat Genet. 2008 May;40(5):616-22 [18385676] Int J Cancer. 2008 Aug 1;123(3):511-8 [18470912] Nat Genet. 2008 Dec;40(12):1404-6 [18978790] PLoS One. 2009;4(2):e4653 [19247474] Biol Psychiatry. 2009 Apr 15;65(8):702-5 [19135651] Cancer Epidemiol Biomarkers Prev. 2009 Apr;18(4):1050-9 [19318430] Am J Respir Crit Care Med. 2009 Sep 1;180(5):462-7 [19498054] Nat Rev Genet. 2009 Oct;10(10):704-14 [19763153] Epidemiology. 2009 Nov;20(6):863-71 [19806059] PLoS One. 2009;4(11):e7951 [19956740] Cancer Epidemiol Biomarkers Prev. 2009 Dec;18(12):3375-83 [19959685] J Thorac Oncol. 2009 Oct;4(10):1195-201 [19641473] Nat Genet. 2010 May;42(5):441-7 [20418890] Nat Rev Cancer. 2010 Jun;10(6):389-402 [20495573] Ann Hum Genet. 2010 Jul;74(4):291-8 [20456319] PLoS Genet. 2010 Aug;6(8). pii: e1001051. doi: 10.1371/journal.pgen.1001051 [20700438] Eur J Epidemiol. 2011 Jun;26(6):433-8 [21344323] J Natl Cancer Inst. 2011 Sep 7;103(17):1342-6 [21747048] Int J Cancer. 2012 Mar 1;130(5):1001-10 [21484788] Cancer Discov. 2011 Oct;1(5):420-9 [22586632] Cell. 2012 Jun 8;149(6):1284-97 [22632761] Nat Genet. 2012 Dec;44(12):1330-5 [23143601] Clin Biochem. 2013 Jul;46(10-11):918-25 [23396164] Synapse. 2013 Sep;67(9):545-52 [23447334] Cancer Discov. 2013 Dec;3(12):1364-77 [24078773] BMC Cancer. 2013;13:607 [24369748] Int Immunopharmacol. 2001 Jul;1(7):1363-74 [11460316] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1940-6207.CAPR-14-0158 ER - TY - JOUR T1 - Research Resource: STR DNA profile and gene expression comparisons of human BG-1 cells and a BG-1/MCF-7 clonal variant. AN - 1629963814; 25321415 AB - Human ovarian cancer BG-1 cells are a valuable in vitro model that has enabled several laboratories to study the estrogenic responses of ovarian cancers. We recently discovered that there are two different BG-1 cell lines being used for experiments, denoted here as BG-1 FR and BG-1 NIEHS, which exhibit striking morphological differences. The objective of this study was to methodically analyze these two BG-1 variants and compare their characteristics. Short tandem repeat analysis revealed that the DNA profile of BG-1 FR cells was unique, yet the Short tandem repeat pattern of BG-1 NIEHS was identical with that of MCF-7 cells. From a cytogenetic analysis, it became apparent that the BG-1 FR line had the same profile as previously reported, whereas the BG-1 NIEHS and MCF-7 cells share a similar genetic display. A significant number of unique chromosomal translocations were observed between the BG-1 NIEHS and MCF-7 cells, suggesting that acquired genotypic differences resulted in the formation of two lines from a common origin. Although all cell types demonstrated a similar estrogen responsiveness in reporter gene assays, a microarray analysis revealed distinct estrogen-responsive gene expression patterns with surprisingly moderate to low overlap. We conclude that BG-1 FR is the original ovarian cancer cell line, whereas the BG-1 NIEHS is a variant from the MCF-7 cells. These findings provide much needed clarification of the identities and characteristics of key cell line models that are widely used to study estrogen action in female reproductive cancers. JF - Molecular endocrinology (Baltimore, Md.) AU - Li, Yin AU - Arao, Yukitomo AU - Hall, Julie M AU - Burkett, Sandra AU - Liu, Liwen AU - Gerrish, Kevin AU - Cavailles, Vincent AU - Korach, Kenneth S AD - Laboratory of Reproductive and Developmental Toxicology (Y.L., Y.A., K.S.K.) and Molecular Genomics Core Facility (L.L., K.G.), National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709; College of Pharmacy and Health Sciences (J.M.H.), Campbell University, Buies Creek, North Carolina 27506; Center for Cancer Research (S.B.), National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702; and Institut de Recherche en Cancérologie de Montpellier (V.C.), Institut de Recherche en Cancerologie de Montpellier and INSERM Unité 896, Universite Montpellier1, F-34298 Montpellier, France. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 2072 EP - 2081 VL - 28 IS - 12 KW - Receptors, Estrogen KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Genotype KW - Translocation, Genetic -- genetics KW - Receptors, Estrogen -- genetics KW - Humans KW - Cell Line, Tumor KW - Female KW - Ovarian Neoplasms -- genetics KW - DNA -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629963814?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Research+Resource%3A+STR+DNA+profile+and+gene+expression+comparisons+of+human+BG-1+cells+and+a+BG-1%2FMCF-7+clonal+variant.&rft.au=Li%2C+Yin%3BArao%2C+Yukitomo%3BHall%2C+Julie+M%3BBurkett%2C+Sandra%3BLiu%2C+Liwen%3BGerrish%2C+Kevin%3BCavailles%2C+Vincent%3BKorach%2C+Kenneth+S&rft.aulast=Li&rft.aufirst=Yin&rft.date=2014-12-01&rft.volume=28&rft.issue=12&rft.spage=2072&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=1944-9917&rft_id=info:doi/10.1210%2Fme.2014-1229 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-01 N1 - Date created - 2014-12-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Pathol. 1998 Nov;153(5):1579-88 [9811350] J Soc Gynecol Investig. 2000 Jan-Feb;7(1 Suppl):S33-7 [10732327] Carcinogenesis. 1998 Nov;19(11):1895-900 [9854999] Endocrinology. 2005 Feb;146(2):760-8 [15528301] Obstet Gynecol. 2000 Sep;96(3):417-21 [10960636] Annu Rev Physiol. 2001;63:165-92 [11181953] Breast Cancer Res. 2000;2(2):139-48 [11056686] Proc Natl Acad Sci U S A. 2001 Jul 3;98(14):8012-7 [11416159] Physiol Rev. 2001 Oct;81(4):1535-65 [11581496] Int J Oncol. 2002 Mar;20(3):489-94 [11836559] Oncogene. 2002 Feb 7;21(7):1097-107 [11850827] Mol Endocrinol. 2002 Mar;16(3):469-86 [11875105] Science. 2002 May 31;296(5573):1642-4 [12040178] Br J Cancer. 2003 Mar 24;88(6):871-8 [12644824] Mol Endocrinol. 2003 May;17(5):792-803 [12586845] Br J Cancer. 2003 Dec;89 Suppl 3:S3-8 [14661040] Mol Endocrinol. 2004 Aug;18(8):1859-75 [15031323] Nucleic Acids Res. 1982 Dec 20;10(24):7895-903 [6897676] Science. 1988 Aug 5;241(4866):705-8 [3041593] Cancer. 1989 Jan 15;63(2):280-8 [2910432] Proc Natl Acad Sci U S A. 1989 Feb;86(4):1218-22 [2919170] J Clin Endocrinol Metab. 1992 Dec;75(6):1497-502 [1464654] Proc Natl Acad Sci U S A. 1993 Dec 1;90(23):11162-6 [8248223] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):316-20 [8552629] Science. 1996 Jul 26;273(5274):494-7 [8662537] Mol Endocrinol. 1997 Mar;11(3):353-65 [9058381] Endocrinology. 1997 Nov;138(11):4613-21 [9348186] Int J Cancer. 1998 Feb 9;75(4):654-8 [9466671] J Clin Endocrinol Metab. 1998 Mar;83(3):1025-8 [9506768] J Steroid Biochem Mol Biol. 2012 Oct;132(1-2):176-85 [22652558] Gynecol Oncol. 2012 Oct;127(1):241-8 [22710073] Steroids. 2013 Jun;78(6):530-7 [23402742] Mol Carcinog. 2013 Sep;52(9):715-25 [22549810] Mol Endocrinol. 2013 Sep;27(9):1429-41 [23885094] J Steroid Biochem Mol Biol. 2005 Jan;93(1):15-24 [15748828] Breast Cancer Res Treat. 2005 Jul;92(2):141-9 [15986123] Endocrinology. 2005 Aug;146(8):3247-62 [15831568] Oncogene. 2005 Jul 21;24(31):4894-907 [15870696] Mol Interv. 2005 Dec;5(6):343-57 [16394250] FASEB J. 2006 Feb;20(2):240-50 [16449796] Environ Health Perspect. 2009 Nov;117(11):1702-6 [20049119] J Endocrinol. 2010 Apr;205(1):15-23 [20019181] Nat Rev Cancer. 2010 Jun;10(6):441-8 [20448633] J Steroid Biochem Mol Biol. 2012 Feb;128(3-5):98-106 [22138011] Mol Med Rep. 2012 Jul;6(1):151-6 [22552626] Cancer Res. 1998 Dec 1;58(23):5367-73 [9850067] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/me.2014-1229 ER - TY - JOUR T1 - ATR inhibitors VE-821 and VX-970 sensitize cancer cells to topoisomerase i inhibitors by disabling DNA replication initiation and fork elongation responses. AN - 1629963582; 25269479 AB - Camptothecin and its derivatives, topotecan and irinotecan, are specific topoisomerase I (Top1) inhibitors and potent anticancer drugs killing cancer cells by producing replication-associated DNA double-strand breaks, and the indenoisoquinoline LMP-400 (indotecan) is a novel Top1 inhibitor in clinical trial. To develop novel drug combinations, we conducted a synthetic lethal siRNA screen using a library that targets nearly 7,000 human genes. Depletion of ATR, the main transducer of replication stress, came as a top candidate gene for camptothecin synthetic lethality. Validation studies using ATR siRNA and the ATR inhibitor VE-821 confirmed marked antiproliferative synergy with camptothecin and even greater synergy with LMP-400. Single-cell analyses and DNA fiber combing assays showed that VE-821 abrogates the S-phase replication elongation checkpoint and the replication origin-firing checkpoint induced by camptothecin and LMP-400. As expected, the combination of Top1 inhibitors with VE-821 inhibited the phosphorylation of ATR and Chk1; however, it strongly induced γH2AX. In cells treated with the combination, the γH2AX pattern changed over time from the well-defined Top1-induced damage foci to an intense peripheral and diffuse nuclear staining, which could be used as response biomarker. Finally, the clinical derivative of VE-821, VX-970, enhanced the in vivo tumor response to irinotecan without additional toxicity. A key implication of our work is the mechanistic rationale and proof of principle it provides to evaluate the combination of Top1 inhibitors with ATR inhibitors in clinical trials. ©2014 American Association for Cancer Research. JF - Cancer research AU - Jossé, Rozenn AU - Martin, Scott E AU - Guha, Rajarshi AU - Ormanoglu, Pinar AU - Pfister, Thomas D AU - Reaper, Philip M AU - Barnes, Christopher S AU - Jones, Julie AU - Charlton, Peter AU - Pollard, John R AU - Morris, Joel AU - Doroshow, James H AU - Pommier, Yves AD - Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland. ; Division of Pre-Clinical Innovation, National Center for Advancing Translational Sciences (NCATS), NIH, Rockville, Maryland. ; Laboratory of Human Toxicology and Pharmacology, Applied/Developmental Research Directorate, Leidos Biomedical Research, Inc, National Laboratory for Cancer Research, Frederick, Maryland. ; Vertex Pharmaceuticals (Europe) Ltd, Abingdon, Oxfordshire, United Kingdom. ; Drug Synthesis and Chemistry Branch, Division of Cancer Treatment, Division of Cancer Treatment and Diagnosis (DTP-DCTD), NCI-NIH, Bethesda, Maryland. ; Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland. Drug Synthesis and Chemistry Branch, Division of Cancer Treatment, Division of Cancer Treatment and Diagnosis (DTP-DCTD), NCI-NIH, Bethesda, Maryland. ; Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland. pommier@nih.gov. Y1 - 2014/12/01/ PY - 2014 DA - 2014 Dec 01 SP - 6968 EP - 6979 VL - 74 IS - 23 KW - 3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide KW - 0 KW - H2AFX protein, human KW - Histones KW - Organothiophosphorus Compounds KW - Pyrazines KW - Sulfones KW - Topoisomerase I Inhibitors KW - irinotecan KW - 0H43101T0J KW - Topotecan KW - 7M7YKX2N15 KW - VX KW - 9A4381183B KW - Protein Kinases KW - EC 2.7.- KW - ATR protein, human KW - EC 2.7.11.1 KW - Ataxia Telangiectasia Mutated Proteins KW - CHEK1 protein, human KW - Checkpoint Kinase 1 KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - TOP1 protein, human KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Camptothecin -- pharmacology KW - DNA Damage KW - Humans KW - Ataxia Telangiectasia Mutated Proteins -- metabolism KW - Cell Line, Tumor KW - Ataxia Telangiectasia Mutated Proteins -- antagonists & inhibitors KW - Phosphorylation -- drug effects KW - Protein Kinases -- metabolism KW - Single-Cell Analysis -- methods KW - Topotecan -- pharmacology KW - Histones -- metabolism KW - Protein Kinases -- genetics KW - Camptothecin -- analogs & derivatives KW - HT29 Cells KW - Histones -- genetics KW - Topoisomerase I Inhibitors -- pharmacology KW - Sulfones -- pharmacology KW - Replication Origin -- drug effects KW - Pyrazines -- pharmacology KW - Organothiophosphorus Compounds -- pharmacology KW - DNA Topoisomerases, Type I -- metabolism KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629963582?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=ATR+inhibitors+VE-821+and+VX-970+sensitize+cancer+cells+to+topoisomerase+i+inhibitors+by+disabling+DNA+replication+initiation+and+fork+elongation+responses.&rft.au=Joss%C3%A9%2C+Rozenn%3BMartin%2C+Scott+E%3BGuha%2C+Rajarshi%3BOrmanoglu%2C+Pinar%3BPfister%2C+Thomas+D%3BReaper%2C+Philip+M%3BBarnes%2C+Christopher+S%3BJones%2C+Julie%3BCharlton%2C+Peter%3BPollard%2C+John+R%3BMorris%2C+Joel%3BDoroshow%2C+James+H%3BPommier%2C+Yves&rft.aulast=Joss%C3%A9&rft.aufirst=Rozenn&rft.date=2014-12-01&rft.volume=74&rft.issue=23&rft.spage=6968&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-13-3369 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-04 N1 - Date created - 2014-12-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Chem Biol. 2010 May 28;17(5):421-33 [20534341] Cancer Res. 2010 Jan 15;70(2):440-6 [20068163] Adv Cancer Res. 2010;108:73-112 [21034966] Clin Cancer Res. 2010 Nov 15;16(22):5447-57 [20924131] PLoS One. 2010;5(11):e15544 [21124906] Cancer Res. 2010 Dec 1;70(23):9693-702 [21098704] Mol Cancer Ther. 2009 May;8(5):1008-14 [19383846] J Med Chem. 2011 Apr 14;54(7):2320-30 [21413798] Biochem J. 2011 Jun 15;436(3):527-36 [21615334] Nat Struct Mol Biol. 2011 Jun;18(6):721-7 [21552262] Nat Chem Biol. 2011 Jul;7(7):428-30 [21490603] Mol Cell. 2011 Jul 22;43(2):192-202 [21777809] Br J Cancer. 2011 Jul 26;105(3):372-81 [21730979] J Biol Chem. 2011 Aug 19;286(33):28707-14 [21705319] Nat Struct Mol Biol. 2011 Dec;18(12):1331-5 [22120667] Curr Cancer Drug Targets. 2011 Oct;11(8):976-86 [21834757] Cancer Res. 2012 Feb 15;72(4):979-89 [22189968] Br J Cancer. 2012 Jul 10;107(2):291-9 [22713662] Cancer Biol Ther. 2012 Sep;13(11):1072-81 [22825331] Cell Death Dis. 2012;3:e441 [23222511] ACS Chem Biol. 2013 Jan 18;8(1):82-95 [23259582] Cell Cycle. 2013 May 15;12(10):1501-9 [23598718] Cancer Res. 2013 Jun 15;73(12):3683-91 [23548269] Nat Cell Biol. 2014 Jan;16(1):2-9 [24366029] Oncotarget. 2014 Jul 30;5(14):5674-85 [25010037] Cytometry A. 2013 Oct;83(10):913-24 [23846844] J Biol Chem. 2002 Feb 8;277(6):4428-34 [11711532] Cancer Res. 1988 Apr 1;48(7):1722-6 [2832051] Blood. 1995 Sep 1;86(5):1903-10 [7655019] Cancer Res. 1997 Sep 15;57(18):4029-35 [9307289] EMBO J. 1999 Mar 1;18(5):1397-406 [10064605] Cell Cycle. 2006 Jul;5(14):1496-8 [16861888] Nat Rev Cancer. 2006 Oct;6(10):789-802 [16990856] Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):591-602 [17255282] Oncogene. 2007 May 14;26(22):3214-26 [17496917] Mol Cell Biol. 2007 Aug;27(16):5806-18 [17515603] Nat Methods. 2007 Oct;4(10):847-9 [17828270] Cancer Res. 2007 Nov 1;67(21):10397-405 [17974983] Cell Cycle. 2007 Nov 15;6(22):2760-7 [17986860] Mol Cancer Ther. 2008 Sep;7(9):2955-66 [18790776] Nat Rev Cancer. 2008 Dec;8(12):957-67 [19005492] Mol Cell Biol. 2009 Jan;29(1):68-82 [18955500] Nucleic Acids Res. 2009 Jan;37(Database issue):D412-6 [18940858] Clin Cancer Res. 2008 Dec 15;14(24):8132-42 [19088028] Nat Cell Biol. 2009 Feb;11(2):123-32 [19136968] J Biol Chem. 2009 Feb 27;284(9):5994-6003 [19049966] Apoptosis. 2009 Apr;14(4):584-96 [19156528] EMBO Rep. 2009 Aug;10(8):887-93 [19557000] Nature. 2009 Oct 22;461(7267):1071-8 [19847258] Cancer Chemother Pharmacol. 2010 Nov;66(6):1079-85 [20165849] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/0008-5472.CAN-13-3369 ER - TY - JOUR T1 - An open-label phase Ib dose-escalation study of TRC105 (anti-endoglin antibody) with bevacizumab in patients with advanced cancer. AN - 1629961331; 25261556 AB - Endoglin, an endothelial cell membrane receptor expressed on angiogenic tumor vessels, is essential for angiogenesis and upregulated in the setting of VEGF inhibition. TRC105 is an anti-endoglin IgG1 monoclonal antibody that potentiates VEGF inhibitors in preclinical models. This study assessed safety, pharmacokinetics, and antitumor activity of TRC105 in combination with bevacizumab. Patients (n = 38) with advanced solid tumors, Eastern Cooperative Group performance status 0-1, and normal organ function were treated with escalating doses of TRC105 plus bevacizumab until disease progression or unacceptable toxicity using a standard 3 + 3 phase I design. TRC105 and bevacizumab were well tolerated at their recommended single-agent doses (10 mg/kg) when the initial dose of TRC105 was delayed by one week and divided over 2 days to limit the frequency of headache. The concurrent administration of bevacizumab and TRC105 did not otherwise potentiate known toxicities of TRC105 or bevacizumab. Hypertension and proteinuria were observed, though not at rates expected for single-agent bevacizumab. Several patients who had previously progressed on bevacizumab or VEGF receptor tyrosine kinase inhibitor (VEGFR TKI) treatment experienced reductions in tumor volume, including two partial responses by RECIST, and 6 remained without progression for longer periods than during their prior VEGF inhibitor therapy. TRC105 was well tolerated with bevacizumab and clinical activity was observed in a VEGF inhibitor-refractory population. Ongoing clinical trials are testing TRC105 in combination with bevacizumab in glioblastoma and with VEGFR TKIs in renal cell carcinoma, hepatocellular carcinoma, and soft tissue sarcoma. ©2014 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Gordon, Michael S AU - Robert, Francisco AU - Matei, Daniela AU - Mendelson, David S AU - Goldman, Jonathan W AU - Chiorean, E Gabriela AU - Strother, Robert M AU - Seon, Ben K AU - Figg, William D AU - Peer, Cody J AU - Alvarez, Delia AU - Adams, Bonne J AU - Theuer, Charles P AU - Rosen, Lee S AD - Pinnacle Oncology Hematology, Scottsdale, Arizona. mgordon@azpoh.com. ; University of Alabama, Birmingham, Alabama. ; Indiana University School of Medicine, Indianapolis, Indiana. ; Pinnacle Oncology Hematology, Scottsdale, Arizona. ; UCLA Department of Medicine, Los Angeles, California. ; Indiana University School of Medicine, Indianapolis, Indiana. University of Washington, Seattle, Washington. ; Roswell Park Cancer Institute, Buffalo, New York. ; Clinical Pharmacology Program, National Cancer Institute, Bethesda, Maryland. ; TRACON Pharmaceuticals, San Diego, California. Y1 - 2014/12/01/ PY - 2014 DA - 2014 Dec 01 SP - 5918 EP - 5926 VL - 20 IS - 23 SN - 1078-0432, 1078-0432 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Monoclonal, Humanized KW - TRC105 KW - Bevacizumab KW - 2S9ZZM9Q9V KW - Index Medicus KW - Antibodies, Monoclonal, Humanized -- pharmacokinetics KW - Neoplasm Staging KW - Antibodies, Monoclonal -- pharmacokinetics KW - Aged, 80 and over KW - Humans KW - Adult KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Maximum Tolerated Dose KW - Antibodies, Monoclonal, Humanized -- administration & dosage KW - Male KW - Female KW - Antibodies, Monoclonal -- administration & dosage KW - Neoplasms -- drug therapy KW - Neoplasms -- diagnosis KW - Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629961331?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=An+open-label+phase+Ib+dose-escalation+study+of+TRC105+%28anti-endoglin+antibody%29+with+bevacizumab+in+patients+with+advanced+cancer.&rft.au=Gordon%2C+Michael+S%3BRobert%2C+Francisco%3BMatei%2C+Daniela%3BMendelson%2C+David+S%3BGoldman%2C+Jonathan+W%3BChiorean%2C+E+Gabriela%3BStrother%2C+Robert+M%3BSeon%2C+Ben+K%3BFigg%2C+William+D%3BPeer%2C+Cody+J%3BAlvarez%2C+Delia%3BAdams%2C+Bonne+J%3BTheuer%2C+Charles+P%3BRosen%2C+Lee+S&rft.aulast=Gordon&rft.aufirst=Michael&rft.date=2014-12-01&rft.volume=20&rft.issue=23&rft.spage=5918&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-1143 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-28 N1 - Date created - 2014-12-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Cancer Res. 2008 Apr 1;14(7):1931-7 [18381930] Curr Oncol Rep. 2014 Feb;16(2):365 [24445497] Nat Rev Cancer. 2008 Aug;8(8):592-603 [18650835] Gynecol Oncol. 2009 Mar;112(3):469-74 [19135712] Cancer Cell. 2009 Mar 3;15(3):220-31 [19249680] Bull Cancer. 2000 Dec;87(12):881-6 [11174117] J Biol Chem. 2002 Nov 15;277(46):43799-808 [12228247] FASEB J. 2003 Jun;17(9):984-92 [12773481] Br J Cancer. 2003 May 6;88(9):1424-31 [12778073] Clin Cancer Res. 2003 Sep 15;9(11):4221-6 [14519649] N Engl J Med. 2004 Jun 3;350(23):2335-42 [15175435] Cancer Res. 2004 Jul 1;64(13):4601-10 [15231672] Cancer Res. 1999 Feb 15;59(4):856-61 [10029075] Science. 1999 May 28;284(5419):1534-7 [10348742] J Clin Oncol. 2005 Feb 1;23(4):792-9 [15681523] Hum Pathol. 2005 Sep;36(9):955-61 [16153457] Neuropathology. 2005 Sep;25(3):201-6 [16193836] Cancer Immunol Immunother. 2006 Feb;55(2):140-50 [15856228] Curr Pharm Des. 2006;12(10):1173-93 [16611099] Acta Otolaryngol. 2006 Jun;126(6):633-9 [16720449] Virchows Arch. 2006 Jun;448(6):768-75 [16612622] BMC Cancer. 2006;6:110 [16650286] Hum Pathol. 2006 Jul;37(7):861-6 [16784986] Int J Gynecol Cancer. 2006 Sep-Oct;16(5):1789-93 [17009973] Gynecol Oncol. 2006 Dec;103(3):1007-11 [16854456] N Engl J Med. 2006 Dec 14;355(24):2542-50 [17167137] Am J Clin Pathol. 2007 Apr;127(4):572-9 [17369132] J Clin Oncol. 2007 May 1;25(13):1753-9 [17470865] J Clin Oncol. 2007 Oct 10;25(29):4536-41 [17876014] J Clin Oncol. 2009 Oct 1;27(28):4733-40 [19720927] J Clin Oncol. 2010 May 1;28(13):2144-50 [20368553] Curr Drug Deliv. 2011 Jan;8(1):135-43 [21034418] Cell. 2011 Sep 16;146(6):873-87 [21925313] Cancer Discov. 2012 Mar;2(3):270-87 [22585997] Clin Cancer Res. 2012 Sep 1;18(17):4820-9 [22767667] PLoS One. 2012;7(12):e50920 [23300529] J Exp Med. 2013 Mar 11;210(3):563-79 [23401487] Cancer Epidemiol Biomarkers Prev. 2014 Jan;23(1):117-25 [24192008] N Engl J Med. 2008 Jul 24;359(4):378-90 [18650514] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-1143 ER - TY - JOUR T1 - A3 adenosine receptor agonist prevents the development of paclitaxel-induced neuropathic pain by modulating spinal glial-restricted redox-dependent signaling pathways. AN - 1629588824; 25242567 AB - Chemotherapy-induced peripheral neuropathy accompanied by chronic neuropathic pain is the major dose-limiting toxicity of several anticancer agents including the taxane paclitaxel (Taxol). A critical mechanism underlying paclitaxel-induced neuropathic pain is the increased production of peroxynitrite in spinal cord generated in response to activation of the superoxide-generating enzyme, NADPH oxidase. Peroxynitrite in turn contributes to the development of neuropathic pain by modulating several redox-dependent events in spinal cord. We recently reported that activation of the Gi/Gq-coupled A3 adenosine receptor (A3AR) with selective A3AR agonists (ie, IB-MECA) blocked the development of chemotherapy induced-neuropathic pain evoked by distinct agents, including paclitaxel, without interfering with anticancer effects. The mechanism or mechanisms of action underlying these beneficial effects has yet to be explored. We now demonstrate that IB-MECA attenuates the development of paclitaxel-induced neuropathic pain by inhibiting the activation of spinal NADPH oxidase and two downstream redox-dependent systems. The first relies on inhibition of the redox-sensitive transcription factor (NFκB) and mitogen activated protein kinases (ERK and p38) resulting in decreased production of neuroexcitatory/proinflammatory cytokines (TNF-α, IL-1β) and increased formation of the neuroprotective/anti-inflammatory IL-10. The second involves inhibition of redox-mediated posttranslational tyrosine nitration and modification (inactivation) of glia-restricted proteins known to play key roles in regulating synaptic glutamate homeostasis: the glutamate transporter GLT-1 and glutamine synthetase. Our results unravel a mechanistic link into biomolecular signaling pathways employed by A3AR activation in neuropathic pain while providing the foundation to consider use of A3AR agonists as therapeutic agents in patients with chemotherapy-induced peripheral neuropathy. Copyright © 2014 International Association for the Study of Pain. All rights reserved. JF - Pain AU - Janes, Kali AU - Esposito, Emanuela AU - Doyle, Timothy AU - Cuzzocrea, Salvatore AU - Tosh, Dillip K AU - Jacobson, Kenneth A AU - Salvemini, Daniela AD - Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, 1402 South Grand Blvd, St Louis, MO 63104, USA. ; Department of Clinical and Experimental Medicine and Pharmacology, University of Messina, Messina 98122, Italy. ; Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0810, USA. ; Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, 1402 South Grand Blvd, St Louis, MO 63104, USA. Electronic address: salvemd@slu.edu. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 2560 EP - 2567 VL - 155 IS - 12 KW - Adenosine A3 Receptor Agonists KW - 0 KW - Antineoplastic Agents, Phytogenic KW - Cytokines KW - Excitatory Amino Acid Transporter 2 KW - NF-kappa B KW - Slc1a2 protein, rat KW - Tumor Necrosis Factor-alpha KW - N(6)-(3-iodobenzyl)-5'-N-methylcarboxamidoadenosine KW - 152918-18-8 KW - NADP KW - 53-59-8 KW - Adenosine KW - K72T3FS567 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Neuropathic pain KW - A3 KW - Spinal cord KW - Neuroinflammation KW - Chemotherapy-induced peripheral neuropathy KW - Excitatory Amino Acid Transporter 2 -- metabolism KW - Animals KW - Hyperalgesia -- etiology KW - Adenosine -- analogs & derivatives KW - Disease Models, Animal KW - NADP -- metabolism KW - Cytokines -- metabolism KW - Adenosine -- therapeutic use KW - Rats KW - Oxidation-Reduction KW - Neuroglia -- metabolism KW - Rats, Sprague-Dawley KW - Antineoplastic Agents, Phytogenic -- toxicity KW - Paclitaxel -- toxicity KW - Excitatory Amino Acid Transporter 2 -- genetics KW - Male KW - Neuralgia -- physiopathology KW - Spinal Cord -- metabolism KW - Adenosine A3 Receptor Agonists -- therapeutic use KW - Signal Transduction -- drug effects KW - Spinal Cord -- pathology KW - Neuralgia -- chemically induced KW - Neuralgia -- pathology KW - Neuralgia -- prevention & control KW - NF-kappa B -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629588824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pain&rft.atitle=A3+adenosine+receptor+agonist+prevents+the+development+of+paclitaxel-induced+neuropathic+pain+by+modulating+spinal+glial-restricted+redox-dependent+signaling+pathways.&rft.au=Janes%2C+Kali%3BEsposito%2C+Emanuela%3BDoyle%2C+Timothy%3BCuzzocrea%2C+Salvatore%3BTosh%2C+Dillip+K%3BJacobson%2C+Kenneth+A%3BSalvemini%2C+Daniela&rft.aulast=Janes&rft.aufirst=Kali&rft.date=2014-12-01&rft.volume=155&rft.issue=12&rft.spage=2560&rft.isbn=&rft.btitle=&rft.title=Pain&rft.issn=1872-6623&rft_id=info:doi/10.1016%2Fj.pain.2014.09.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-15 N1 - Date created - 2014-12-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochem Pharmacol. 2010 Jan 15;79(2):180-7 [19686702] Neurochem Int. 2010 Jan;56(1):35-41 [19723551] Free Radic Res. 2010 Jun;44(6):694-709 [20370565] Neurologia. 2010 Mar;25(2):116-31 [20487712] J Neurosci. 2010 Nov 17;30(46):15400-8 [21084596] Neuroreport. 2010 Sep 15;21(13):892-6 [21150487] Curr Opin Support Palliat Care. 2011 Mar;5(1):1-7 [21192267] Pharmacol Rev. 2011 Mar;63(1):1-34 [21303899] Free Radic Biol Med. 2011 Sep 1;51(5):951-66 [21277369] Free Radic Biol Med. 2011 Oct 1;51(7):1289-301 [21777669] J Pain. 2012 Mar;13(3):293-303 [22285612] J Neurochem. 2006 Jul;98(2):566-75 [16805847] Drug Discov Today. 2012 Apr;17(7-8):359-66 [22033198] J Neurochem. 2012 Apr;121(2):287-301 [22243365] FASEB J. 2012 May;26(5):1855-65 [22345405] J Neurosci. 2012 May 2;32(18):6149-60 [22553021] J Biol Chem. 2013 Feb 1;288(5):3070-84 [23250749] Brain Res Bull. 2013 Jun;95:21-7 [23562605] Neuroscience. 2013 Sep 5;247:201-12 [23707800] Toxicol Appl Pharmacol. 2013 Sep 1;271(2):239-48 [23707771] Neuroscience. 2013 Dec 19;254:301-11 [24070631] Nat Rev Neurol. 2014 Jun;10(6):326-36 [24840972] J Pain. 2014 Jul;15(7):712-25 [24755282] J Biol Chem. 2014 Jul 25;289(30):21082-97 [24876379] Free Radic Res. 2001 Apr;34(4):325-36 [11328670] FASEB J. 2001 Sep;15(11):1886-94 [11532968] Prog Brain Res. 2001;132:267-86 [11544995] Pain. 2001 Dec;94(3):293-304 [11731066] J Biol Chem. 2002 Apr 26;277(17):15021-7 [11839754] Neurochem Int. 2002 Aug-Sep;41(2-3):123-42 [12020613] Anticancer Drugs. 2002 Jun;13(5):437-43 [12045454] J Neurochem. 2002 Sep;82(5):1179-91 [12358765] Eur J Neurosci. 2003 May;17(10):2106-18 [12786977] Diabetes. 2003 Oct;52(10):2603-14 [14514646] Glia. 2004 May;46(4):410-8 [15095371] J Immunol. 2004 Sep 15;173(6):3589-93 [15356101] Annu Rev Pharmacol Toxicol. 1980;20:441-62 [7387124] Nature. 1992 Dec 3;360(6403):467-71 [1280334] Proc Natl Acad Sci U S A. 1993 Nov 1;90(21):10086-90 [8234260] Neuron. 1994 Sep;13(3):713-25 [7917301] J Biol Chem. 1996 Mar 15;271(11):5976-9 [8626378] J Neurosci. 1996 Oct 1;16(19):6125-33 [8815895] J Immunol. 1996 Nov 15;157(10):4634-40 [8906843] Neuroreport. 1996 Sep 2;7(13):2181-5 [8930985] Trends Pharmacol Sci. 1998 May;19(5):184-91 [9652191] J Neurosci. 1998 Aug 15;18(16):6138-46 [9698308] Arch Biochem Biophys. 1999 Jun 1;366(1):82-8 [10334867] Arch Int Pharmacodyn Ther. 1957 Sep 1;111(4):409-19 [13471093] Oncogene. 2005 Jan 20;24(4):672-9 [15580312] Nat Rev Mol Cell Biol. 2005 Feb;6(2):150-66 [15688001] Arch Biochem Biophys. 2005 Apr 1;436(1):136-44 [15752718] FEBS Lett. 2007 Jan 9;581(1):84-90 [17174954] Physiol Rev. 2007 Jan;87(1):245-313 [17237347] Brain Behav Immun. 2007 Jul;21(5):686-98 [17174526] J Clin Invest. 2007 Nov;117(11):3530-9 [17975673] Exp Mol Med. 2007 Dec 31;39(6):812-9 [18160852] Neuropharmacology. 2009 Jan;56(1):254-63 [18793655] FASEB J. 2009 Apr;23(4):1011-22 [19028840] Handb Exp Pharmacol. 2009;(193):399-441 [19639290] Neoplasia. 2009 Nov;11(11):1132-45 [19881949] Trends Pharmacol Sci. 2009 Nov;30(11):581-91 [19762094] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.pain.2014.09.016 ER - TY - JOUR T1 - Gene expression profiles of NO- and HNO-donor treated breast cancer cells: insights into tumor response and resistance pathways. AN - 1629588671; 25153034 AB - Nitric oxide (NO) synthase 2 (NOS2), a major inflammatory protein, modulates disease progression via NO in a number of pathologies, including cancer. The role of NOS2-derived NO is not only flux-dependent, which is higher in mouse vs human cells, but also varies based on spatial and temporal distribution both within tumor cells and in the tumor microenvironment. NO donors have been utilized to mimic NO flux conditions and to investigate the effects of varied NO concentrations. As a wide range of effects mediated by NO and other nitrogen oxides such as nitroxyl (HNO) have been elucidated, multiple NO- and HNO-releasing compounds have been developed as potential therapeutics, including as tumor modulators. One of the challenges is to determine differences in biomarker expression from extracellular vs intracellular generation of NO or HNO. Taking advantage of new NO and HNO releasing agents, we have characterized the gene expression profile of estrogen receptor-negative human breast cancer (MDA-MB-231) cells following exposure to aspirin, the NO donor DEA/NO, the HNO donor IPA/NO andtheir intracellularly-activated prodrug conjugates DEA/NO-aspirin and IPA/NO-aspirin. Comparison of the gene expression profiles demonstrated that several genes were uniquely expressed with respect to NO or HNO, such as miR-21, HSP70, cystathionine γ-lyase and IL24. These findings provide insight into targets and pathways that could be therapeutically exploited by the redox related species NO and HNO. Published by Elsevier Inc. JF - Nitric oxide : biology and chemistry AU - Cheng, Robert Y S AU - Basudhar, Debashree AU - Ridnour, Lisa A AU - Heinecke, Julie L AU - Kesarwala, Aparna H AU - Glynn, Sharon AU - Switzer, Christopher H AU - Ambs, Stefan AU - Miranda, Katrina M AU - Wink, David A AD - Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. Electronic address: robert.cheng2@nih.gov. ; Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA; Department of Chemistry, University of Arizona, Tucson, AZ 85721, USA. ; Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. ; Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. ; Prostate Cancer Institute, NUI Galway, Ireland. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. ; Department of Chemistry, University of Arizona, Tucson, AZ 85721, USA. Y1 - 2014/12/01/ PY - 2014 DA - 2014 Dec 01 SP - 17 EP - 28 VL - 43 KW - Nitric Oxide Donors KW - 0 KW - Nitric Oxide KW - 31C4KY9ESH KW - Nitric Oxide Synthase KW - EC 1.14.13.39 KW - Index Medicus KW - Nitroxyl KW - Cell signaling KW - Cancer biology KW - Breast cancer KW - Nitric oxide synthase KW - Nitric oxide KW - Breast Neoplasms -- genetics KW - Gene Expression Profiling KW - Animals KW - Humans KW - Breast Neoplasms -- therapy KW - Mice KW - Cell Line, Tumor KW - Nitric Oxide Synthase -- metabolism KW - Signal Transduction KW - Female KW - Drug Resistance, Neoplasm -- drug effects KW - Nitric Oxide Donors -- pharmacology KW - Nitric Oxide -- pharmacology KW - Gene Expression Regulation, Neoplastic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629588671?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nitric+oxide+%3A+biology+and+chemistry&rft.atitle=Gene+expression+profiles+of+NO-+and+HNO-donor+treated+breast+cancer+cells%3A+insights+into+tumor+response+and+resistance+pathways.&rft.au=Cheng%2C+Robert+Y+S%3BBasudhar%2C+Debashree%3BRidnour%2C+Lisa+A%3BHeinecke%2C+Julie+L%3BKesarwala%2C+Aparna+H%3BGlynn%2C+Sharon%3BSwitzer%2C+Christopher+H%3BAmbs%2C+Stefan%3BMiranda%2C+Katrina+M%3BWink%2C+David+A&rft.aulast=Cheng&rft.aufirst=Robert+Y&rft.date=2014-12-01&rft.volume=43&rft.issue=&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Nitric+oxide+%3A+biology+and+chemistry&rft.issn=1089-8611&rft_id=info:doi/10.1016%2Fj.niox.2014.08.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-01 N1 - Date created - 2014-12-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - 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2013;13:468 [24112473] Ageing Res Rev. 2013 Sep;12(4):1056-68 [23688930] J Med Chem. 2013 Oct 24;56(20):7804-20 [24102516] Biochem Biophys Res Commun. 2014 Jan 17;443(3):802-7 [24342610] Cancer Biol Ther. 2014 Feb;15(2):194-9 [24100579] Proc Natl Acad Sci U S A. 2014 Apr 29;111(17):6323-8 [24733928] FEBS Lett. 2001 Oct 5;506(2):135-9 [11591387] Lancet Oncol. 2001 Mar;2(3):149-56 [11902565] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.niox.2014.08.003 ER - TY - JOUR T1 - Transcriptome analysis of pancreatic cancer reveals a tumor suppressor function for HNF1A. AN - 1629586167; 25233928 AB - Pancreatic ductal adenocarcinoma (PDAC) is driven by the accumulation of somatic mutations, epigenetic modifications and changes in the micro-environment. New approaches to investigating disruptions of gene expression networks promise to uncover key regulators and pathways in carcinogenesis. We performed messenger RNA-sequencing in pancreatic normal (n = 10) and tumor (n = 8) derived tissue samples, as well as in pancreatic cancer cell lines (n = 9), to determine differential gene expression (DE) patterns. Sub-network enrichment analyses identified HNF1A as the regulator of the most significantly and consistently dysregulated expression sub-network in pancreatic tumor tissues and cells (median P = 7.56×10(-7), median rank = 1, range = 1-25). To explore the effects of HNF1A expression in pancreatic tumor-derived cells, we generated stable HNF1A-inducible clones in two pancreatic cancer cell lines (PANC-1 and MIA PaCa-2) and observed growth inhibition (5.3-fold, P = 4.5×10(-5) for MIA PaCa-2 clones; 7.2-fold, P = 2.2×10(-5) for PANC-1 clones), and a G0/G1 cell cycle arrest and apoptosis upon induction. These effects correlated with HNF1A-induced down-regulation of 51 of 84 cell cycle genes (e.g. E2F1, CDK2, CDK4, MCM2/3/4/5, SKP2 and CCND1), decreased expression of anti-apoptotic genes (e.g. BIRC2/5/6 and AKT) and increased expression of pro-apoptotic genes (e.g. CASP4/9/10 and APAF1). In light of the established role of HNF1A in the regulation of pancreatic development and homeostasis, our data suggest that it also functions as an important tumor suppressor in the pancreas. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Hoskins, Jason W AU - Jia, Jinping AU - Flandez, Marta AU - Parikh, Hemang AU - Xiao, Wenming AU - Collins, Irene AU - Emmanuel, Mickey A AU - Ibrahim, Abdisamad AU - Powell, John AU - Zhang, Lizhi AU - Malats, Nuria AU - Bamlet, William R AU - Petersen, Gloria M AU - Real, Francisco X AU - Amundadottir, Laufey T AD - Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA, Epithelial Carcinogenesis Group, CNIO-Spanish National Cancer Research Centre, E-28029 Madrid, Spain, Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute and Bioinformatics and Molecular Analysis Section, Division of Computational Bioscience, Center for Information Technology, National Institutes of Health, Bethesda, MD 20892, USA, Department of Laboratory Medicine and Pathology and Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55905, USA and Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Spain. ; Epithelial Carcinogenesis Group, CNIO-Spanish National Cancer Research Centre, E-28029 Madrid, Spain. ; Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute and. ; Bioinformatics and Molecular Analysis Section, Division of Computational Bioscience, Center for Information Technology, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Laboratory Medicine and Pathology and. ; Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55905, USA and. ; Epithelial Carcinogenesis Group, CNIO-Spanish National Cancer Research Centre, E-28029 Madrid, Spain, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Spain. ; Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA, Epithelial Carcinogenesis Group, CNIO-Spanish National Cancer Research Centre, E-28029 Madrid, Spain, Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute and Bioinformatics and Molecular Analysis Section, Division of Computational Bioscience, Center for Information Technology, National Institutes of Health, Bethesda, MD 20892, USA, Department of Laboratory Medicine and Pathology and Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN 55905, USA and Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Spain amundadottirl@mail.nih.gov. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 2670 EP - 2678 VL - 35 IS - 12 KW - Biomarkers, Tumor KW - 0 KW - HNF1A protein, human KW - Hepatocyte Nuclear Factor 1-alpha KW - RNA, Messenger KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Apoptosis KW - Humans KW - Gene Regulatory Networks KW - Reverse Transcriptase Polymerase Chain Reaction KW - Cell Proliferation KW - RNA, Messenger -- genetics KW - Blotting, Western KW - Cells, Cultured KW - Pancreas -- metabolism KW - Flow Cytometry KW - Cell Cycle KW - Immunoenzyme Techniques KW - Biomarkers, Tumor -- metabolism KW - Gene Expression Profiling KW - Biomarkers, Tumor -- genetics KW - Pancreatic Neoplasms -- pathology KW - Pancreatic Neoplasms -- metabolism KW - Hepatocyte Nuclear Factor 1-alpha -- genetics KW - Hepatocyte Nuclear Factor 1-alpha -- metabolism KW - Genes, Tumor Suppressor KW - Carcinoma, Pancreatic Ductal -- metabolism KW - Carcinoma, Pancreatic Ductal -- pathology KW - Carcinoma, Pancreatic Ductal -- genetics KW - Pancreatic Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629586167?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transcriptome+analysis+of+pancreatic+cancer+reveals+a+tumor+suppressor+function+for+HNF1A.&rft.au=Hoskins%2C+Jason+W%3BJia%2C+Jinping%3BFlandez%2C+Marta%3BParikh%2C+Hemang%3BXiao%2C+Wenming%3BCollins%2C+Irene%3BEmmanuel%2C+Mickey+A%3BIbrahim%2C+Abdisamad%3BPowell%2C+John%3BZhang%2C+Lizhi%3BMalats%2C+Nuria%3BBamlet%2C+William+R%3BPetersen%2C+Gloria+M%3BReal%2C+Francisco+X%3BAmundadottir%2C+Laufey+T&rft.aulast=Hoskins&rft.aufirst=Jason&rft.date=2014-12-01&rft.volume=35&rft.issue=12&rft.spage=2670&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu193 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-14 N1 - Date created - 2014-12-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Exp Nephrol. 1999 Sep-Dec;7(5-6):407-12 [10559638] Nat Genet. 2009 Sep;41(9):986-90 [19648918] Bioinformatics. 2003 Dec 12;19(18):2502-4 [14668247] Science. 2004 Feb 27;303(5662):1378-81 [14988562] Science. 1987 Oct 30;238(4827):688-92 [3499668] Bioinformatics. 2010 Jan 1;26(1):139-40 [19910308] Nat Genet. 2010 Mar;42(3):224-8 [20101243] Development. 2010 May;137(9):1573-82 [20388655] Arch Intern Med. 2010 May 10;170(9):791-802 [20458087] BMC Cancer. 2010;10:379 [20646298] PLoS One. 2010;5(7):e11824 [20686608] Nature. 2010 Oct 28;467(7319):1114-7 [20981102] Cancer Cell. 2011 Jun 14;19(6):728-39 [21665147] Cancer Res. 2011 Jul 1;71(13):4352-8 [21498636] BMC Cancer. 2011;11:427 [21975049] Hepatology. 2011 Dec;54(6):2036-47 [21898499] Mol Carcinog. 2012 Jan;51(1):14-24 [22162228] Nat Genet. 2012 Jan;44(1):62-6 [22158540] Gut. 2012 Mar;61(3):449-58 [21730103] Gastroenterology. 2012 Apr;142(4):730-733.e9 [22226782] Cancer Discov. 2012 Jan;2(1):41-6 [22585167] Ann Oncol. 2012 Jul;23(7):1880-8 [22104574] Gut. 2012 Aug;61(8):1187-96 [21948943] Nat Genet. 2012 Aug;44(8):841-7 [22836096] Carcinogenesis. 2012 Jul;33(7):1384-90 [22523087] Nature. 2012 Nov 15;491(7424):399-405 [23103869] Cancer Causes Control. 2013 Jan;24(1):13-25 [23112111] J Natl Cancer Inst. 2013 Jul 17;105(14):1027-35 [23847240] BMC Med Genomics. 2013;6:33 [24053169] Gut. 2014 Apr;63(4):647-55 [23598351] Cancer Res. 2014 May 15;74(10):2785-95 [24648346] Nature. 2010 Oct 28;467(7319):1109-13 [20981101] Lab Invest. 1994 Sep;71(3):423-31 [7523764] Nature. 2004 Nov 18;432(7015):307-15 [15549092] Diabetes Obes Metab. 2005 Jul;7(4):318-26 [15955117] Genes Dev. 2006 May 15;20(10):1218-49 [16702400] Hum Mutat. 2006 Sep;27(9):854-69 [16917892] Diabetologia. 2006 Dec;49(12):2882-91 [17033837] Cancer Cell. 2007 Mar;11(3):291-302 [17349585] J Bioinform Comput Biol. 2007 Apr;5(2B):429-56 [17636854] Gastroenterology. 2008 Sep;135(3):724-8 [18692502] Science. 2008 Sep 26;321(5897):1801-6 [18772397] Nucleic Acids Res. 2009 Jan;37(Database issue):D674-9 [18832364] Mol Cell Biol. 2009 Jun;29(11):2945-59 [19289501] Nucleic Acids Res. 2009 Jul;37(Web Server issue):W135-40 [19417065] Bioinformatics. 2009 Jul 15;25(14):1754-60 [19451168] Am J Epidemiol. 2009 Aug 15;170(4):403-13 [19561064] Diabetes. 2002 Aug;51(8):2355-62 [12145145] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu193 ER - TY - JOUR T1 - Resveratrol prevents tumorigenesis in mouse model of Kras activated sporadic colorectal cancer by suppressing oncogenic Kras expression. AN - 1629586076; 25280562 AB - Sporadic and non-hereditary mutations account for the majority of colorectal cancers (CRC). After the loss of adenomatous polyposis coli (APC) function and activation of the β-catenin/LEF signaling pathway, activating mutations in Kras are major drivers of sporadic CRC. Preventing the outgrowth of cells that develop sporadic mutations will decrease CRC. Resveratrol, a naturally occurring polyphenolic compound has anti-inflammatory, anti-oxidant and anti-cancer activities. We used a genetically engineered mouse model for sporadic CRC where the APC locus is knocked out and Kras is activated specifically in the distal colon to determine the effects of resveratrol on preventing and treating CRC. Feeding mice a diet supplemented with 150 or 300 ppm resveratrol (105 and 210mg daily human equivalent dose, respectively) before tumors were visible by colonoscopy resulted in a 60% inhibition of tumor production. In the 40% of mice that did develop tumors Kras expression was lost in the tumors. In a therapeutic assay where tumors were allowed to develop prior to treatment, feeding tumor bearing mice with resveratrol resulted in a complete remission in 33% of the mice and a 97% decrease in tumor size in the remaining mice. Analysis of miRNA expression in non-tumoral and tumoral colonic tissue of resveratrol treated mice showed an increased expression of miR-96, a miRNA previously shown to regulate Kras translation. These data indicate that resveratrol can prevent the formation and growth of colorectal tumors by downregulating Kras expression. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Saud, Shakir M AU - Li, Weidong AU - Morris, Nicole L AU - Matter, Matthias S AU - Colburn, Nancy H AU - Kim, Young S AU - Young, Matthew R AD - Nutritional Science Research Group, Division of Cancer Prevention, National Cancer Institute, Rockville, MD, USA, Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick, MD, USA. ; Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick, MD, USA, Oncology Department, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China. ; Laboratory Animal Sciences Program, Leidos Biomedical Research, Inc., Frederick, MD, USA and. ; Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA. ; Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick, MD, USA. ; Nutritional Science Research Group, Division of Cancer Prevention, National Cancer Institute, Rockville, MD, USA. ; Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick, MD, USA, youngma@mail.nih.gov. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 2778 EP - 2786 VL - 35 IS - 12 KW - Adenomatous Polyposis Coli Protein KW - 0 KW - Anticarcinogenic Agents KW - RNA, Messenger KW - Stilbenes KW - Kras2 protein, mouse KW - EC 3.6.5.2 KW - Proto-Oncogene Proteins p21(ras) KW - resveratrol KW - Q369O8926L KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Cell Proliferation -- drug effects KW - Animals KW - Humans KW - Disease Models, Animal KW - Mice KW - Reverse Transcriptase Polymerase Chain Reaction KW - RNA, Messenger -- genetics KW - Mice, Knockout KW - Blotting, Western KW - Tumor Cells, Cultured KW - Mutation -- genetics KW - Female KW - Immunoenzyme Techniques KW - Male KW - Cell Transformation, Neoplastic -- pathology KW - Anticarcinogenic Agents -- therapeutic use KW - Colorectal Neoplasms -- pathology KW - Stilbenes -- therapeutic use KW - Colorectal Neoplasms -- etiology KW - Cell Transformation, Neoplastic -- drug effects KW - Proto-Oncogene Proteins p21(ras) -- antagonists & inhibitors KW - Adenomatous Polyposis Coli Protein -- physiology KW - Colorectal Neoplasms -- prevention & control KW - Cell Transformation, Neoplastic -- genetics KW - Proto-Oncogene Proteins p21(ras) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629586076?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Resveratrol+prevents+tumorigenesis+in+mouse+model+of+Kras+activated+sporadic+colorectal+cancer+by+suppressing+oncogenic+Kras+expression.&rft.au=Saud%2C+Shakir+M%3BLi%2C+Weidong%3BMorris%2C+Nicole+L%3BMatter%2C+Matthias+S%3BColburn%2C+Nancy+H%3BKim%2C+Young+S%3BYoung%2C+Matthew+R&rft.aulast=Saud&rft.aufirst=Shakir&rft.date=2014-12-01&rft.volume=35&rft.issue=12&rft.spage=2778&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu209 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-14 N1 - Date created - 2014-12-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cold Spring Harb Perspect Biol. 2013 Jan;5(1):a007898 [23169527] Gastroenterology. 2013 Apr;144(4):705-17 [23415801] Ann N Y Acad Sci. 2013 Jul;1290:12-20 [23855461] Ann N Y Acad Sci. 2013 Jul;1290:74-82 [23855468] Cancer Res. 2013 Sep 1;73(17):5473-84 [23824743] Oncogene. 2014 May 8;33(19):2454-63 [23752186] Nat Genet. 2000 Feb;24(2):144-52 [10655059] Nutr Cancer. 2001;39(1):102-7 [11588890] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630] Dig Dis Sci. 2002 May;47(5):1073-9 [12018902] Scand J Gastroenterol. 2002 Sep;37(9):1048-53 [12374230] Biochem Pharmacol. 2003 Apr 1;65(7):1053-60 [12663041] Ann N Y Acad Sci. 2003 Mar;983:197-207 [12724224] Carcinogenesis. 2004 Apr;25(4):527-33 [14688025] Lancet. 1992 Sep 12;340(8820):626-30 [1355210] Hum Pathol. 1994 Nov;25(11):1160-71 [7959660] Cell. 1996 Oct 18;87(2):159-70 [8861899] Oncogene. 1998 Sep 17;17(11 Reviews):1395-413 [9779987] Nat Rev Genet. 2006 Aug;7(8):606-19 [16847462] J Exp Clin Cancer Res. 2006 Jun;25(2):189-93 [16918129] Gastroenterology. 2006 Oct;131(4):1096-109 [17030180] PLoS Genet. 2006 Sep 15;2(9):e146 [17002498] Nat Protoc. 2006;1(6):2900-4 [17406549] Nature. 2007 Oct 25;449(7165):1003-7 [17934449] FASEB J. 2008 Mar;22(3):659-61 [17942826] J Agric Food Chem. 2008 Jun 25;56(12):4813-8 [18522405] Oncol Rep. 2008 Jul;20(1):3-11 [18575712] Nutr Rev. 2008 Aug;66 Suppl 1:S1-6 [18673478] Proc Natl Acad Sci U S A. 2010 Jan 26;107(4):1565-70 [20080688] Cancer Prev Res (Phila). 2010 Apr;3(4):549-59 [20332304] Cancer Res. 2010 Jul 15;70(14):6015-25 [20610624] Cancer Res. 2010 Sep 1;70(17):6715-24 [20736375] Cell Res. 2011 Jan;21(1):131-45 [21135874] Ann N Y Acad Sci. 2011 Jan;1215:150-60 [21261654] PLoS One. 2011;6(1):e16530 [21304978] Clin Cancer Res. 2011 Nov 15;17(22):7015-23 [21976550] Carcinogenesis. 2012 Jan;33(1):131-9 [22016468] Cell. 2012 Jun 8;149(6):1192-205 [22682243] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu209 ER - TY - JOUR T1 - Genetic polymorphisms in the 9p21 region associated with risk of multiple cancers. AN - 1629585949; 25239644 AB - The chromosome 9p21 region has been implicated in the pathogenesis of multiple cancers. We analyzed 9p21 single nucleotide polymorphisms (SNPs) from eight genome-wide association studies (GWAS) with data deposited in dbGaP, including studies of esophageal squamous cell carcinoma (ESCC), gastric cancer (GC), pancreatic cancer, renal cell carcinoma (RCC), lung cancer (LC), breast cancer (BrC), bladder cancer (BC) and prostate cancer (PrC). The number of subjects ranged from 2252 (PrC) to 7619 (LC). SNP-level analyses for each cancer were conducted by logistic regression or random-effects meta-analysis. A subset-based statistical approach (ASSET) was performed to combine SNP-level P values across multiple cancers. We calculated gene-level P values using the adaptive rank truncated product method. We identified that rs1063192 and rs2157719 in the CDKN2A/2B region were significantly associated with ESCC and rs2764736 (3' of TUSC1) was associated with BC (P ≤ 2.59 × 10(-6)). ASSET analyses identified four SNPs significantly associated with multiple cancers: rs3731239 (CDKN2A intronic) with ESCC, GC and BC (P = 3.96 × 10(-) (4)); rs10811474 (3' of IFNW1) with RCC and BrC (P = 0.001); rs12683422 (LINGO2 intronic) with RCC and BC (P = 5.93 × 10(-) (4)) and rs10511729 (3' of ELAVL2) with LC and BrC (P = 8.63 × 10(-) (4)). At gene level, CDKN2B, CDKN2A and CDKN2B-AS1 were significantly associated with ESCC (P ≤ 4.70 × 10(-) (5)). Rs10511729 and rs10811474 were associated with cis-expression of 9p21 genes in corresponding cancer tissues in the expression quantitative trait loci analysis. In conclusion, we identified several genetic variants in the 9p21 region associated with the risk of multiple cancers, suggesting that this region may contribute to a shared susceptibility across different cancer types. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Li, Wen-Qing AU - Pfeiffer, Ruth M AU - Hyland, Paula L AU - Shi, Jianxin AU - Gu, Fangyi AU - Wang, Zhaoming AU - Bhattacharjee, Samsiddhi AU - Luo, Jun AU - Xiong, Xiaoqin AU - Yeager, Meredith AU - Deng, Xiang AU - Hu, Nan AU - Taylor, Philip R AU - Albanes, Demetrius AU - Caporaso, Neil E AU - Gapstur, Susan M AU - Amundadottir, Laufey AU - Chanock, Stephen J AU - Chatterjee, Nilanjan AU - Landi, Maria Teresa AU - Tucker, Margaret A AU - Goldstein, Alisa M AU - Yang, Xiaohong R AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institute of Health, Bethesda, MD, USA, Department of Dermatology, Warren Alpert Medical School, Brown University, Providence, RI, USA, wen-qing_li@brown.edu. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institute of Health, Bethesda, MD, USA. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institute of Health, Bethesda, MD, USA, Cancer Genomics Research Laboratory, NCI-Frederick, SAIC-Frederick Inc., Frederick, MD, USA. ; National Institute of Biomedical Genomics, Kalyani, India. ; Information Management Services, Inc., Calverton, MD, USA and. ; Information Management Services, Inc., Calverton, MD, USA and wen-qing_li@brown.edu royang@mail.nih.gov. ; Epidemiology Research Program, American Cancer Society, Atlanta, GA, USA. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 2698 EP - 2705 VL - 35 IS - 12 KW - Biomarkers, Tumor KW - 0 KW - Index Medicus KW - Genotype KW - Polymerase Chain Reaction KW - Risk Factors KW - Humans KW - Prognosis KW - Genome-Wide Association Study KW - Biomarkers, Tumor -- genetics KW - Quantitative Trait Loci KW - Genetic Predisposition to Disease KW - Polymorphism, Single Nucleotide -- genetics KW - Neoplasms -- genetics KW - Chromosomes, Human, Pair 9 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629585949?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+polymorphisms+in+the+9p21+region+associated+with+risk+of+multiple+cancers.&rft.au=Li%2C+Wen-Qing%3BPfeiffer%2C+Ruth+M%3BHyland%2C+Paula+L%3BShi%2C+Jianxin%3BGu%2C+Fangyi%3BWang%2C+Zhaoming%3BBhattacharjee%2C+Samsiddhi%3BLuo%2C+Jun%3BXiong%2C+Xiaoqin%3BYeager%2C+Meredith%3BDeng%2C+Xiang%3BHu%2C+Nan%3BTaylor%2C+Philip+R%3BAlbanes%2C+Demetrius%3BCaporaso%2C+Neil+E%3BGapstur%2C+Susan+M%3BAmundadottir%2C+Laufey%3BChanock%2C+Stephen+J%3BChatterjee%2C+Nilanjan%3BLandi%2C+Maria+Teresa%3BTucker%2C+Margaret+A%3BGoldstein%2C+Alisa+M%3BYang%2C+Xiaohong+R&rft.aulast=Li&rft.aufirst=Wen-Qing&rft.date=2014-12-01&rft.volume=35&rft.issue=12&rft.spage=2698&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu203 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-14 N1 - Date created - 2014-12-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Genet. 2007 Oct;39(10):1181-6 [17898773] Nucleic Acids Res. 2013 Jan;41(Database issue):D64-9 [23155063] Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):12028-33 [18685102] Nature. 2008 Oct 23;455(7216):1061-8 [18772890] Nat Genet. 2009 Aug;41(8):909-14 [19578363] Nat Genet. 2009 Aug;41(8):920-5 [19578364] Nat Genet. 2009 Aug;41(8):905-8 [19578366] Nat Genet. 2009 Aug;41(8):899-904 [19578367] Nat Genet. 2009 Sep;41(9):986-90 [19648918] Am J Hum Genet. 2009 Nov;85(5):679-91 [19836008] Genet Epidemiol. 2009 Dec;33(8):700-9 [19333968] Nat Genet. 2010 Mar;42(3):224-8 [20101243] Int J Cancer. 2010 May 1;126(9):2079-89 [19739119] Oncogene. 2000 Nov 23;19(50):5747-54 [11126361] J Urol. 2001 Sep;166(3):1088-92 [11490304] Hum Mutat. 2004 Jun;23(6):630 [15146471] Genes Dev. 1999 Feb 15;13(4):449-61 [10049360] Mod Pathol. 2005 Jul;18(7):959-63 [15832197] Cancer Res. 2006 Aug 15;66(16):8100-8 [16912187] Nat Genet. 2007 May;39(5):645-9 [17401363] Nat Genet. 2007 Jul;39(7):870-4 [17529973] Nucleic Acids Res. 2013 Jan;41(Database issue):D56-63 [23193274] Cell. 2013 Jan 31;152(3):633-41 [23374354] Circulation. 2013 Feb 19;127(7):799-810 [23315372] Br J Cancer. 2013 Apr 2;108(6):1378-86 [23361049] PLoS One. 2013;8(6):e66114 [23776618] Carcinogenesis. 2013 Jul;34(7):1536-42 [23504502] Genes Chromosomes Cancer. 2004 Mar;39(3):205-16 [14732922] PLoS Genet. 2010 Apr;6(4):e1000899 [20386740] Nat Genet. 2010 Jun;42(6):504-7 [20453838] Nat Genet. 2010 Jul;42(7):599-603 [20512145] Nat Genet. 2010 Sep;42(9):764-7 [20729852] Nat Genet. 2010 Nov;42(11):978-84 [20972438] Fam Cancer. 2010 Dec;9(4):625-33 [20574843] Nat Genet. 2011 Jan;43(1):60-5 [21131975] Hum Genet. 2011 Jul;130(1):59-78 [21678065] BMC Bioinformatics. 2011;12:323 [21816040] Hum Mol Genet. 2011 Dec 15;20(24):5012-23 [21926416] Am J Hum Genet. 2012 May 4;90(5):821-35 [22560090] Hum Mol Genet. 2012 Jun 15;21(12):2836-42 [22419738] Hum Mol Genet. 2012 Nov 15;21(22):4980-95 [22899653] Am J Hum Genet. 2012 Nov 2;91(5):928-34 [23103227] Hum Genet. 2012 Dec;131(12):1877-88 [22886559] PLoS Genet. 2008 Apr;4(4):e1000054 [18437204] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu203 ER - TY - JOUR T1 - Identification of fragile X syndrome specific molecular markers in human fibroblasts: a useful model to test the efficacy of therapeutic drugs. AN - 1628238948; 25224527 AB - Fragile X syndrome (FXS) is the most frequent cause of inherited intellectual disability and autism. It is caused by the absence of the fragile X mental retardation 1 (FMR1) gene product, fragile X mental retardation protein (FMRP), an RNA-binding protein involved in the regulation of translation of a subset of brain mRNAs. In Fmr1 knockout mice, the absence of FMRP results in elevated protein synthesis in the brain as well as increased signaling of many translational regulators. Whether protein synthesis is also dysregulated in FXS patients is not firmly established. Here, we demonstrate that fibroblasts from FXS patients have significantly elevated rates of basal protein synthesis along with increased levels of phosphorylated mechanistic target of rapamycin (p-mTOR), phosphorylated extracellular signal regulated kinase 1/2, and phosphorylated p70 ribosomal S6 kinase 1 (p-S6K1). The treatment with small molecules that inhibit S6K1 and a known FMRP target, phosphoinositide 3-kinase (PI3K) catalytic subunit p110β, lowered the rates of protein synthesis in both control and patient fibroblasts. Our data thus demonstrate that fibroblasts from FXS patients may be a useful in vitro model to test the efficacy and toxicity of potential therapeutics prior to clinical trials, as well as for drug screening and designing personalized treatment approaches. © 2014 WILEY PERIODICALS, INC. JF - Human mutation AU - Kumari, Daman AU - Bhattacharya, Aditi AU - Nadel, Jeffrey AU - Moulton, Kristen AU - Zeak, Nicole M AU - Glicksman, Anne AU - Dobkin, Carl AU - Brick, David J AU - Schwartz, Philip H AU - Smith, Carolyn B AU - Klann, Eric AU - Usdin, Karen AD - Laboratory of Cell and Molecular Biology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 1485 EP - 1494 VL - 35 IS - 12 KW - Biomarkers KW - 0 KW - FMR1 protein, human KW - RNA, Messenger KW - Fragile X Mental Retardation Protein KW - 139135-51-6 KW - Phosphatidylinositol 3-Kinases KW - EC 2.7.1.- KW - Ribosomal Protein S6 Kinases KW - EC 2.7.11.1 KW - Leucine KW - GMW67QNF9C KW - Index Medicus KW - S6K1 KW - protein synthesis KW - FMRP KW - Fragile X syndrome KW - fibroblasts KW - FMR1 KW - Protein Biosynthesis KW - Animals KW - Phosphatidylinositol 3-Kinases -- metabolism KW - Humans KW - Fibroblasts -- cytology KW - Mice KW - RNA, Messenger -- genetics KW - Fibroblasts -- metabolism KW - Mice, Knockout KW - Ribosomal Protein S6 Kinases -- metabolism KW - Cells, Cultured KW - Leucine -- metabolism KW - Case-Control Studies KW - Fragile X Mental Retardation Protein -- genetics KW - Drug Evaluation, Preclinical KW - Male KW - Fragile X Syndrome -- genetics KW - Biomarkers -- metabolism KW - Fragile X Syndrome -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1628238948?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+mutation&rft.atitle=Identification+of+fragile+X+syndrome+specific+molecular+markers+in+human+fibroblasts%3A+a+useful+model+to+test+the+efficacy+of+therapeutic+drugs.&rft.au=Kumari%2C+Daman%3BBhattacharya%2C+Aditi%3BNadel%2C+Jeffrey%3BMoulton%2C+Kristen%3BZeak%2C+Nicole+M%3BGlicksman%2C+Anne%3BDobkin%2C+Carl%3BBrick%2C+David+J%3BSchwartz%2C+Philip+H%3BSmith%2C+Carolyn+B%3BKlann%2C+Eric%3BUsdin%2C+Karen&rft.aulast=Kumari&rft.aufirst=Daman&rft.date=2014-12-01&rft.volume=35&rft.issue=12&rft.spage=1485&rft.isbn=&rft.btitle=&rft.title=Human+mutation&rft.issn=1098-1004&rft_id=info:doi/10.1002%2Fhumu.22699 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-08 N1 - Date created - 2014-11-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cell. 2011 Jul 22;146(2):247-61 [21784246] PLoS One. 2011;6(10):e26549 [22046307] Biochem J. 2012 Jan 1;441(1):1-21 [22168436] Annu Rev Pathol. 2012;7:219-45 [22017584] Neurobiol Dis. 2012 Mar;45(3):1145-52 [22227453] Genes Brain Behav. 2012 Apr;11(3):332-41 [22268788] J Neurochem. 2012 May;121(4):672-9 [22393900] Biochem J. 2010 Oct 15;431(2):245-55 [20704563] J Neurosci. 2010 Nov 17;30(46):15616-27 [21084617] Neurobiol Dis. 2011 Feb;41(2):469-80 [21047554] Neuron. 2012 Apr 12;74(1):49-56 [22500629] Mol Med. 2012;18:336-45 [22207187] Sci Transl Med. 2012 Sep 19;4(152):152ra128 [22993295] Neuron. 2012 Oct 18;76(2):325-37 [23083736] Hum Mutat. 2013 Jan;34(1):157-66 [22887750] Neuron. 2013 Jan 23;77(2):243-50 [23352161] J Cereb Blood Flow Metab. 2013 Apr;33(4):499-507 [23299245] Nat Med. 2013 May;19(5):603-7 [23542787] J Mol Diagn. 2013 Jul;15(4):508-17 [23660422] J Neurosci Res. 2013 Oct;91(10):1247-62 [23893392] Nat Neurosci. 2013 Nov;16(11):1530-6 [23584741] Nat Med. 2013 Nov;19(11):1473-7 [24141422] Biol Psychiatry. 2014 Feb 1;75(3):198-206 [24041505] Science. 2014 Feb 28;343(6174):1002-5 [24578575] Am J Med Genet A. 2014 Jul;164A(7):1648-58 [24700618] Am J Hum Genet. 2000 Jan;66(1):6-15 [10631132] Cereb Cortex. 2000 Oct;10(10):1038-44 [11007554] Hum Mol Genet. 2001 Jul 1;10(14):1449-54 [11448936] Am J Hum Genet. 2002 Oct;71(4):923-32 [12232854] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216] Dev Med Child Neurol. 1992 Sep;34(9):826-32 [1526353] Hum Mol Genet. 1992 Sep;1(6):397-400 [1301913] Nat Genet. 1993 Jan;3(1):36-43 [8490651] Nat Genet. 1993 Aug;4(4):335-40 [8401578] Cell. 1994 Jul 15;78(1):23-33 [8033209] Hum Mol Genet. 1995 Mar;4(3):359-66 [7795588] Am J Med Genet. 1996 Aug 9;64(2):296-301 [8844069] J Med Genet. 1998 Feb;35(2):103-11 [9507388] Neuron. 2005 Mar 3;45(5):753-64 [15748850] J Neurosci. 2005 May 18;25(20):5087-95 [15901791] J Neurosci. 2007 May 16;27(20):5338-48 [17507556] Am J Med Genet A. 2008 Jan 1;146A(1):60-5 [18074381] J Physiol. 2008 Mar 15;586(6):1503-8 [18202092] Neurochem Res. 2008 Jun;33(6):1028-35 [18080753] Cell Stem Cell. 2007 Nov;1(5):568-77 [18371394] Neuron. 2008 Oct 23;60(2):201-14 [18957214] Neuron. 2009 Jan 15;61(1):10-26 [19146809] J Neurosci. 2010 Jan 13;30(2):694-702 [20071534] Mol Cell Neurosci. 2010 Jan;43(1):43-50 [19837168] Neurotherapeutics. 2010 Jul;7(3):264-74 [20643379] J Neurosci. 2010 Aug 11;30(32):10624-38 [20702695] J Mol Diagn. 2010 Sep;12(5):589-600 [20616364] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/humu.22699 ER - TY - JOUR T1 - Perceived and objective diet quality in US adults: a cross-sectional analysis of the National Health and Nutrition Examination Survey (NHANES) AN - 1627977482; 20913351 AB - The Dietary Approaches to Stop Hypertension (DASH) dietary pattern has been shown to reduce cardiometabolic risk. Little is understood about the relationship between objective diet quality and perceived diet quality (PDQ), a potential psychosocial barrier to appropriate dietary intake. We compared PDQ and diet quality measured by a nutrient-based DASH index score in the USA. Cross-sectional study. Participants in the 2005-2006 National Health and Nutrition Examination Survey (NHANES) rated diet quality on a 5-point Likert scale and PDQ scores were generated (low, medium, high). A single 24 h dietary recall was used to estimate DASH index scores (range 0-9 points) by assigning 0, 0.5 or 1 point (optimal) for nine target nutrients: total fat, saturated fat, protein, cholesterol, fibre, Ca, Mg, K and Na. Nationally representative sample of the US population. Adults aged greater than or equal to 19 years in 2005-2006 NHANES (n 4419). Participants with high PDQ (33 %) had higher DASH index scores (mean 3.0 (sd 0.07)) than those with low PDQ (mean 2.5 (sd 0.06), P < 0.001), but average scores did not align with targets for intermediate or optimal DASH accordance. Adults with high PDQ reported higher total fat, saturated fat and Na intakes compared with optimal DASH nutrient goals. Differences between those with high v. low PDQ were similar for Whites and Blacks, but there was no difference between PDQ groups for Mexican Americans. Among Whites and Blacks, but not Mexican Americans, high PDQ may be associated with higher diet quality, but not necessarily a diet meeting DASH nutrient goals. This disconnect between PDQ and actual diet quality may serve as a target in obesity prevention. JF - Public Health Nutrition AU - Powell-Wiley, Tiffany M AU - Miller, Paige E AU - Agyemang, Priscilla AU - Agurs-Collins, Tanya AU - Reedy, Jill AD - Cardiovascular and Pulmonary Branch, Division of Intramural Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 10 - Room 5E3340, Bethesda, MD 20892, USA, tiffany.powell@nih.gov Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 2641 EP - 2649 PB - Cambridge University Press, The Edinburgh Building, Cambridge CB2 2RU United Kingdom VL - 17 IS - 12 SN - 1368-9800, 1368-9800 KW - Risk Abstracts KW - Diets KW - Obesity KW - Cholesterol KW - Ingestion KW - Nutrition KW - Health risks KW - USA KW - Prevention KW - Perception KW - Proteins KW - Ethnic groups KW - Hypertension KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627977482?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+Health+Nutrition&rft.atitle=Perceived+and+objective+diet+quality+in+US+adults%3A+a+cross-sectional+analysis+of+the+National+Health+and+Nutrition+Examination+Survey+%28NHANES%29&rft.au=Powell-Wiley%2C+Tiffany+M%3BMiller%2C+Paige+E%3BAgyemang%2C+Priscilla%3BAgurs-Collins%2C+Tanya%3BReedy%2C+Jill&rft.aulast=Powell-Wiley&rft.aufirst=Tiffany&rft.date=2014-12-01&rft.volume=17&rft.issue=12&rft.spage=2641&rft.isbn=&rft.btitle=&rft.title=Public+Health+Nutrition&rft.issn=13689800&rft_id=info:doi/10.1017%2FS1368980014000196 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Number of references - 39 N1 - Last updated - 2014-12-24 N1 - SubjectsTermNotLitGenreText - Diets; Health risks; Obesity; Prevention; Perception; Proteins; Cholesterol; Ingestion; Nutrition; Ethnic groups; Hypertension; USA DO - http://dx.doi.org/10.1017/S1368980014000196 ER - TY - JOUR T1 - Peritubular myoid cells participate in male mouse spermatogonial stem cell maintenance. AN - 1627697485; 25181385 AB - Peritubular myoid (PM) cells surround the seminiferous tubule and together with Sertoli cells form the cellular boundary of the spermatogonial stem cell (SSC) niche. However, it remains unclear what role PM cells have in determining the microenvironment in the niche required for maintenance of the ability of SSCs to undergo self-renewal and differentiation into spermatogonia. Mice with a targeted disruption of the androgen receptor gene (Ar) in PM cells experienced a progressive loss of spermatogonia, suggesting that PM cells require testosterone (T) action to produce factors influencing SSC maintenance in the niche. Other studies showed that glial cell line-derived neurotrophic factor (GDNF) is required for SSC self-renewal and differentiation of SSCs in vitro and in vivo. This led us to hypothesize that T-regulated GDNF expression by PM cells contributes to the maintenance of SSCs. This hypothesis was tested using an adult mouse PM cell primary culture system and germ cell transplantation. We found that T induced GDNF expression at the mRNA and protein levels in PM cells. Furthermore, when thymus cell antigen 1-positive spermatogonia isolated from neonatal mice were cocultured with PM cells with or without T and transplanted to the testes of germ cell-depleted mice, the number and length of transplant-derived colonies was increased considerably by in vitro T treatment. These results support the novel hypothesis that T-dependent regulation of GDNF expression in PM cells has a significant influence on the microenvironment of the niche and SSC maintenance. JF - Endocrinology AU - Chen, Liang-Yu AU - Brown, Paula R AU - Willis, William B AU - Eddy, Edward M AD - Gamete Biology Group (L.-Y.C., W.B.W., E.M.E.) and Reproductive Developmental Biology Group (P.R.B.), Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 4964 EP - 4974 VL - 155 IS - 12 KW - Glial Cell Line-Derived Neurotrophic Factor KW - 0 KW - Testosterone KW - 3XMK78S47O KW - Abridged Index Medicus KW - Index Medicus KW - Coculture Techniques KW - Animals KW - Mice, Inbred C57BL KW - Spermatogonia -- physiology KW - Male KW - Adult Stem Cells -- transplantation KW - Testis -- physiology KW - Glial Cell Line-Derived Neurotrophic Factor -- metabolism KW - Testosterone -- physiology KW - Adult Stem Cells -- physiology KW - Testis -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627697485?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Peritubular+myoid+cells+participate+in+male+mouse+spermatogonial+stem+cell+maintenance.&rft.au=Chen%2C+Liang-Yu%3BBrown%2C+Paula+R%3BWillis%2C+William+B%3BEddy%2C+Edward+M&rft.aulast=Chen&rft.aufirst=Liang-Yu&rft.date=2014-12-01&rft.volume=155&rft.issue=12&rft.spage=4964&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=1945-7170&rft_id=info:doi/10.1210%2Fen.2014-1406 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-08 N1 - Date created - 2014-11-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cell Stem Cell. 2012 Oct 5;11(4):567-78 [23040482] J Cell Sci. 2013 Feb 15;126(Pt 4):1009-20 [23239029] Development. 2009 Apr;136(7):1191-9 [19270176] FASEB J. 2009 Dec;23(12):4218-30 [19692648] Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6210-5 [20308578] J Endocrinol. 2010 May;205(2):133-45 [20147357] Endocrinology. 2010 May;151(5):2343-8 [20228170] Endocrinology. 2010 Jul;151(7):3374-85 [20444943] Hum Reprod. 2010 Sep;25(9):2181-7 [20601681] Biol Reprod. 2010 Nov;83(5):759-66 [20650881] Science. 2000 Feb 25;287(5457):1489-93 [10688798] Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8346-51 [10900001] Biol Reprod. 2001 Feb;64(2):464-72 [11159348] Endocrinology. 2001 Jun;142(6):2405-8 [11356688] Oncogene. 2001 Aug 2;20(34):4696-709 [11498792] Mech Dev. 2002 Apr;113(1):29-39 [11900972] Biol Reprod. 2002 Jun;66(6):1579-84 [12021034] Endocrinology. 2002 Sep;143(9):3351-60 [12193547] Dev Biol. 2003 Jun 1;258(1):209-25 [12781694] Biol Reprod. 2003 Aug;69(2):612-6 [12700182] Biol Reprod. 2003 Aug;69(2):701-7 [12700185] Biol Reprod. 2004 Sep;71(3):722-31 [15115718] Am J Anat. 1967 Nov;121(3):523-57 [5582405] Cell Tissue Kinet. 1971 Jul;4(4):335-49 [5127357] Nature. 1977 Sep 22;269(5626):338-40 [198666] Endocrinology. 1984 Nov;115(5):1925-32 [6541571] J Cell Biol. 1985 Jun;100(6):1941-7 [3889013] Endocrinology. 1989 Feb;124(2):845-54 [2463904] Mol Endocrinol. 1989 Apr;3(4):625-34 [2725526] J Endocrinol. 1990 Apr;125(1):131-8 [2338529] Mutat Res. 1993 Dec;290(2):193-200 [7694110] Biol Reprod. 2013 May;88(5):131 [23536371] PLoS One. 2014;9(3):e90088 [24619130] Development. 1996 Sep;122(9):2813-22 [8787755] Biol Reprod. 1996 Jul;55(1):25-31 [8793054] Anat Embryol (Berl). 1998 Aug;198(2):101-10 [9725769] Mol Reprod Dev. 1999 Jun;53(2):142-8 [10331452] Biol Reprod. 1999 Sep;61(3):842-7 [10456866] Mol Reprod Dev. 2005 Oct;72(2):171-81 [16010662] Biol Reprod. 2005 Nov;73(5):1011-6 [16014811] Biol Reprod. 2006 Feb;74(2):314-21 [16237148] Int J Hematol. 2005 Dec;82(5):381-8 [16533739] J Endocrinol. 2006 Jul;190(1):59-71 [16837611] Biol Reprod. 2006 Aug;75(2):167-75 [16571874] J Mol Cell Cardiol. 2006 Oct;41(4):724-31 [16887142] Proc Natl Acad Sci U S A. 2006 Nov 21;103(47):17718-23 [17095600] Methods Enzymol. 2006;419:259-82 [17141059] Biol Reprod. 2007 Jan;76(1):55-62 [17021343] J Biol Chem. 2007 Aug 31;282(35):25842-51 [17597063] Biol Reprod. 2007 Oct;77(4):723-33 [17625109] Neurosci Res. 2007 Nov;59(3):277-87 [17765347] Stem Cells. 2008 Jan;26(1):266-78 [17962702] Genes Cells. 2008 Apr;13(4):365-74 [18363967] Mol Cell Endocrinol. 2008 Jun 25;288(1-2):95-103 [18485583] Endocrinology. 1994 Sep;135(3):1227-34 [8070367] Arch Histol Cytol. 1996 Mar;59(1):1-13 [8727359] FEBS Lett. 2011 Aug 4;585(15):2437-44 [21726557] Biol Reprod. 2011 Oct;85(4):763-9 [21653894] PLoS One. 2011;6(12):e28367 [22174794] Endocrinology. 2012 Feb;153(2):887-900 [22147017] Stem Cells. 2012 Apr;30(4):732-40 [22232066] Development. 2012 May;139(10):1734-43 [22491947] PLoS One. 2012;7(4):e35136 [22514715] Physiol Rev. 2012 Apr;92(2):577-95 [22535892] Biol Reprod. 2012 May;86(5):150, 1-8 [22357548] Am J Physiol Endocrinol Metab. 2012 Oct 1;303(7):E886-98 [22850685] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/en.2014-1406 ER - TY - JOUR T1 - A phase I trial of veliparib (ABT-888) and temozolomide in children with recurrent CNS tumors: a pediatric brain tumor consortium report. AN - 1625347261; 24908656 AB - A phase I trial of veliparib (ABT-888), an oral poly(ADP-ribose) polymerase (PARP) inhibitor, and temozolomide (TMZ) was conducted in children with recurrent brain tumors to (i) estimate the maximum tolerated doses (MTDs) or recommended phase II doses (RP2Ds) of veliparib and TMZ; (ii) describe the toxicities of this regimen; and (iii) evaluate the plasma pharmacokinetic parameters and extent of PARP inhibition in peripheral blood mononuclear cells (PBMCs) following veliparib. TMZ was given once daily and veliparib twice daily for 5 days every 28 days. Veliparib concentrations and poly(ADP-ribose) (PAR) levels in PBMCs were measured on days 1 and 4. Analysis of pharmacokinetic and PBMC PAR levels were performed twice during study conduct to rationally guide dose modifications and to determine biologically optimal MTD/RP2D. Twenty-nine evaluable patients were enrolled. Myelosuppression (grade 4 neutropenia and thrombocytopenia) were dose limiting. The RP2Ds are veliparib 25 mg/m(2) b.i.d. and TMZ 135 mg/m(2)/d. Only 2 out of 12 patients treated at RP2Ds experienced dose-limiting toxicities. Although no objective response was observed, 4 patients had stable disease >6 months in duration, including 1 with glioblastoma multiforme and 1 with ependymoma. At the RP2D of veliparib, pediatric pharmacokinetic parameters were similar to those in adults. Veliparib and TMZ at the RP2D were well tolerated in children with recurrent brain tumors. A phase I/II trial to evaluate the tolerability and efficacy of veliparib, TMZ, and radiation in children with newly diagnosed brainstem gliomas is in progress. © The Author(s) 2014. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. JF - Neuro-oncology AU - Su, Jack M AU - Thompson, Patrick AU - Adesina, Adekunle AU - Li, Xiao-Nan AU - Kilburn, Lindsay AU - Onar-Thomas, Arzu AU - Kocak, Mehmet AU - Chyla, Brenda AU - McKeegan, Evelyn AU - Warren, Katherine E AU - Goldman, Stewart AU - Pollack, Ian F AU - Fouladi, Maryam AU - Chen, Alice AU - Giranda, Vincent AU - Boyett, James AU - Kun, Larry AU - Blaney, Susan M AD - Texas Children's Cancer Center, Baylor College of Medicine (J.M.S., P.T., A.A., X-N.L., S.M.B.); Children's National Medical Center (L.K.); St. Jude Children's Research Hospital (A.O-T., J.B., L.K.); University of Tennessee Health Science Center (M.K.); AbbVie Pharmaceuticals (B.C., E.M., V.G.); National Cancer Institute, Pediatric Oncology Branch (K.E.W.); Children's Hospital of Chicago (S.G.); Children's Hospital of Pittsburgh (I.F.P.); Cincinnati Children's Hospital Medical Center (M.F.); Cancer Therapy Evaluation Program, National Cancer Institute (A.C.). Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 1661 EP - 1668 VL - 16 IS - 12 KW - Antineoplastic Agents, Alkylating KW - 0 KW - Benzimidazoles KW - Poly(ADP-ribose) Polymerase Inhibitors KW - veliparib KW - 01O4K0631N KW - Dacarbazine KW - 7GR28W0FJI KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - temozolomide KW - YF1K15M17Y KW - Index Medicus KW - PARP inhibition KW - ABT-888 KW - pediatric phase I study KW - CNS tumors KW - Infant KW - Young Adult KW - Poly(ADP-ribose) Polymerases -- blood KW - Humans KW - Leukocytes, Mononuclear -- metabolism KW - Adult KW - Child KW - Maximum Tolerated Dose KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Dacarbazine -- therapeutic use KW - Antineoplastic Agents, Alkylating -- therapeutic use KW - Brain Neoplasms -- drug therapy KW - Dacarbazine -- analogs & derivatives KW - Benzimidazoles -- adverse effects KW - Antineoplastic Agents, Alkylating -- adverse effects KW - Benzimidazoles -- therapeutic use KW - Antineoplastic Agents, Alkylating -- administration & dosage KW - Benzimidazoles -- pharmacokinetics KW - Dacarbazine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1625347261?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+trial+of+veliparib+%28ABT-888%29+and+temozolomide+in+children+with+recurrent+CNS+tumors%3A+a+pediatric+brain+tumor+consortium+report.&rft.au=Su%2C+Jack+M%3BThompson%2C+Patrick%3BAdesina%2C+Adekunle%3BLi%2C+Xiao-Nan%3BKilburn%2C+Lindsay%3BOnar-Thomas%2C+Arzu%3BKocak%2C+Mehmet%3BChyla%2C+Brenda%3BMcKeegan%2C+Evelyn%3BWarren%2C+Katherine+E%3BGoldman%2C+Stewart%3BPollack%2C+Ian+F%3BFouladi%2C+Maryam%3BChen%2C+Alice%3BGiranda%2C+Vincent%3BBoyett%2C+James%3BKun%2C+Larry%3BBlaney%2C+Susan+M&rft.aulast=Su&rft.aufirst=Jack&rft.date=2014-12-01&rft.volume=16&rft.issue=12&rft.spage=1661&rft.isbn=&rft.btitle=&rft.title=Neuro-oncology&rft.issn=1523-5866&rft_id=info:doi/10.1093%2Fneuonc%2Fnou103 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-06 N1 - Date created - 2014-11-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Oncol. 2002 Dec 15;20(24):4684-91 [12488414] Nat Rev Mol Cell Biol. 2003 Jun;4(6):435-45 [12778123] Int J Radiat Oncol Biol Phys. 2004 Feb 1;58(2):410-9 [14751510] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7303-7 [9207086] J Biol Chem. 1998 Jun 5;273(23):14461-7 [9603959] Nat Rev Genet. 2006 Jan;7(1):45-54 [16369571] Nucleic Acids Res. 2006;34(6):1685-91 [16556909] Eur J Cancer. 2006 Sep;42(14):2335-42 [16899365] Clin Cancer Res. 2007 May 1;13(9):2728-37 [17473206] Clin Cancer Res. 2007 May 15;13(10):3033-42 [17505006] Cancer. 2007 Oct 1;110(7):1542-50 [17705175] Mol Interv. 2007 Dec;7(6):325-34 [18199854] Radiother Oncol. 2008 Aug;88(2):258-68 [18456354] Anal Biochem. 2008 Oct 15;381(2):240-7 [18674509] J Clin Oncol. 2009 Jun 1;27(16):2705-11 [19364967] Pediatr Blood Cancer. 2009 Dec 15;53(7):1227-30 [19533660] Clin Cancer Res. 2009 Dec 1;15(23):7277-90 [19934293] Cancer Chemother Pharmacol. 2010 Feb;65(3):419-25 [19526240] J Clin Oncol. 2010 Mar 10;28(8):1337-44 [20142589] Nat Rev Cancer. 2010 Apr;10(4):293-301 [20200537] Cancer Res. 2010 Jul 1;70(13):5457-64 [20530668] Lancet. 2010 Jul 24;376(9737):235-44 [20609467] Lancet. 2010 Jul 24;376(9737):245-51 [20609468] J Clin Oncol. 2010 Aug 1;28(22):3555-61 [20547991] Mol Cancer Ther. 2011 Jul;10(7):1185-93 [21571912] Radiother Oncol. 2011 Jun;99(3):331-8 [21719137] Cancer Res. 2011 Sep 1;71(17):5626-34 [21795476] J Clin Oncol. 2011 Sep 10;29(26):3529-34 [21825264] Neuro Oncol. 2011 Nov;13(11):1171-7 [21849329] PLoS One. 2011;6(10):e26152 [22028822] Blood. 2011 Dec 8;118(24):6368-79 [21917757] Oncotarget. 2011 Dec;2(12):984-96 [22184287] Clin Cancer Res. 2012 Mar 15;18(6):1726-34 [22307137] Mol Pharmacol. 2012 Oct;82(4):767-76 [22833573] PLoS One. 2012;7(10):e46614 [23071597] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/neuonc/nou103 ER - TY - JOUR T1 - Abasic phosphorothioate oligomers inhibit HIV-1 reverse transcription and block virus transmission across polarized ectocervical organ cultures. AN - 1625339001; 25224013 AB - In the absence of universally available antiretroviral (ARV) drugs or a vaccine against HIV-1, microbicides may offer the most immediate hope for controlling the AIDS pandemic. The most advanced and clinically effective microbicides are based on ARV agents that interfere with the earliest stages of HIV-1 replication. Our objective was to identify and characterize novel ARV-like inhibitors, as well as demonstrate their efficacy at blocking HIV-1 transmission. Abasic phosphorothioate 2' deoxyribose backbone (PDB) oligomers were evaluated in a variety of mechanistic assays and for their ability to inhibit HIV-1 infection and virus transmission through primary human cervical mucosa. Cellular and biochemical assays were used to elucidate the antiviral mechanisms of action of PDB oligomers against both lab-adapted and primary CCR5- and CXCR4-utilizing HIV-1 strains, including a multidrug-resistant isolate. A polarized cervical organ culture was used to test the ability of PDB compounds to block HIV-1 transmission to primary immune cell populations across ectocervical tissue. The antiviral activity and mechanisms of action of PDB-based compounds were dependent on oligomer size, with smaller molecules preventing reverse transcription and larger oligomers blocking viral entry. Importantly, irrespective of molecular size, PDBs potently inhibited virus infection and transmission within genital tissue samples. Furthermore, the PDB inhibitors exhibited excellent toxicity and stability profiles and were found to be safe for vaginal application in vivo. These results, coupled with the previously reported intrinsic anti-inflammatory properties of PDBs, support further investigations in the development of PDB-based topical microbicides for preventing the global spread of HIV-1. Copyright © 2014, American Society for Microbiology. All Rights Reserved. JF - Antimicrobial agents and chemotherapy AU - Fraietta, Joseph A AU - Mueller, Yvonne M AU - Lozenski, Karissa L AU - Ratner, Deena AU - Boesteanu, Alina C AU - Hancock, Aidan S AU - Lackman-Smith, Carol AU - Zentner, Isaac J AU - Chaiken, Irwin M AU - Chung, Suhman AU - LeGrice, Stuart F J AU - Snyder, Beth A AU - Mankowski, Marie K AU - Jones, Natalie M AU - Hope, Jennifer L AU - Gupta, Phalguni AU - Anderson, Sharon H AU - Wigdahl, Brian AU - Katsikis, Peter D AD - Department of Microbiology and Immunology and Center for Immunology and Vaccine Science, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Philadelphia, Pennsylvania, USA. ; Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. ; Southern Research Institute, Frederick, Maryland, USA. ; Department of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, Pennsylvania, USA. ; HIV Drug Resistance Program, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA. ; Department of Obstetrics & Gynecology, Drexel University College of Medicine, Philadelphia, Pennsylvania, USA Main Line Fertility Center, Bryn Mawr, Pennsylvania, USA. ; Department of Microbiology and Immunology and Center for Immunology and Vaccine Science, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Philadelphia, Pennsylvania, USA peter.katsikis@drexelmed.edu. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 7056 EP - 7071 VL - 58 IS - 12 KW - CCR5 protein, human KW - 0 KW - CXCR4 protein, human KW - Phosphorothioate Oligonucleotides KW - Receptors, CCR5 KW - Receptors, CXCR4 KW - Reverse Transcriptase Inhibitors KW - Deoxyribose KW - 533-67-5 KW - Index Medicus KW - Vagina -- drug effects KW - Epithelial Cells -- virology KW - Animals KW - Humans KW - Gene Expression KW - Receptors, CXCR4 -- antagonists & inhibitors KW - Mice KW - Sperm Motility -- drug effects KW - Mucous Membrane -- drug effects KW - Structure-Activity Relationship KW - Epithelial Cells -- drug effects KW - Mucous Membrane -- virology KW - Receptors, CCR5 -- genetics KW - Vagina -- virology KW - Mice, Inbred C57BL KW - Deoxyribose -- chemistry KW - Organ Culture Techniques KW - Receptors, CCR5 -- metabolism KW - Female KW - Male KW - Phosphorothioate Oligonucleotides -- chemical synthesis KW - Cervix Uteri -- drug effects KW - HIV-1 -- genetics KW - Reverse Transcriptase Inhibitors -- pharmacology KW - HIV-1 -- growth & development KW - Cervix Uteri -- virology KW - HIV-1 -- enzymology KW - Phosphorothioate Oligonucleotides -- pharmacology KW - Reverse Transcriptase Inhibitors -- chemical synthesis KW - HIV-1 -- drug effects KW - Virus Internalization -- drug effects KW - Reverse Transcription -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1625339001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+agents+and+chemotherapy&rft.atitle=Abasic+phosphorothioate+oligomers+inhibit+HIV-1+reverse+transcription+and+block+virus+transmission+across+polarized+ectocervical+organ+cultures.&rft.au=Fraietta%2C+Joseph+A%3BMueller%2C+Yvonne+M%3BLozenski%2C+Karissa+L%3BRatner%2C+Deena%3BBoesteanu%2C+Alina+C%3BHancock%2C+Aidan+S%3BLackman-Smith%2C+Carol%3BZentner%2C+Isaac+J%3BChaiken%2C+Irwin+M%3BChung%2C+Suhman%3BLeGrice%2C+Stuart+F+J%3BSnyder%2C+Beth+A%3BMankowski%2C+Marie+K%3BJones%2C+Natalie+M%3BHope%2C+Jennifer+L%3BGupta%2C+Phalguni%3BAnderson%2C+Sharon+H%3BWigdahl%2C+Brian%3BKatsikis%2C+Peter+D&rft.aulast=Fraietta&rft.aufirst=Joseph&rft.date=2014-12-01&rft.volume=58&rft.issue=12&rft.spage=7056&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+agents+and+chemotherapy&rft.issn=1098-6596&rft_id=info:doi/10.1128%2FAAC.02991-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-07 N1 - Date created - 2014-11-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Virol. 2000 Apr;74(8):3740-51 [10729149] Nat Med. 2000 Apr;6(4):475-9 [10742159] Clin Microbiol Rev. 2001 Apr;14(2):327-35 [11292641] Manushi. 1997 Mar-Apr;(99):37-8 [12348108] AIDS Anal Afr. 2000 Feb-Mar;10(5):2 [12322486] Lancet. 2002 Sep 28;360(9338):971-7 [12383665] AIDS Res Hum Retroviruses. 2002 Nov 20;18(17):1281-90 [12487816] Clin Chim Acta. 1973 Nov 15;48(4):393-401 [4202600] Cancer Treat Rep. 1986 Mar;70(3):359-62 [3955547] J Virol Methods. 1988 Aug;20(4):309-21 [2460479] Virology. 1990 Jan;174(1):103-16 [1688473] Stud Fam Plann. 1989 Nov-Dec;20(6 Pt 1):297-307 [2623725] AIDS Res Hum Retroviruses. 1991 Mar;7(3):295-302 [1712216] Antisense Res Dev. 1993 Spring;3(1):19-31 [8495104] Soc Sci Med. 1993 Jun;36(12):1635-44 [8327927] Antimicrob Agents Chemother. 1998 Mar;42(3):487-94 [9517921] AIDS Res Hum Retroviruses. 1998 Apr;14 Suppl 1:S119-23 [9581895] J Womens Health. 1998 Nov;7(9):1081-6 [9861583] Soc Sci Med. 2005 Jan;60(2):319-30 [15522488] PLoS Med. 2005 May;2(5):e142 [15916473] J Virol. 2005 Nov;79(22):14355-70 [16254370] J Biomol Screen. 2006 Feb;11(1):65-74 [16314403] Nat Rev Immunol. 2006 May;6(5):371-82 [16639430] J Immunol. 2006 Nov 15;177(10):6584-7 [17082568] J Immunol. 2006 Dec 1;177(11):8164-70 [17114492] J Clin Invest. 2007 May;117(5):1116 [17476340] Nature. 2007 Sep 6;449(7158):101-4 [17805298] PLoS One. 2007;2(12):e1312 [18091987] PLoS One. 2008;3(1):e1474 [18213382] Immunity. 2008 Mar;28(3):315-23 [18342006] Antimicrob Agents Chemother. 2008 May;52(5):1768-81 [18316528] Nature. 2008 May 15;453(7193):289-90 [18480799] Nat Med. 2008 Jul;14(7):762-6 [18552857] Antimicrob Agents Chemother. 2008 Sep;52(9):3169-79 [18625767] Methods Mol Biol. 2009;485:55-72 [19020818] PLoS One. 2008;3(11):e3784 [19023429] Nature. 2009 Apr 23;458(7241):1034-8 [19262509] Cont Lens Anterior Eye. 2009 Aug;32(4):187-9 [19553155] Nat Med. 2009 Aug;15(8):951-4 [19525965] Antimicrob Agents Chemother. 2010 Apr;54(4):1512-9 [20086149] Antimicrob Agents Chemother. 2010 Sep;54(9):3913-21 [20547794] Science. 2010 Sep 3;329(5996):1168-74 [20643915] Antimicrob Agents Chemother. 2010 Oct;54(10):4064-73 [20625151] Lancet. 2010 Oct 16;376(9749):1329-37 [20851460] ChemMedChem. 2010 Nov 8;5(11):1871-9 [20677318] N Engl J Med. 2010 Dec 30;363(27):2587-99 [21091279] Annu Rev Med. 2011;62:127-39 [21054171] Lancet. 2011 Jul 16;378(9787):269-78 [21763938] Antimicrob Agents Chemother. 2012 Feb;56(2):805-15 [22083472] PLoS Pathog. 2012;8(4):e1002634 [22496655] AIDS. 2012 Apr 24;26(7):F13-9 [22333749] J Biol Chem. 2012 May 11;287(20):16801-11 [22437836] Best Pract Res Clin Obstet Gynaecol. 2012 Aug;26(4):441-9 [22429786] J Acquir Immune Defic Syndr. 2012 Aug 15;60(5):455-61 [22592582] Acta Neurochir (Wien). 2013 Jul;155(7):1287-92 [23649989] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/AAC.02991-14 ER - TY - JOUR T1 - What happens when people discontinue taking medications? Lessons from COMBINE AN - 1625335697; 4619060 AB - We use intensive longitudinal data methods to illuminate processes affecting patients' drinking in relation to the discontinuation of medications within an alcohol treatment study. Although previous work has focused on broad measures of medication adherence, we focus on dynamic changes in drinking both before and after patients discontinue. We conducted secondary data analyses using the COMBINE (Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence) study, focused on participants who discontinued medications prior to the planned end of treatment. Using an interrupted time-series analysis, we analysed drinking in the weeks before and after discontinuation and also studied outcomes at the end of the COMBINE follow-up. We describe the subsample of COMBINE participants who discontinued medications (n=450), and compare them with those who were medication-adherent (n=559) and with those who discontinued but had substantial missing data (n=217). The primary outcomes were percentage of days abstinent (PDA) and percentage of heavy drinking days (PHDD). Medication adherence data were used to approximate the date of discontinuation. For many patients, an increase in drinking began weeks before discontinuation (PDA: F(1,4803) =19.07, P<0.001; PHDD: F(1,4804)=8.58, P=0.003) then escalated at discontinuation (PDA: F(1,446)=5.05, P=0.025; PHDD: F(1,446)=4.52, P=0.034). Among other effects, the amount of change was moderated by the reason for discontinuation (e.g. adverse event; PDA: F(2,4803)=3.85, P=0.021; PHDD: F(2,4804)=5.36, P=0.005) and also whether it occurred in the first or second half of treatment (PDA: F(1,4803)=5.23, P=0.022; PHDD: F(1,4804)=8.79, P=0.003). A patient's decision to stop taking medications during alcohol treatment appears to take place during a weeks-long process of disengagement from treatment. Patients who discontinue medications early in treatment or without medical consultation appear to drink more frequently and more heavily. Reprinted by permission of Blackwell Publishing JF - Addiction AU - Falk, Daniel AU - Stout, Robert L AU - Braciszewski, Jordan M AU - Subbaraman, Meenakshi Sabina AU - Kranzler, Henry R AU - O'malley, Stephanie S AD - Pacific Institute for Research and Evaluation ; University of California, Berkeley ; University of Pennsylvania ; Yale University ; National Institute on Alcohol Abuse and Alcoholism Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 2044 EP - 2052 VL - 109 IS - 12 SN - 0965-2140, 0965-2140 KW - Sociology KW - Alcohol KW - Medical care KW - Pharmaceuticals KW - Medicine KW - Patients KW - Medical treatment KW - Addiction KW - Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1625335697?accountid=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=What+happens+when+people+discontinue+taking+medications%3F+Lessons+from+COMBINE&rft.au=Falk%2C+Daniel%3BStout%2C+Robert+L%3BBraciszewski%2C+Jordan+M%3BSubbaraman%2C+Meenakshi+Sabina%3BKranzler%2C+Henry+R%3BO%27malley%2C+Stephanie+S&rft.aulast=Falk&rft.aufirst=Daniel&rft.date=2014-12-01&rft.volume=109&rft.issue=12&rft.spage=2044&rft.isbn=&rft.btitle=&rft.title=Addiction&rft.issn=09652140&rft_id=info:doi/10.1111%2Fadd.12700 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-11-17 N1 - Last updated - 2014-11-17 N1 - SubjectsTermNotLitGenreText - 7875 5775 13521; 7890 5792 10484; 3755; 9474; 9271 7890 5792 10484; 909; 561 6220; 7894 DO - http://dx.doi.org/10.1111/add.12700 ER - TY - JOUR T1 - Unrelated solubility-enhancing fusion partners MBP and NusA utilize a similar mode of action AN - 1622606905; 20891073 AB - The tendency of recombinant proteins to accumulate in the form of insoluble aggregates in Escherichia coli is a major hindrance to their overproduction. One of the more effective approaches to circumvent this problem is to use translation fusion partners {solubility-enhancers (SEs)}. E. coli maltose-binding protein (MBP) and N-utilization substance A (NusA) are arguably the most effective solubilizing agents that have been discovered so far. Here, we show that although these two proteins are structurally, functionally, and physicochemically distinct, they influence the solubility and folding of their fusion partners in a very similar manner. These SEs act as "holdases" that prevent the aggregation of their fusion partners. Subsequent folding of the passenger proteins, when it occurs, is either spontaneous or chaperone-mediated. Biotechnol. Bioeng. 2014; 111: 2407-2411. copyright 2014 Wiley Periodicals, Inc. The structures of MBP (PDB:10MP) and NusA (PDB:1L2F) are radically different, as illustrated by these ribbon models, but they utilize a similar mechanism of action to enhance the solubility of their fusion partners. Amino- and carboxy-termini are labeled N and C, respectively. Passenger proteins are fused to the C-termini. Alpha helices and beta sheets are colored cyan and pink, respectively. JF - Biotechnology and Bioengineering AU - Raran-Kurussi, Sreejith AU - Waugh, David S AD - Protein Engineering Section, Macromolecular Crystallography Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, Maryland. Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 2407 EP - 2411 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 111 IS - 12 SN - 0006-3592, 0006-3592 KW - Biotechnology and Bioengineering Abstracts KW - Protein structure KW - Translation KW - Solubility KW - Escherichia coli KW - maltose-binding protein KW - Models KW - W 30925:Genetic Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622606905?accountid=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=Clinical+and+Vaccine+Immunology&rft.atitle=Successful+Protection+against+Tularemia+in+C57BL%2F6+Mice+Is+Correlated+with+Expansion+of+Francisella+tularensis-Specific+Effector+T+Cells&rft.au=Griffin%2C+Amanda+J%3BCrane%2C+Deborah+D%3BWehrly%2C+Tara+D%3BBosio%2C+Catharine+M&rft.aulast=Griffin&rft.aufirst=Amanda&rft.date=2015-01-01&rft.volume=22&rft.issue=1&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=15566811&rft_id=info:doi/10.1128%2FCVI.00648-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Protein structure; Translation; Solubility; maltose-binding protein; Models; Escherichia coli DO - http://dx.doi.org/10.1002/bit.25317 ER - TY - JOUR T1 - Linking polymorphic p53 response elements with gene expression in airway epithelial cells of smokers and cancer risk. AN - 1622065517; 25179167 AB - Chronic cigarette smoking exposes airway epithelial cells to thousands of carcinogens, oxidants and DNA-damaging agents, creating a field of molecular injury in the airway and altering gene expression. Studies of cytologically normal bronchial epithelial cells from smokers have identified transcription-based biomarkers that may prove useful in early diagnosis of lung cancer, including a number of p53-regulated genes. The ability of p53 to regulate transcription is critical for tumor suppression, and this suggests that single-nucleotide polymorphisms (SNPs) in functional p53 binding sites (p53 response elements, or p53REs) that affect gene expression could influence susceptibility to cancer. To connect p53RE SNP genotype with gene expression and cancer risk, we identified a set of 204 SNPs in putative p53REs, and performed cis expression quantitative trait loci (eQTL) analysis, assessing associations between SNP genotypes and mRNA levels of adjacent genes in bronchial epithelial cells obtained from 44 cigarette smokers. To further test and validate these genotype-expression associations, we searched published eQTL studies from independent populations and determined that 53% (39/74) of the bronchial epithelial eQTLs were observed in at least one of other studies. SNPs in p53REs were also evaluated for effects on p53-DNA binding using a quantitative in vitro protein-DNA binding assay. Last, based on linkage disequilibrium, we found 6 p53RE SNPs associated with gene expression were identified as cancer risk SNPs by either genome-wide association studies or candidate gene studies. We provide an approach for identifying and evaluating potentially functional SNPs that may modulate the airway gene expression response to smoking and may influence susceptibility to cancers. JF - Human genetics AU - Wang, Xuting AU - Pittman, Gary S AU - Bandele, Omari J AU - Bischof, Jason J AU - Liu, Gang AU - Brothers, John F AU - Spira, Avrum AU - Bell, Douglas A AD - Environmental Genomics Section, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Mail Drop: C3-03, 111 TW Alexander Drive, PO Box 12233, Research Triangle Park, NC, 27709, USA. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 1467 EP - 1476 VL - 133 IS - 12 KW - TP53 protein, human KW - 0 KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Polymorphism, Single Nucleotide KW - Oligonucleotide Array Sequence Analysis KW - Humans KW - Quantitative Trait Loci KW - Genetic Association Studies KW - Linkage Disequilibrium KW - Protein Binding KW - Respiratory Mucosa -- pathology KW - Binding Sites KW - Risk KW - Base Sequence KW - Respiratory Mucosa -- metabolism KW - Genetic Predisposition to Disease KW - Transcriptome KW - Epithelial Cells -- metabolism KW - Tumor Suppressor Protein p53 -- physiology KW - Lung Neoplasms -- etiology KW - Smoking -- metabolism KW - Smoking -- adverse effects KW - Response Elements KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622065517?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+genetics&rft.atitle=Linking+polymorphic+p53+response+elements+with+gene+expression+in+airway+epithelial+cells+of+smokers+and+cancer+risk.&rft.au=Wang%2C+Xuting%3BPittman%2C+Gary+S%3BBandele%2C+Omari+J%3BBischof%2C+Jason+J%3BLiu%2C+Gang%3BBrothers%2C+John+F%3BSpira%2C+Avrum%3BBell%2C+Douglas+A&rft.aulast=Wang&rft.aufirst=Xuting&rft.date=2014-12-01&rft.volume=133&rft.issue=12&rft.spage=1467&rft.isbn=&rft.btitle=&rft.title=Human+genetics&rft.issn=1432-1203&rft_id=info:doi/10.1007%2Fs00439-014-1483-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-12 N1 - Date created - 2014-11-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Genet. 2008 Feb;40(2):124-5 [18227866] Nat Genet. 2007 Oct;39(10):1217-24 [17873874] PLoS Biol. 2008 May 6;6(5):e107 [18462017] N Engl J Med. 2008 Sep 25;359(13):1367-80 [18815398] PLoS Genet. 2008 Oct;4(10):e1000214 [18846210] Cancer Prev Res (Phila). 2008 Nov;1(6):396-403 [19138985] PLoS Genet. 2009 May;5(5):e1000462 [19424414] Proc Natl Acad Sci U S A. 2009 Jun 9;106(23):9362-7 [19474294] PLoS One. 2010;5(5):e10693 [20502693] PLoS One. 2010;5(8):e11934 [20689807] Nucleic Acids Res. 2011 Jan;39(1):178-89 [20817676] Nat Genet. 2012 Oct;44(10):1084-9 [22941192] Nature. 2012 Nov 1;491(7422):56-65 [23128226] Cell Death Differ. 2012 Dec;19(12):1992-2002 [22790872] Genome Res. 2013 Apr;23(4):716-26 [23345460] Nat Genet. 2013 Oct;45(10):1238-43 [24013639] Hum Mutat. 2003 Mar;21(3):229-39 [12619108] Ann Oncol. 1999;10 Suppl 5:S7-11 [10582132] Cell. 2013 Oct 10;155(2):410-22 [24120139] Cancer Cell. 2003 Apr;3(4):387-402 [12726864] Cancer Epidemiol Biomarkers Prev. 2004 Mar;13(3):445-53 [15006922] Clin Cancer Res. 2004 Apr 1;10(7):2379-85 [15073114] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10143-8 [15210990] Nature. 2004 Aug 12;430(7001):743-7 [15269782] J Clin Invest. 1997 Oct 15;100(8):2133-7 [9329980] J Natl Cancer Inst. 1999 Feb 17;91(4):332-9 [10050866] Cancer. 1953 Sep;6(5):963-8 [13094644] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078] Proc Natl Acad Sci U S A. 2005 May 3;102(18):6431-6 [15843459] Nature. 2005 Oct 27;437(7063):1365-9 [16251966] PLoS Genet. 2005 Dec;1(6):e78 [16362079] Nat Genet. 2006 Oct;38(10):1133-41 [16964264] Nat Med. 2007 Mar;13(3):361-6 [17334370] Hum Mol Genet. 2007 May 15;16(10):1188-200 [17409198] Am J Hum Genet. 2007 Sep;81(3):559-75 [17701901] Nat Rev Mol Cell Biol. 2008 May;9(5):402-12 [18431400] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00439-014-1483-8 ER - TY - JOUR T1 - Wuzhi tablet (Schisandra Sphenanthera extract) protects against acetaminophen-induced hepatotoxicity by inhibition of CYP-mediated bioactivation and regulation of NRF2-ARE and p53/p21 pathways. AN - 1619319008; 25217484 AB - Schisandra sphenanthera is widely used as a tonic and restorative in many countries to enhance the function of liver and other organs. Wuzhi tablet (WZ) is a preparation of an ethanol extract of Schisandra sphenanthera. Our previous study demonstrated that WZ exerted a protective effect toward acetaminophen (APAP)-induced hepatotoxicity. However, the molecular mechanisms of this protection remain unclear. This study aimed to determine what molecular pathways contributed to the hepatoprotective effects of WZ against APAP toxicity. Administration of WZ 3 days before APAP treatment significantly attenuated APAP hepatotoxicity in a dose-dependent manner and reduced APAP-induced JNK activation. Treatment with WZ resulted in potent inhibition of CYP2E1, CYP3A11, and CYP1A2 activities and then caused significant inhibition of the formation of the oxidized APAP metabolite N-acetyl-p-benzoquinone imine-reduced glutathione. The expression of NRF2 was increased after APAP and/or WZ treatment, whereas KEAP1 levels were decreased. The protein expression of NRF2 target genes including Gclc, Gclm, Ho-1, and Nqo1 was significantly increased by WZ treatment. Furthermore, APAP increased the levels of p53 and its downstream gene p21 to trigger cell cycle arrest and apoptosis, whereas WZ pretreatment could inhibit p53/p21 signaling to induce cell proliferation-associated proteins including cyclin D1, CDK4, PCNA, and ALR to promote hepatocyte proliferation. This study demonstrated that WZ prevented APAP-induced liver injury by inhibition of cytochrome P450-mediated APAP bioactivation, activation of the NRF2-antioxidant response element pathway to induce detoxification and antioxidation, and regulation of the p53, p21, cyclin D1, CDK4, PCNA, and ALR to facilitate liver regeneration after APAP-induced liver injury. U.S. Government work not protected by U.S. copyright. JF - Drug metabolism and disposition: the biological fate of chemicals AU - Fan, Xiaomei AU - Jiang, Yiming AU - Wang, Ying AU - Tan, Huasen AU - Zeng, Hang AU - Wang, Yongtao AU - Chen, Pan AU - Qu, Aijuan AU - Gonzalez, Frank J AU - Huang, Min AU - Bi, Huichang AD - School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China (X.F., Y.J., Yo.W., H.T., H.Z., Yi. W., M.H., H.B.); The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China (P.C.); and Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland (A.Q., F.J.G). ; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China (X.F., Y.J., Yo.W., H.T., H.Z., Yi. W., M.H., H.B.); The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China (P.C.); and Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland (A.Q., F.J.G) bihchang@mail.sysu.edu.cn. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 1982 EP - 1990 VL - 42 IS - 12 KW - Antioxidants KW - 0 KW - Cyclin-Dependent Kinase Inhibitor p21 KW - Drugs, Chinese Herbal KW - NF-E2-Related Factor 2 KW - Nfe2l2 protein, mouse KW - Plant Extracts KW - Protective Agents KW - Tablets KW - Tumor Suppressor Protein p53 KW - wuzhi KW - Acetaminophen KW - 362O9ITL9D KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Carboxylic Ester Hydrolases KW - EC 3.1.1.- KW - arylesterase KW - EC 3.1.1.2 KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Animals KW - Hepatocytes -- drug effects KW - Acetaminophen -- adverse effects KW - Liver -- metabolism KW - Mice KW - Protective Agents -- pharmacology KW - Tablets -- pharmacology KW - Plant Extracts -- pharmacology KW - Antioxidants -- pharmacology KW - Liver -- drug effects KW - Signal Transduction -- drug effects KW - Mice, Inbred C57BL KW - Male KW - Hepatocytes -- metabolism KW - Carboxylic Ester Hydrolases -- metabolism KW - Schisandra -- chemistry KW - Cyclin-Dependent Kinase Inhibitor p21 -- metabolism KW - Tumor Suppressor Protein p53 -- metabolism KW - Drugs, Chinese Herbal -- pharmacology KW - Chemical and Drug Induced Liver Injury -- metabolism KW - Chemical and Drug Induced Liver Injury -- drug therapy KW - NF-E2-Related Factor 2 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619319008?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.atitle=Wuzhi+tablet+%28Schisandra+Sphenanthera+extract%29+protects+against+acetaminophen-induced+hepatotoxicity+by+inhibition+of+CYP-mediated+bioactivation+and+regulation+of+NRF2-ARE+and+p53%2Fp21+pathways.&rft.au=Fan%2C+Xiaomei%3BJiang%2C+Yiming%3BWang%2C+Ying%3BTan%2C+Huasen%3BZeng%2C+Hang%3BWang%2C+Yongtao%3BChen%2C+Pan%3BQu%2C+Aijuan%3BGonzalez%2C+Frank+J%3BHuang%2C+Min%3BBi%2C+Huichang&rft.aulast=Fan&rft.aufirst=Xiaomei&rft.date=2014-12-01&rft.volume=42&rft.issue=12&rft.spage=1982&rft.isbn=&rft.btitle=&rft.title=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.issn=1521-009X&rft_id=info:doi/10.1124%2Fdmd.114.059535 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-01 N1 - Date created - 2014-11-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/dmd.114.059535 ER - TY - JOUR T1 - Subpicomolar diphenyleneiodonium inhibits microglial NADPH oxidase with high specificity and shows great potential as a therapeutic agent for neurodegenerative diseases. AN - 1614700436; 25043383 AB - Activation of microglial NADPH oxidase (NOX2) plays a critical role in mediating neuroinflammation, which is closely linked with the pathogenesis of a variety of neurodegenerative diseases, including Parkinson's disease (PD). The inhibition of NOX2-generated superoxide has become an effective strategy for developing disease-modifying therapies for PD. However, the lack of specific and potent NOX2 inhibitors has hampered the progress of this approach. Diphenyleneiodonium (DPI) is a widely used, long-acting NOX2 inhibitor. However, due to its non-specificity for NOX2 and high cytotoxicity at standard doses (µM), DPI has been precluded from human studies. In this study, using ultra-low doses of DPI, we aimed to: (1) investigate whether these problems could be circumvented and (2) determine whether ultra-low doses of DPI were able to preserve its utility as a potent NOX2 inhibitor. We found that DPI at subpicomolar concentrations (10(-14) and 10(-13) M) displays no toxicity in primary midbrain neuron-glia cultures. More importantly, we observed that subpicomolar DPI inhibited phorbol myristate acetate (PMA)-induced activation of NOX2. The same concentrations of DPI did not inhibit the activities of a series of flavoprotein-containing enzymes. Furthermore, potent neuroprotective efficacy was demonstrated in a post-treatment study. When subpicomolar DPI was added to neuron-glia cultures pretreated with lipopolysaccharide, 1-methyl-4-phenylpyridinium or rotenone, it potently protected the dopaminergic neurons. In summary, DPI's unique combination of high specificity toward NOX2, low cytotoxicity and potent neuroprotective efficacy in post-treatment regimens suggests that subpicomolar DPI may be an ideal candidate for further animal studies and potential clinical trials. © 2014 Wiley Periodicals, Inc. JF - Glia AU - Wang, Qingshan AU - Chu, Chun-Hsien AU - Oyarzabal, Esteban AU - Jiang, Lulu AU - Chen, Shih-Heng AU - Wilson, Belinda AU - Qian, Li AU - Hong, Jau-Shyong AD - Neuropharmacology Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 2034 EP - 2043 VL - 62 IS - 12 KW - Aif1 protein, rat KW - 0 KW - Calcium-Binding Proteins KW - Enzyme Inhibitors KW - Glial Fibrillary Acidic Protein KW - Microfilament Proteins KW - Nitrites KW - Onium Compounds KW - Superoxides KW - 11062-77-4 KW - diphenyleneiodonium KW - 6HJ411TU98 KW - Nitric Oxide Synthase Type II KW - EC 1.14.13.39 KW - Tyrosine 3-Monooxygenase KW - EC 1.14.16.2 KW - Xanthine Oxidase KW - EC 1.17.3.2 KW - NADPH-Ferrihemoprotein Reductase KW - EC 1.6.2.4 KW - NADPH Oxidase KW - EC 1.6.3.1 KW - Electron Transport Complex I KW - EC 1.6.5.3 KW - Thioredoxin-Disulfide Reductase KW - EC 1.8.1.9 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - microglia KW - Parkinson's disease KW - oxidative stress KW - neuroinflammation KW - NADPH oxidase KW - Xanthine Oxidase -- metabolism KW - Animals KW - Tyrosine 3-Monooxygenase -- metabolism KW - Microfilament Proteins -- metabolism KW - Cell Count KW - Nitrites -- metabolism KW - Neurons -- drug effects KW - Electron Transport Complex I -- metabolism KW - Glial Fibrillary Acidic Protein -- metabolism KW - Dopamine -- metabolism KW - NADPH-Ferrihemoprotein Reductase -- metabolism KW - Mesencephalon -- cytology KW - Superoxides -- metabolism KW - Cells, Cultured KW - Thioredoxin-Disulfide Reductase -- metabolism KW - Neurons -- physiology KW - Nitric Oxide Synthase Type II -- metabolism KW - Calcium-Binding Proteins -- metabolism KW - NADPH Oxidase -- metabolism KW - Onium Compounds -- pharmacology KW - Enzyme Inhibitors -- pharmacology KW - Microglia -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1614700436?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Glia&rft.atitle=Subpicomolar+diphenyleneiodonium+inhibits+microglial+NADPH+oxidase+with+high+specificity+and+shows+great+potential+as+a+therapeutic+agent+for+neurodegenerative+diseases.&rft.au=Wang%2C+Qingshan%3BChu%2C+Chun-Hsien%3BOyarzabal%2C+Esteban%3BJiang%2C+Lulu%3BChen%2C+Shih-Heng%3BWilson%2C+Belinda%3BQian%2C+Li%3BHong%2C+Jau-Shyong&rft.aulast=Wang&rft.aufirst=Qingshan&rft.date=2014-12-01&rft.volume=62&rft.issue=12&rft.spage=2034&rft.isbn=&rft.btitle=&rft.title=Glia&rft.issn=1098-1136&rft_id=info:doi/10.1002%2Fglia.22724 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-19 N1 - Date created - 2014-10-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: FASEB J. 2005 Apr;19(6):550-7 [15791005] Antioxid Redox Signal. 2014 Jun 10;20(17):2741-54 [24070014] Prog Neurobiol. 2005 Jun;76(2):77-98 [16081203] Ann N Y Acad Sci. 2005 Aug;1053:107-20 [16179514] J Biol Chem. 2006 Oct 13;281(41):30336-46 [16895900] Nat Rev Neurosci. 2007 Jan;8(1):57-69 [17180163] Biochem Soc Trans. 2007 Nov;35(Pt 5):1119-21 [17956292] Parkinsonism Relat Disord. 2007;13 Suppl 3:S316-20 [18267257] Trends Immunol. 2008 Aug;29(8):357-65 [18599350] Curr Drug Metab. 2008 Oct;9(8):686-96 [18855607] Lancet Neurol. 2009 Apr;8(4):382-97 [19296921] J Pharmacol Sci. 2009 Oct;111(2):147-54 [19834286] Mol Biochem Parasitol. 2010 May;171(1):17-24 [20093143] Brain. 2010 Mar;133(Pt 3):808-21 [20123724] Prog Brain Res. 2010;184:113-32 [20887872] J Biol Chem. 2010 Nov 5;285(45):35169-79 [20817944] J Neurosci. 2011 Jan 19;31(3):1081-92 [21248133] Nat Rev Drug Discov. 2011 Jun;10(6):453-71 [21629295] Parkinsonism Relat Disord. 2012 Jan;18 Suppl 1:S210-2 [22166438] J Neuroinflammation. 2012;9:32 [22340895] Trends Pharmacol Sci. 2012 Jun;33(6):295-303 [22503440] Cell Mol Life Sci. 2012 Jul;69(14):2409-27 [22581365] Cell Mol Life Sci. 2012 Jul;69(14):2387-407 [22643836] Cold Spring Harb Perspect Med. 2012 Jul;2(7):a009290 [22762023] Glia. 2013 Jun;61(6):855-68 [23536230] Methods Mol Biol. 2013;1041:231-40 [23813383] Nat Med. 1999 Dec;5(12):1403-9 [10581083] J Neurosci. 2002 Feb 1;22(3):782-90 [11826108] Proc Natl Acad Sci U S A. 2003 May 13;100(10):6145-50 [12721370] Environ Health Perspect. 2003 Jun;111(8):1065-73 [12826478] J Biol Chem. 2004 Jan 9;279(2):1415-21 [14578353] Nat Rev Immunol. 2004 Mar;4(3):181-9 [15039755] Free Radic Biol Med. 2004 Jul 15;37(2):216-28 [15203193] Biochem J. 1993 Feb 15;290 ( Pt 1):41-9 [8439298] Biochemistry. 1999 Mar 23;38(12):3694-703 [10090757] FASEB J. 2005 Apr;19(6):489-96 [15790998] Traffic. 2013 Nov;14(11):1118-31 [23980663] Curr Opin Neurol. 2005 Jun;18(3):315-21 [15891419] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/glia.22724 ER - TY - JOUR T1 - PET and NIR optical imaging using self-illuminating (64)Cu-doped chelator-free gold nanoclusters. AN - 1566409017; 25224367 AB - Self-illuminating fluorescence imaging without autofluorescence background interference has recently aroused more research interests in molecular imaging. Currently, only a few self-illuminating probes were developed, based mainly on toxic quantum dots such as CdSe, CdTe. Herein, we report a novel design of nontoxic self-illuminating gold nanocluster ((64)Cu-doped AuNCs) for dual-modality positron emission tomography (PET) and near-infrared (NIR) fluorescence imaging based on Cerenkov resonance energy transfer (CRET). PET radionuclide (64)Cu was introduced by a chelator-free doping method, which played dual roles as the energy donor and the PET imaging source. Meanwhile, AuNCs acted as the energy acceptor for NIR fluorescence imaging. (64)Cu-doped AuNCs exhibited efficient CRET-NIR and PET imaging both in vitro and in vivo. In a U87MG glioblastoma xenograft model, (64)Cu-doped AuNCs showed high tumor uptake (14.9 %ID/g at 18 h) and produced satisfactory tumor self-illuminating NIR images in the absence of external excitation. This self-illuminating nanocluster with non-toxicity and good biocompatibility can be employed as a novel imaging contrast agent for biomedical applications, especially for molecular imaging. Published by Elsevier Ltd. JF - Biomaterials AU - Hu, Hao AU - Huang, Peng AU - Weiss, Orit Jacobson AU - Yan, Xuefeng AU - Yue, Xuyi AU - Zhang, Molly Gu AU - Tang, Yuxia AU - Nie, Liming AU - Ma, Ying AU - Niu, Gang AU - Wu, Kaichun AU - Chen, Xiaoyuan AD - State Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi'an, China; Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, MD, USA. ; Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, MD, USA. ; Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, MD, USA; Center for Molecular Imaging and Translational Medicine, State Key Laboratory of Molecular Vaccinology and Molecular Diagnostics, School of Public Health, Xiamen University, Xiamen, China. ; State Key Laboratory of Cancer Biology & Xijing Hospital of Digestive Diseases, Fourth Military Medical University, Xi'an, China. Electronic address: kaicwu@fmmu.edu.cn. ; Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, MD, USA. Electronic address: shawn.chen@nih.gov. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 9868 EP - 9876 VL - 35 IS - 37 KW - Isotopes KW - 0 KW - Gold KW - 7440-57-5 KW - Copper KW - 789U1901C5 KW - Index Medicus KW - Gold nanocluster KW - Positron emission tomography KW - Optical imaging KW - (64)Cu doping KW - Cerenkov effect KW - Animals KW - Infrared Rays KW - Humans KW - Mice KW - Cell Line, Tumor KW - Optical Imaging -- methods KW - Nanostructures -- chemistry KW - Positron-Emission Tomography -- methods KW - Glioblastoma -- diagnosis KW - Gold -- chemistry KW - Copper -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566409017?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomaterials&rft.atitle=PET+and+NIR+optical+imaging+using+self-illuminating+%2864%29Cu-doped+chelator-free+gold+nanoclusters.&rft.au=Hu%2C+Hao%3BHuang%2C+Peng%3BWeiss%2C+Orit+Jacobson%3BYan%2C+Xuefeng%3BYue%2C+Xuyi%3BZhang%2C+Molly+Gu%3BTang%2C+Yuxia%3BNie%2C+Liming%3BMa%2C+Ying%3BNiu%2C+Gang%3BWu%2C+Kaichun%3BChen%2C+Xiaoyuan&rft.aulast=Hu&rft.aufirst=Hao&rft.date=2014-12-01&rft.volume=35&rft.issue=37&rft.spage=9868&rft.isbn=&rft.btitle=&rft.title=Biomaterials&rft.issn=1878-5905&rft_id=info:doi/10.1016%2Fj.biomaterials.2014.08.038 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-03 N1 - Date created - 2014-09-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2006 Feb;114(2):165-72 [16451849] Nat Biotechnol. 2006 Mar;24(3):339-43 [16501578] Nat Biotechnol. 2006 Mar;24(3):326-8 [16525407] Curr Med Chem. 2006;13(8):897-909 [16611074] Annu Rev Phys Chem. 2007;58:409-31 [17105412] J Am Chem Soc. 2009 Jan 28;131(3):888-9 [19123810] Nanotechnology. 2010 Feb 5;21(5):055103 [20023317] J Nucl Med. 2010 Jul;51(7):1123-30 [20554722] Biomaterials. 2011 May;32(13):3447-58 [21303717] Chem Asian J. 2011 May 2;6(5):1156-62 [21341374] Philos Trans A Math Phys Eng Sci. 2011 Nov 28;369(1955):4605-19 [22006909] J Nucl Med. 2011 Dec;52(12):2009-18 [22080446] ACS Nano. 2011 Dec 27;5(12):9718-25 [22053819] Int J Nanomedicine. 2012;7:3433-43 [22848169] Adv Mater. 2012 Sep 25;24(37):5104-10 [22718562] Nat Med. 2013 Apr;19(4):500-5 [23455711] Biomaterials. 2013 Jun;34(19):4643-54 [23523428] Angew Chem Int Ed Engl. 2013 Dec 9;52(50):13319-23 [24166933] Angew Chem Int Ed Engl. 2014 Jan 3;53(1):156-9 [24272951] Adv Healthc Mater. 2014 Jan;3(1):133-41 [23873780] J Am Chem Soc. 2014 Feb 5;136(5):1706-9 [24401138] Chem Commun (Camb). 2014 May 25;50(40):5143-55 [24266029] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.biomaterials.2014.08.038 ER - TY - JOUR T1 - Changes in human pluripotent stem cell gene expression after genotoxic stress exposures. AN - 1637571708; 25426256 AB - Human pluripotent stem cells (hPSCs) represent heterogeneous populations, including induced pluripotent stem cells (iPSCs), endogenous plastic somatic cells, and embryonic stem cells (ESCs). Human ESCs are derived from the inner cell mass of the blastocyst, and they are characterized by the abilities to self-renew indefinitely, and to give rise to all cell types of embryonic lineage (pluripotency) under the guidance of the appropriate chemical, mechanical and environmental cues. The combination of these critical features is unique to hESCs, and set them apart from other human cells. The expectations are high to utilize hESCs for treating injuries and degenerative diseases; for modeling of complex illnesses and development; for screening and testing of pharmacological products; and for examining toxicity, mutagenicity, teratogenicity, and potential carcinogenic effects of a variety of environmental factors, including ionizing radiation (IR). Exposures to genotoxic stresses, such as background IR, are unavoidable; moreover, IR is widely used in diagnostic and therapeutic procedures in medicine on a routine basis. One of the key outcomes of cell exposures to IR is the change in gene expression, which may underlie the ultimate hESCs fate after such a stress. However, gaps in our knowledge about basic biology of hESCs impose a serious limitation to fully realize the potential of hESCs in practice. The purpose of this review is to examine the available evidence of alterations in gene expression in human pluripotent stem cells after genotoxic stress, and to discuss strategies for future research in this important area. JF - World journal of stem cells AU - Sokolov, Mykyta V AU - Neumann, Ronald D AD - Mykyta V Sokolov, Ronald D Neumann, Nuclear Medicine Division, Department of Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, Bethesda, MD 20892, United States. Y1 - 2014/11/26/ PY - 2014 DA - 2014 Nov 26 SP - 598 EP - 605 VL - 6 IS - 5 KW - Ionizing radiation KW - Gene expression alterations KW - Human pluripotent stem cells KW - Genotoxic stress UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1637571708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=World+journal+of+stem+cells&rft.atitle=Changes+in+human+pluripotent+stem+cell+gene+expression+after+genotoxic+stress+exposures.&rft.au=Sokolov%2C+Mykyta+V%3BNeumann%2C+Ronald+D&rft.aulast=Sokolov&rft.aufirst=Mykyta&rft.date=2014-11-26&rft.volume=6&rft.issue=5&rft.spage=598&rft.isbn=&rft.btitle=&rft.title=World+journal+of+stem+cells&rft.issn=&rft_id=info:doi/10.4252%2Fwjsc.v6.i5.598 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-26 N1 - Date created - 2014-11-26 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4252/wjsc.v6.i5.598 ER - TY - JOUR T1 - Association of serum alpha -tocopherol, beta -carotene, and retinol with liver cancer incidence and chronic liver disease mortality AN - 1635028256; 21050931 AB - Background: Micronutrients may influence the development or progression of liver cancer and liver disease. We evaluated the association of serum alpha -tocopherol, beta -carotene, and retinol with incident liver cancer and chronic liver disease (CLD) mortality in a prospective cohort of middle-aged Finnish male smokers. Methods: Baseline and 3-year follow-up serum were available from 29 046 and 22 805 men, respectively. After 24 years of follow-up, 208 men were diagnosed with liver cancer and 237 died from CLD. Hazards ratios and 95% confidence intervals were calculated for highest vs lowest quartiles from multivariate proportional hazards models. Results: Higher beta -carotene and retinol levels were associated with less liver cancer ( beta -carotene: 0.35, 0.22-0.55, P-trend <0.0001; retinol: 0.58, 0.39-0.85, P-trend=0.0009) and CLD mortality ( beta -carotene: 0.47, 0.30-0.75, P-trend=0.001; retinol: 0.55, 0.38-0.78, P-trend=0.0007). alpha -Tocopherol was associated with CLD mortality (0.63, 0.40-0.99, P-trend=0.06), but not with liver cancer (1.06, 0.64-1.74, P-trend=0.77). Participants with higher levels of beta -carotene and retinol, but not alpha -tocopherol, at both baseline and year 3 had lower risk of each outcome than those with lower levels. Conclusions: Our findings suggest that higher concentrations of beta -carotene and retinol are associated with incident liver cancer and CLD. However, such data do not indicate that supplementation should be considered for these diseases. JF - British Journal of Cancer AU - Lai, G Y AU - Weinstein, S J AU - Albanes, D AU - Taylor, P R AU - Virtamo, J AU - McGlynn, K A AU - Freedman, N D AD - 1] Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, 9609 Medical Center Drive, Bethesda, MD 20892, USA [2] Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Room 6E316, Bethesda, MD 20892, USA Y1 - 2014/11/25/ PY - 2014 DA - 2014 Nov 25 SP - 2163 EP - 2171 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 111 IS - 11 SN - 0007-0920, 0007-0920 KW - Risk Abstracts KW - Health risks KW - Mortality KW - Liver KW - Micronutrients KW - Cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635028256?accountid=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=Association+of+serum+alpha+-tocopherol%2C+beta+-carotene%2C+and+retinol+with+liver+cancer+incidence+and+chronic+liver+disease+mortality&rft.au=Lai%2C+G+Y%3BWeinstein%2C+S+J%3BAlbanes%2C+D%3BTaylor%2C+P+R%3BVirtamo%2C+J%3BMcGlynn%2C+K+A%3BFreedman%2C+N+D&rft.aulast=Lai&rft.aufirst=G&rft.date=2014-11-25&rft.volume=111&rft.issue=11&rft.spage=2163&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2014.365 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2015-02-12 N1 - SubjectsTermNotLitGenreText - Mortality; Health risks; Liver; Micronutrients; Cancer DO - http://dx.doi.org/10.1038/bjc.2014.365 ER - TY - JOUR T1 - Dialogue between skin microbiota and immunity AN - 1811903667; PQ0003455265 AB - Human skin, the body's largest organ, functions as a physical barrier to bar the entry of foreign pathogens, while concomitantly providing a home to myriad commensals. Over a human's life span, keratinized skin cells, immune cells, and microbes all interact to integrate the processes of maintaining skin's physical and immune barrier under homeostatic healthy conditions and also under multiple stresses, such as wounding or infection. In this Review, we explore the intricate interactions of microbes and immune cells on the skin surface and within associated appendages to regulate this orchestrated maturation in the context of both host physiological changes and environmental challenges. JF - Science AU - Belkaid, Yasmine AU - Segre, Julia A AD - Program in Barrier Immunity and Repair and Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institute of Health (NIH), Bethesda, MD, USA, ybelkaid@niaid.nih.gov Y1 - 2014/11/21/ PY - 2014 DA - 2014 Nov 21 SP - 954 EP - 959 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 346 IS - 6212 SN - 0036-8075, 0036-8075 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Skin KW - Commensals KW - Stress KW - Pathogens KW - Immunity KW - Infection KW - Wounding KW - A 01450:Environmental Pollution & Waste Treatment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1811903667?accountid=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=Dialogue+between+skin+microbiota+and+immunity&rft.au=Belkaid%2C+Yasmine%3BSegre%2C+Julia+A&rft.aulast=Belkaid&rft.aufirst=Yasmine&rft.date=2014-11-21&rft.volume=346&rft.issue=6212&rft.spage=954&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1260144 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-08-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Skin; Commensals; Stress; Immunity; Pathogens; Infection; Wounding DO - http://dx.doi.org/10.1126/science.1260144 ER - TY - CPAPER T1 - Immuno-spin trapping of alpha-synuclein radical formed in Maneb and paraquat-induced models of Parkinson's disease T2 - 21st Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2014) AN - 1645171810; 6325161 JF - 21st Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2014) AU - Kumar, Ashutosh Y1 - 2014/11/19/ PY - 2014 DA - 2014 Nov 19 KW - Synuclein KW - Neurodegenerative diseases KW - Movement disorders KW - Parkinson's disease KW - Trapping KW - Models KW - Radicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645171810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=21st+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2014%29&rft.atitle=Immuno-spin+trapping+of+alpha-synuclein+radical+formed+in+Maneb+and+paraquat-induced+models+of+Parkinson%27s+disease&rft.au=Kumar%2C+Ashutosh&rft.aulast=Kumar&rft.aufirst=Ashutosh&rft.date=2014-11-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=21st+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfrbm.org/pdf/SFRBM2014-OralPresentations.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Nrf2 in Human (and Mouse) Diseases T2 - 21st Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2014) AN - 1645169186; 6325136 JF - 21st Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2014) AU - Kleeberger, Steven Y1 - 2014/11/19/ PY - 2014 DA - 2014 Nov 19 KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645169186?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=21st+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2014%29&rft.atitle=Nrf2+in+Human+%28and+Mouse%29+Diseases&rft.au=Kleeberger%2C+Steven&rft.aulast=Kleeberger&rft.aufirst=Steven&rft.date=2014-11-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=21st+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfrbm.org/sections/annual-meeting/21st-annual-meeting-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Peripherally restricted, selective cannabinoid CB2 receptor agonist LEI-101 prevents cisplatin-induced nephrotoxicity by attenuating oxidative/nitrative stress and inflammation T2 - 21st Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2014) AN - 1645168979; 6325165 JF - 21st Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2014) AU - Pacher, Pal Y1 - 2014/11/19/ PY - 2014 DA - 2014 Nov 19 KW - Cannabinoid CB2 receptors KW - Stress KW - Inflammation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645168979?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=21st+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2014%29&rft.atitle=Peripherally+restricted%2C+selective+cannabinoid+CB2+receptor+agonist+LEI-101+prevents+cisplatin-induced+nephrotoxicity+by+attenuating+oxidative%2Fnitrative+stress+and+inflammation&rft.au=Pacher%2C+Pal&rft.aulast=Pacher&rft.aufirst=Pal&rft.date=2014-11-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=21st+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfrbm.org/pdf/SFRBM2014-OralPresentations.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Goals and Priorities of the National Institute of Environmental Health Sciences (NIEHS) T2 - 21st Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2014) AN - 1645168841; 6325148 JF - 21st Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2014) AU - Reinlib, Leslie Y1 - 2014/11/19/ PY - 2014 DA - 2014 Nov 19 KW - Priorities KW - Environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645168841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=21st+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2014%29&rft.atitle=Goals+and+Priorities+of+the+National+Institute+of+Environmental+Health+Sciences+%28NIEHS%29&rft.au=Reinlib%2C+Leslie&rft.aulast=Reinlib&rft.aufirst=Leslie&rft.date=2014-11-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=21st+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfrbm.org/sections/annual-meeting/21st-annual-meeting-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Malaria vector diversity in Southeast Asia and beyond: Challenges and opportunities T2 - 62nd Annual Meeting of the Entomological Society of America (Entomology 2014) AN - 1645158326; 6323004 JF - 62nd Annual Meeting of the Entomological Society of America (Entomology 2014) AU - St Laurent, Brandyce Y1 - 2014/11/16/ PY - 2014 DA - 2014 Nov 16 KW - Species diversity KW - Vectors KW - Malaria KW - Southeast Asia UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645158326?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Entomological+Society+of+America+%28Entomology+2014%29&rft.atitle=Malaria+vector+diversity+in+Southeast+Asia+and+beyond%3A+Challenges+and+opportunities&rft.au=St+Laurent%2C+Brandyce&rft.aulast=St+Laurent&rft.aufirst=Brandyce&rft.date=2014-11-16&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=62nd+Annual+Meeting+of+the+Entomological+Society+of+America+%28Entomology+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://esa.confex.com/esa/2014/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - JOUR T1 - Diminished Systemic and Antigen-Specific Type 1, Type 17, and Other Proinflammatory Cytokines in Diabetic and Prediabetic Individuals With Latent Mycobacterium tuberculosis Infection AN - 1694971749; PQ0001607954 AB - Background. Diabetes mellitus type 2 (DM) is known to be a major risk factor for the development of active tuberculosis, although its influence on latent Mycobacterium tuberculosis infection (hereafter, "latent infection") remains poorly characterized. Methods. We examined circulating plasma cytokine levels in individuals with latent infection with DM or pre-DM (ie, intermediate hyperglycemia) and compared them to levels in patients with latent infection and normal glycemic control. Results. In persons with DM or pre-DM, latent infection is characterized by diminished circulating levels of type 1 (interferon gamma , interleukin 2, and tumor necrosis factor alpha ) and type 17 (interleukin 17F) cytokines. This was associated with decreased systemic levels of other proinflammatory cytokines (interleukin 1 beta and interleukin 18) and the antiinflammatory cytokine interleukin 10 but not with decreased systemic levels of type 2 cytokines. Moreover, latently infected individuals with DM had diminished levels of spontaneous and M. tuberculosis antigen-specific levels of type 1 and type 17 cytokines when antigen-stimulated whole blood was examined. Finally, there was no significant correlation between the levels of any of the cytokines measured (with the exception of interleukin 22) with hemoglobin A1c levels. Conclusions. Our data reveal that latent infection in the presence of DM or pre-DM, is characterized by diminished production of cytokines, implicated in the control of M. tuberculosis activation, allowing for a potential immunological mechanism that could account for the increased risk of active tuberculosis in latently infected individuals with DM. JF - Journal of Infectious Diseases AU - Kumar, Nathella Pavan AU - George, Parakkal Jovvian AU - Kumaran, Paul AU - Dolla, Chandra Kumar AU - Nutman, Thomas B AU - Babu, Subash AD - National Institutes of Health-International Center for Excellence in Research; National Institute for Research in Tuberculosis, sbabu@mail.nih.gov Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 SP - 1670 EP - 1678 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 210 IS - 10 SN - 0022-1899, 0022-1899 KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - bacterial KW - cytokines KW - diabetes KW - pre-diabetes KW - tuberculosis KW - gamma -Interferon KW - Latent infection KW - Data processing KW - Interleukin 2 KW - Interleukin 1 KW - Interleukin 10 KW - Inflammation KW - Hemoglobin KW - Diabetes mellitus KW - Blood KW - Interleukin 22 KW - Hyperglycemia KW - Risk factors KW - Interleukin 18 KW - Cytokines KW - Tuberculosis KW - Tumor necrosis factor- alpha KW - Mycobacterium tuberculosis KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694971749?accountid=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=Diminished+Systemic+and+Antigen-Specific+Type+1%2C+Type+17%2C+and+Other+Proinflammatory+Cytokines+in+Diabetic+and+Prediabetic+Individuals+With+Latent+Mycobacterium+tuberculosis+Infection&rft.au=Kumar%2C+Nathella+Pavan%3BGeorge%2C+Parakkal+Jovvian%3BKumaran%2C+Paul%3BDolla%2C+Chandra+Kumar%3BNutman%2C+Thomas+B%3BBabu%2C+Subash&rft.aulast=Kumar&rft.aufirst=Nathella&rft.date=2014-11-15&rft.volume=210&rft.issue=10&rft.spage=1670&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiu329 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-07-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Latent infection; gamma -Interferon; Data processing; Interleukin 2; Interleukin 1; Interleukin 10; Inflammation; Diabetes mellitus; Hemoglobin; Blood; Interleukin 22; Hyperglycemia; Risk factors; Interleukin 18; Cytokines; Tuberculosis; Tumor necrosis factor- alpha; Mycobacterium tuberculosis DO - http://dx.doi.org/10.1093/infdis/jiu329 ER - TY - JOUR T1 - Antigen-Presenting Phagocytic Cells Ingest Malaria Parasites and Increase HIV Replication in a Tumor Necrosis Factor alpha -Dependent Manner AN - 1694971070; PQ0001607943 AB - Background. Plasmodium falciparum infection induces human immunodeficiency virus (HIV) replication and accelerates a decline in CD4 super(+) T-cell count. The mechanisms contributing to these interactions have not been fully elucidated. Methods. We infected peripheral blood mononuclear cells (PBMCs) with HIV type 1 (HIV-1) and then cocultured them with P. falciparum-infected red blood cells (iRBCs) or uninfected RBCs (uRBCs). Levels of HIV-1 p24 antigen and activation-associated cytokines were measured in culture supernatants. T-cell surface activation was assessed by flow cytometry. Results. It has been reported that iRBCs increase HIV replication, compared with uRBCs; that neutralizing tumor necrosis factor alpha (TNF- alpha ) abrogates this increase; and that hemozoin enhances HIV production. In this study, we confirmed that TNF- alpha plays an important role in this interaction. We show that iRBCs increased CD4 super(+) T-cell expression of HLA-DR super(+)/CD38 super(+) (P = .001), that monocyte/macrophage depletion reduced HIV production by 40%-50% (P < .001), and that hemozoin-laden monocytes/macrophages that were preincubated with iRBCs also stimulated HIV production. Conclusions. iRBCs activate CD4 super(+) T cells and stimulate HIV replication in a TNF- alpha -dependent manner following malarial antigen processing by monocytes/macrophages. These results suggest that the persistent elevation of HIV replication during and after acute bouts of P. falciparum malaria may be due, at least in part, to ongoing stimulation of CD4 super(+) T cells by hemozoin-loaded antigen-presenting cells within lymphoid tissues. JF - Journal of Infectious Diseases AU - Orlovi, Marika AU - Vaida, Florin AU - Williamson, Kathryn AU - Deng, Qianqian AU - Smith, David M AU - Duffy, Patrick E AU - Schooley, Robert T AD - University of California-San Diego, La Jolla; Seattle Biomedical Research Institute, Washington, duffype@niaid.nih.gov Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 SP - 1562 EP - 1572 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 210 IS - 10 SN - 0022-1899, 0022-1899 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - HIV KW - P. falciparum KW - interaction KW - mechanism of increased viral load KW - malaria KW - co-infection KW - Histocompatibility antigen HLA KW - Macrophages KW - Parasites KW - hemozoin KW - Human diseases KW - Erythrocytes KW - Cell culture KW - Malaria KW - Infection KW - Public health KW - Flow cytometry KW - CD4 antigen KW - Peripheral blood mononuclear cells KW - Antigens KW - Infectious diseases KW - Phagocytes KW - Human immunodeficiency virus 1 KW - Lymphocytes T KW - Cytokines KW - Antigen processing KW - Antigen-presenting cells KW - Monocytes KW - p24 protein KW - Replication KW - Plasmodium falciparum KW - Tumors KW - Lymphoid tissue KW - Human immunodeficiency virus KW - Tumor necrosis factor- alpha KW - Tumours KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22360:AIDS and HIV KW - K 03400:Human Diseases KW - Q1 08604:Stock assessment and management KW - F 06910:Microorganisms & Parasites KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694971070?accountid=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=Antigen-Presenting+Phagocytic+Cells+Ingest+Malaria+Parasites+and+Increase+HIV+Replication+in+a+Tumor+Necrosis+Factor+alpha+-Dependent+Manner&rft.au=Orlovi%2C+Marika%3BVaida%2C+Florin%3BWilliamson%2C+Kathryn%3BDeng%2C+Qianqian%3BSmith%2C+David+M%3BDuffy%2C+Patrick+E%3BSchooley%2C+Robert+T&rft.aulast=Orlovi&rft.aufirst=Marika&rft.date=2014-11-15&rft.volume=210&rft.issue=10&rft.spage=1562&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiu317 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-07-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Flow cytometry; Macrophages; Parasites; Human diseases; Antigens; Replication; Malaria; Tumours; Public health; Histocompatibility antigen HLA; p24 protein; hemozoin; Erythrocytes; Cell culture; Infection; Lymphoid tissue; Peripheral blood mononuclear cells; CD4 antigen; Phagocytes; Lymphocytes T; Cytokines; Antigen processing; Tumor necrosis factor- alpha; Monocytes; Antigen-presenting cells; Infectious diseases; Human immunodeficiency virus; Tumors; Human immunodeficiency virus 1; Plasmodium falciparum DO - http://dx.doi.org/10.1093/infdis/jiu317 ER - TY - CPAPER T1 - Non-apoptotic functions of the mitochondria-caspase cascade at pre- and post-synaptic sites T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647640155; 6326285 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Li, Z. Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Mitochondria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647640155?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Non-apoptotic+functions+of+the+mitochondria-caspase+cascade+at+pre-+and+post-synaptic+sites&rft.au=Li%2C+Z.&rft.aulast=Li&rft.aufirst=Z.&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Fear extinction facilitation by fluoxetine is mediated by basolateral amygdala endocannabinoids T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647639575; 6326372 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Gunduz Cinar, O AU - Flynn, S AU - Cinar, R AU - Ramikie, T AU - Kunos, G AU - Patel, S AU - Holmes, A Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Fluoxetine KW - Cannabinoids KW - Extinction KW - Amygdala KW - Fear conditioning UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639575?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Fear+extinction+facilitation+by+fluoxetine+is+mediated+by+basolateral+amygdala+endocannabinoids&rft.au=Gunduz+Cinar%2C+O%3BFlynn%2C+S%3BCinar%2C+R%3BRamikie%2C+T%3BKunos%2C+G%3BPatel%2C+S%3BHolmes%2C+A&rft.aulast=Gunduz+Cinar&rft.aufirst=O&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - PET imaging of translocator protein, a neuroinflammatory biomarker, in vivo in patients with temporal lobe epilepsy T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647639556; 6326205 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Dickstein, L AU - Zanotti-Fregonara, P AU - Dustin, I AU - Hong, J AU - Liow, J AU - Pike, V AU - Zoghbi, S AU - Innis, R AU - Theodore, W Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Temporal lobe KW - Bioindicators KW - Epilepsy KW - Positron emission tomography KW - Biomarkers KW - biomarkers KW - Imaging techniques KW - Inflammation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639556?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=PET+imaging+of+translocator+protein%2C+a+neuroinflammatory+biomarker%2C+in+vivo+in+patients+with+temporal+lobe+epilepsy&rft.au=Dickstein%2C+L%3BZanotti-Fregonara%2C+P%3BDustin%2C+I%3BHong%2C+J%3BLiow%2C+J%3BPike%2C+V%3BZoghbi%2C+S%3BInnis%2C+R%3BTheodore%2C+W&rft.aulast=Dickstein&rft.aufirst=L&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Neuron and astroglia preserve microglial endotoxin tolerance through macrophage colony-stimulating factor T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647639535; 6325946 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Chu, C AU - Wang, S AU - Wang, Q AU - Chen, S AU - Gao, H AU - Lu, R. AU - Hong, J Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Macrophages KW - Endotoxins KW - Astrocytes KW - Neurons KW - Macrophage colony-stimulating factor UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639535?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Expert+opinion+on+drug+safety&rft.atitle=Class+act%3A+safety+comparison+of+approved+tyrosine+kinase+inhibitors+for+non-small-cell+lung+carcinoma.&rft.au=Burotto%2C+Mauricio%3BAli%2C+Syed+Abbas%3BO%27Sullivan+Coyne%2C+Geraldine&rft.aulast=Burotto&rft.aufirst=Mauricio&rft.date=2015-01-01&rft.volume=14&rft.issue=1&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+drug+safety&rft.issn=1744-764X&rft_id=info:doi/10.1517%2F14740338.2014.973400 L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Neural encoding of the immediate and future value of novel choice options in amygdala, ventral striatum, and orbitofrontal cortex T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647639471; 6326260 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Costa, V AU - Kakalios, L AU - Averbeck, B Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Cortex KW - Neostriatum KW - Amygdala UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639471?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Neural+encoding+of+the+immediate+and+future+value+of+novel+choice+options+in+amygdala%2C+ventral+striatum%2C+and+orbitofrontal+cortex&rft.au=Costa%2C+V%3BKakalios%2C+L%3BAverbeck%2C+B&rft.aulast=Costa&rft.aufirst=V&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Development of the intrinsic functional connectivity of reward and salience circuitries T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647639445; 6326424 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Ernst, M AU - Benson, B AU - Kundru, P AU - Luh, W AU - Bandettini, P AU - Pine, D Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Reinforcement UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639445?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Development+of+the+intrinsic+functional+connectivity+of+reward+and+salience+circuitries&rft.au=Ernst%2C+M%3BBenson%2C+B%3BKundru%2C+P%3BLuh%2C+W%3BBandettini%2C+P%3BPine%2C+D&rft.aulast=Ernst&rft.aufirst=M&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Irreproducible results? NIH perspectives on the causes and solutions T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647639368; 6326146 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Collins, F Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Nervous sytems KW - Neuroscience UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639368?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Irreproducible+results%3F+NIH+perspectives+on+the+causes+and+solutions&rft.au=Collins%2C+F&rft.aulast=Collins&rft.aufirst=F&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Heat responses in larval zebrafish: escape, thermotaxis and arousal T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647639332; 6326392 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Yokogawa, T AU - Iadarola, M AU - Burgess, H Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Heat KW - Arousal KW - Larvae KW - Thermotaxis KW - Freshwater fish KW - Danio rerio UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647639332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Heat+responses+in+larval+zebrafish%3A+escape%2C+thermotaxis+and+arousal&rft.au=Yokogawa%2C+T%3BIadarola%2C+M%3BBurgess%2C+H&rft.aulast=Yokogawa&rft.aufirst=T&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - ALS and C9orf72 in the genomics age: Facts, uncertainties, and the way forward T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647638088; 6326000 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Traynor, B Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Age KW - Amyotrophic lateral sclerosis KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=ALS+and+C9orf72+in+the+genomics+age%3A+Facts%2C+uncertainties%2C+and+the+way+forward&rft.au=Traynor%2C+B&rft.aulast=Traynor&rft.aufirst=B&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Trajectory-based processing reflected in slow cortical potentials and fMRI signals T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647637945; 6325991 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - He, B. Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Cortex KW - Functional magnetic resonance imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647637945?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Trajectory-based+processing+reflected+in+slow+cortical+potentials+and+fMRI+signals&rft.au=He%2C+B.&rft.aulast=He&rft.aufirst=B.&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Rapid and continuous activity-dependent plasticity of sensory input to the mouse olfactory bulb in vivo T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647637843; 6325896 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Cheetham, C AU - Belluscio, L Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Plasticity KW - Olfactory bulb UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647637843?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Rapid+and+continuous+activity-dependent+plasticity+of+sensory+input+to+the+mouse+olfactory+bulb+in+vivo&rft.au=Cheetham%2C+C%3BBelluscio%2C+L&rft.aulast=Cheetham&rft.aufirst=C&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Exercise and the functional integration of new neurons into the hippocampus T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647635323; 6326629 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - van Praag, H Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Integration KW - Hippocampus KW - Neurons KW - Physical training UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635323?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Exercise+and+the+functional+integration+of+new+neurons+into+the+hippocampus&rft.au=van+Praag%2C+H&rft.aulast=van+Praag&rft.aufirst=H&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Sensorimotor predictive coding in the auditory cortex during vocal production in the macaque monkey T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647635027; 6326545 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Fukushima, M AU - Mullarkey, M AU - Doyle, A AU - Saunders, R AU - Fujii, N AU - Averbeck, B AU - Mishkin, M Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Prediction KW - Coding KW - sensorimotor system KW - Cortex (auditory) KW - Macaca UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647635027?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Sensorimotor+predictive+coding+in+the+auditory+cortex+during+vocal+production+in+the+macaque+monkey&rft.au=Fukushima%2C+M%3BMullarkey%2C+M%3BDoyle%2C+A%3BSaunders%2C+R%3BFujii%2C+N%3BAverbeck%2C+B%3BMishkin%2C+M&rft.aulast=Fukushima&rft.aufirst=M&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Resting functional connectivity of the extended amygdala T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647634966; 6327246 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Torrisi, S Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Amygdala UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647634966?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Resting+functional+connectivity+of+the+extended+amygdala&rft.au=Torrisi%2C+S&rft.aulast=Torrisi&rft.aufirst=S&rft.date=2014-11-15&rft.volume=19&rft.issue=10&rft.spage=1339&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+therapeutic+targets&rft.issn=1744-7631&rft_id=info:doi/10.1517%2F14728222.2015.1068759 L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Mechanisms of polarized sorting in neurons T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647634944; 6326796 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Bonifacino, J Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Neurons UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647634944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Mechanisms+of+polarized+sorting+in+neurons&rft.au=Bonifacino%2C+J&rft.aulast=Bonifacino&rft.aufirst=J&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Functional role of pre-Botzinger complex excitatory neurons in respiratory rhythm generation: Optogenetic studies T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647634871; 6327214 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Koizumi, H AU - Koshiya, N AU - Zhang, R AU - Mosher, B AU - Smith, J Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Optics KW - Genetics KW - Information processing KW - Neurons KW - Respiration KW - Rhythms KW - Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647634871?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Functional+role+of+pre-Botzinger+complex+excitatory+neurons+in+respiratory+rhythm+generation%3A+Optogenetic+studies&rft.au=Koizumi%2C+H%3BKoshiya%2C+N%3BZhang%2C+R%3BMosher%2C+B%3BSmith%2C+J&rft.aulast=Koizumi&rft.aufirst=H&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Object information in hippocampus and visual cortex during perception and retrieval from long-term memory T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647634056; 6326925 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Lee, S AU - King, M AU - Kravitz, D AU - Baker, C Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Cortex (visual) KW - Hippocampus KW - Long term memory KW - Perception UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647634056?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Object+information+in+hippocampus+and+visual+cortex+during+perception+and+retrieval+from+long-term+memory&rft.au=Lee%2C+S%3BKing%2C+M%3BKravitz%2C+D%3BBaker%2C+C&rft.aulast=Lee&rft.aufirst=S&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Face-selective regions of the marmoset extrastriate visual cortex - revealed by fMRI & electrocorticography T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647634035; 6326886 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Hung, C AU - Yen, C AU - Ciuchta, J AU - Day-Cooney, J AU - Papoti, D AU - Bock, N AU - Russ, B AU - Leopold, D AU - Silva, A Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Cortex (visual) KW - Functional magnetic resonance imaging KW - Callithrix UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647634035?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Face-selective+regions+of+the+marmoset+extrastriate+visual+cortex+-+revealed+by+fMRI+%26amp%3B+electrocorticography&rft.au=Hung%2C+C%3BYen%2C+C%3BCiuchta%2C+J%3BDay-Cooney%2C+J%3BPapoti%2C+D%3BBock%2C+N%3BRuss%2C+B%3BLeopold%2C+D%3BSilva%2C+A&rft.aulast=Hung&rft.aufirst=C&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Profound putamen catecholamine depletion in Gaucher/Parkinson disease: Role of decreased vesicular sequestration T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647633913; 6326524 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Goldstein, D AU - Sullivan, P AU - Tayebi, N AU - Aflaki, E AU - Sidransky, E Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Neurodegenerative diseases KW - Catecholamines KW - Movement disorders KW - Parkinson's disease KW - Putamen UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647633913?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Profound+putamen+catecholamine+depletion+in+Gaucher%2FParkinson+disease%3A+Role+of+decreased+vesicular+sequestration&rft.au=Goldstein%2C+D%3BSullivan%2C+P%3BTayebi%2C+N%3BAflaki%2C+E%3BSidransky%2C+E&rft.aulast=Goldstein&rft.aufirst=D&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Transient inactivation of basal forebrain subregions shapes spontaneous fMRI correlations in the macaque T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647633667; 6326643 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Turchi, J AU - Chang, C AU - Monosov, I AU - Smith, K AU - Yu, D. AU - Ye, F. AU - Zhu, C AU - Cortes, C AU - Mishkin, M AU - Duyn, J AU - Leopold, D Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Inactivation KW - Forebrain (basal) KW - Functional magnetic resonance imaging KW - Macaca UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647633667?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Transient+inactivation+of+basal+forebrain+subregions+shapes+spontaneous+fMRI+correlations+in+the+macaque&rft.au=Turchi%2C+J%3BChang%2C+C%3BMonosov%2C+I%3BSmith%2C+K%3BYu%2C+D.%3BYe%2C+F.%3BZhu%2C+C%3BCortes%2C+C%3BMishkin%2C+M%3BDuyn%2C+J%3BLeopold%2C+D&rft.aulast=Turchi&rft.aufirst=J&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Transgenic marmoset models of brain function and cerebrovascular disorders T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647633641; 6327114 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Silva, A Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Cerebrovascular diseases KW - Brain KW - Models KW - Callithrix UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647633641?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Transgenic+marmoset+models+of+brain+function+and+cerebrovascular+disorders&rft.au=Silva%2C+A&rft.aulast=Silva&rft.aufirst=A&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Intersectional genetic strategies to unravel the function of the LC/NE system during embryonic development T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647633603; 6326960 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Jensen, P Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Embryogenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647633603?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Intersectional+genetic+strategies+to+unravel+the+function+of+the+LC%2FNE+system+during+embryonic+development&rft.au=Jensen%2C+P&rft.aulast=Jensen&rft.aufirst=P&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - CPAPER T1 - Electrophysiological and behavioral contributions to the resting-state fMRI signal T2 - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AN - 1647633523; 6326642 JF - 44th Annual Meeting of the Society for Neuroscience (Neuroscience 2014) AU - Chang, C AU - Leopold, D AU - Scholvinck, M AU - Liu, X AU - Mandelkow, H AU - Duyn, J Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 KW - Functional magnetic resonance imaging KW - Electrophysiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647633523?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.atitle=Electrophysiological+and+behavioral+contributions+to+the+resting-state+fMRI+signal&rft.au=Chang%2C+C%3BLeopold%2C+D%3BScholvinck%2C+M%3BLiu%2C+X%3BMandelkow%2C+H%3BDuyn%2C+J&rft.aulast=Chang&rft.aufirst=C&rft.date=2014-11-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=44th+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={54C85D94-6D69-4B09-AFAA-502C0E680CA7} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-31 N1 - Last updated - 2015-01-23 ER - TY - JOUR T1 - Phase I trial of bortezomib (PS-341; NSC 681239) and "nonhybrid" (bolus) infusion schedule of alvocidib (flavopiridol; NSC 649890) in patients with recurrent or refractory indolent B-cell neoplasms. AN - 1625343809; 25248382 AB - This phase I study was conducted to determine the dose-limiting toxicities (DLT) and maximum tolerated dose (MTD) for the combination of bortezomib and alvocidib in patients with B-cell malignancies (multiple myeloma, indolent lymphoma, Waldenstrom macroglobulinemia, and mantle cell lymphoma). Patients received bortezomib (intravenous push), followed by alvocidib (1-hour infusion), on days 1, 4, 8, and 11 of a 21-day treatment cycle. Patients experiencing responses or stable disease continued on treatment at the investigator's discretion. A standard 3+3 dose-escalation design was used to identify the MTD based on DLTs, and pharmacokinetic and pharmacodynamic studies were conducted. A total of 44 patients were enrolled, with 39 patients assessed for response. The MTD was established as 1.3 mg/m(2) for bortezomib and 40 mg/m(2) for alvocidib. The most common hematologic toxicities included leukopenia, lymphopenia, neutropenia, and thrombocytopenia. The most common nonhematologic toxicities included diarrhea, fatigue, and sensory neuropathy. Three complete remissions (8%) and 10 partial remissions (26%) were observed for a total response rate of 33%. Pharmacokinetic findings with the current dosing regimen were consistent with the comparable literature and the hybrid dosing regimen. Pharmacodynamic study results did not correlate with clinical responses. The combination of bortezomib and alvocidib is tolerable, and an MTD has been established for this schedule. The regimen appears to be efficacious in patients with relapsed/refractory multiple myeloma or indolent non-Hodgkin lymphoma. As the nonhybrid regimen is less cumbersome than the previous hybrid dosing schedule regimen, the current schedule is recommended for successor studies. ©2014 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Holkova, Beata AU - Kmieciak, Maciej AU - Perkins, E Brent AU - Bose, Prithviraj AU - Baz, Rachid C AU - Roodman, G David AU - Stuart, Robert K AU - Ramakrishnan, Viswanathan AU - Wan, Wen AU - Peer, Cody J AU - Dawson, Jana AU - Kang, Loveleen AU - Honeycutt, Connie AU - Tombes, Mary Beth AU - Shrader, Ellen AU - Weir-Wiggins, Caryn AU - Wellons, Martha AU - Sankala, Heidi AU - Hogan, Kevin T AU - Colevas, A Dimitrios AU - Doyle, L Austin AU - Figg, William D AU - Coppola, Domenico AU - Roberts, John D AU - Sullivan, Daniel AU - Grant, Steven AD - Massey Cancer Center and Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia. bholkova@mcvh-vcu.edu. ; Massey Cancer Center and. ; Massey Cancer Center and Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia. ; Chemical Biology and Molecular Medicine Program, H. Lee Moffitt Cancer Center & Research Institute, Tampa, Florida. ; Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania. ; Department of Medicine, Medical University of South Carolina, Charleston, South Carolina. ; Department of Biostatistics, Virginia Commonwealth University, Richmond, Virginia. ; Center for Cancer Research, NCI, NIH, Bethesda, Maryland. ; James A. Haley Veterans' Hospital, Tampa, Florida. ; Cancer Therapy Evaluation Program, NCI, NIH, Bethesda, Maryland. Departments of. ; Massey Cancer Center and Massey Cancer Center and Massey Cancer Center and Massey Cancer Center and Massey Cancer Center and. Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 SP - 5652 EP - 5662 VL - 20 IS - 22 SN - 1078-0432, 1078-0432 KW - Boronic Acids KW - 0 KW - Flavonoids KW - Piperidines KW - Pyrazines KW - alvocidib KW - 45AD6X575G KW - Bortezomib KW - 69G8BD63PP KW - Index Medicus KW - Drug Administration Schedule KW - Combined Modality Therapy KW - Humans KW - Piperidines -- pharmacokinetics KW - Aged KW - Boronic Acids -- pharmacokinetics KW - Recurrence KW - Pyrazines -- pharmacokinetics KW - Flavonoids -- administration & dosage KW - Pyrazines -- administration & dosage KW - Boronic Acids -- administration & dosage KW - Adult KW - Drug Monitoring KW - Treatment Outcome KW - Piperidines -- administration & dosage KW - Middle Aged KW - Flavonoids -- pharmacokinetics KW - Retreatment KW - Male KW - Female KW - Lymphoproliferative Disorders -- diagnosis KW - Lymphoproliferative Disorders -- drug therapy KW - B-Lymphocytes -- pathology KW - Lymphoproliferative Disorders -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1625343809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+I+trial+of+bortezomib+%28PS-341%3B+NSC+681239%29+and+%22nonhybrid%22+%28bolus%29+infusion+schedule+of+alvocidib+%28flavopiridol%3B+NSC+649890%29+in+patients+with+recurrent+or+refractory+indolent+B-cell+neoplasms.&rft.au=Holkova%2C+Beata%3BKmieciak%2C+Maciej%3BPerkins%2C+E+Brent%3BBose%2C+Prithviraj%3BBaz%2C+Rachid+C%3BRoodman%2C+G+David%3BStuart%2C+Robert+K%3BRamakrishnan%2C+Viswanathan%3BWan%2C+Wen%3BPeer%2C+Cody+J%3BDawson%2C+Jana%3BKang%2C+Loveleen%3BHoneycutt%2C+Connie%3BTombes%2C+Mary+Beth%3BShrader%2C+Ellen%3BWeir-Wiggins%2C+Caryn%3BWellons%2C+Martha%3BSankala%2C+Heidi%3BHogan%2C+Kevin+T%3BColevas%2C+A+Dimitrios%3BDoyle%2C+L+Austin%3BFigg%2C+William+D%3BCoppola%2C+Domenico%3BRoberts%2C+John+D%3BSullivan%2C+Daniel%3BGrant%2C+Steven&rft.aulast=Holkova&rft.aufirst=Beata&rft.date=2014-11-15&rft.volume=20&rft.issue=22&rft.spage=5652&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-0805 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-09 N1 - Date created - 2014-11-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Oncol. 2006 Apr 10;24(11):1770-83 [16603719] Haematologica. 2006 Mar;91(3):390-3 [16503551] Blood. 2007 Jan 15;109(2):399-404 [17003373] Curr Drug Targets. 2007 Jun;8(6):751-9 [17584030] N Engl J Med. 2008 Aug 28;359(9):906-17 [18753647] J Clin Oncol. 2009 Dec 10;27(35):6012-8 [19826119] J Clin Oncol. 2010 Jan 20;28(3):418-23 [20008633] Blood. 2010 Jan 21;115(3):475-80 [19965689] Haematologica. 2010 Jul;95(7):1098-105 [20460644] J Clin Oncol. 2010 Oct 10;28(29):4521-30 [20697091] Blood. 2011 Mar 10;117(10):2807-12 [21239695] J Clin Oncol. 2011 May 10;29(14):1855-63 [21482995] Clin Cancer Res. 2011 May 15;17(10):3388-97 [21447728] J Clin Oncol. 2011 Sep 1;29(25):3389-95 [21810687] Haematologica. 2012 Nov;97(11):1736-42 [22733022] J Clin Oncol. 2005 Dec 20;23(36):9408-21 [16361640] J Clin Oncol. 1999 Apr;17(4):1244 [10561185] Blood. 2000 Jul 15;96(2):393-7 [10887097] J Biol Chem. 2001 Aug 24;276(34):31793-9 [11431468] Blood. 2002 Jul 1;100(1):194-9 [12070027] Ann Hematol. 2002 Jul;81(7):362-7 [12185504] J Clin Oncol. 2002 Oct 1;20(19):4074-82 [12351605] Clin Cancer Res. 2002 Nov;8(11):3527-38 [12429644] Semin Oncol. 2003 Apr;30(2):127-31 [12720121] J Clin Oncol. 2003 May 1;21(9):1740-5 [12735303] N Engl J Med. 2003 Jun 26;348(26):2609-17 [12826635] Oncogene. 2003 Oct 16;22(46):7108-22 [14562039] J Biol Chem. 2004 Feb 6;279(6):4750-9 [14630924] Blood. 2004 Jul 15;104(2):509-18 [15039284] Mol Cancer Ther. 2004 Jul;3(7):873-5 [15252148] Clin Cancer Res. 2004 Aug 1;10(15):5038-47 [15297405] Br J Haematol. 1998 Sep;102(5):1115-23 [9753033] J Clin Oncol. 2005 Jan 20;23(3):630-9 [15659509] Blood. 2005 Apr 15;105(8):3255-62 [15613543] N Engl J Med. 2005 Jun 16;352(24):2487-98 [15958804] Mol Cell Biol. 2005 Jul;25(13):5429-44 [15964800] J Clin Oncol. 2006 Oct 20;24(30):4867-74 [17001068] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-0805 ER - TY - JOUR T1 - Epigenetic control of Ccr7 expression in distinct lineages of lung dendritic cells. AN - 1622066632; 25297875 AB - Adaptive immune responses to inhaled allergens are induced following CCR7-dependent migration of precursor of dendritic cell (pre-DC)-derived conventional DCs (cDCs) from the lung to regional lymph nodes. However, monocyte-derived (moDCs) in the lung express very low levels of Ccr7 and consequently do not migrate efficiently to LN. To investigate the molecular mechanisms that underlie this dichotomy, we studied epigenetic modifications at the Ccr7 locus of murine cDCs and moDCs. When expanded from bone marrow precursors, moDCs were enriched at the Ccr7 locus for trimethylation of histone 3 lysine 27 (H3K27me3), a modification associated with transcriptional repression. Similarly, moDCs prepared from the lung also displayed increased levels of H3K27me3 at the Ccr7 promoter compared with migratory cDCs from that organ. Analysis of DC progenitors revealed that epigenetic modification of Ccr7 does not occur early during DC lineage commitment because monocytes and pre-DCs both had low levels of Ccr7-associated H3K27me3. Rather, Ccr7 is gradually silenced during the differentiation of monocytes to moDCs. Thus, epigenetic modifications of the Ccr7 locus control the migration and therefore the function of DCs in vivo. These findings suggest that manipulating epigenetic mechanisms might be a novel approach to control DC migration and thereby improve DC-based vaccines and treat inflammatory diseases of the lung. Copyright © 2014 by The American Association of Immunologists, Inc. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Moran, Timothy P AU - Nakano, Hideki AU - Kondilis-Mangum, Hrisavgi D AU - Wade, Paul A AU - Cook, Donald N AD - Department of Pediatrics, Duke University Medical Center, Durham, NC 27710; ; Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709; and. ; Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. ; Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709; and cookd@niehs.nih.gov. Y1 - 2014/11/15/ PY - 2014 DA - 2014 Nov 15 SP - 4904 EP - 4913 VL - 193 IS - 10 KW - Ccr7 protein, mouse KW - 0 KW - Histones KW - Receptors, CCR7 KW - Abridged Index Medicus KW - Index Medicus KW - Cell Movement KW - Animals KW - Primary Cell Culture KW - Cell Differentiation KW - Transcription, Genetic KW - Bone Marrow Cells -- immunology KW - Mice KW - Cell Proliferation KW - Mice, Transgenic KW - Cell Lineage -- immunology KW - Lymph Nodes -- cytology KW - Promoter Regions, Genetic KW - Bone Marrow Cells -- cytology KW - Methylation KW - Signal Transduction KW - Lymph Nodes -- immunology KW - Lung -- immunology KW - Receptors, CCR7 -- immunology KW - Dendritic Cells -- immunology KW - Monocytes -- cytology KW - Histones -- immunology KW - Monocytes -- immunology KW - Lung -- cytology KW - Epigenesis, Genetic KW - Dendritic Cells -- cytology KW - Histones -- genetics KW - Receptors, CCR7 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622066632?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epigenetic+control+of+Ccr7+expression+in+distinct+lineages+of+lung+dendritic+cells.&rft.au=Moran%2C+Timothy+P%3BNakano%2C+Hideki%3BKondilis-Mangum%2C+Hrisavgi+D%3BWade%2C+Paul+A%3BCook%2C+Donald+N&rft.aulast=Moran&rft.aufirst=Timothy&rft.date=2014-11-15&rft.volume=193&rft.issue=10&rft.spage=4904&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.1401104 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-24 N1 - Date created - 2014-11-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: ILAR J. 2012;53(3-4):232-9 [23744963] Immunity. 2013 Feb 21;38(2):322-35 [23352232] Annu Rev Immunol. 2013;31:563-604 [23516985] Epigenomics. 2013 Apr;5(2):195-204 [23566096] Mol Aspects Med. 2013 Jul-Aug;34(4):813-25 [22789989] Immunity. 2013 May 23;38(5):970-83 [23706669] Methods Mol Biol. 2013;1032:19-29 [23943441] PLoS One. 2013;8(8):e70387 [23950928] Adv Immunol. 2013;120:239-67 [24070387] PLoS One. 2013;8(10):e76217 [24098447] J Leukoc Biol. 2013 Nov;94(5):903-11 [23898045] J Immunol. 2013 Nov 15;191(10):4903-7 [24123684] Immunity. 2013 Nov 14;39(5):925-38 [24184057] Immunol Rev. 2010 Mar;234(1):45-54 [20193011] Cell. 2010 Oct 29;143(3):416-29 [21029863] BMC Genomics. 2010;11:642 [21087476] J Immunol. 2011 Mar 15;186(6):3556-62 [21317385] Eur J Immunol. 2011 Jun;41(6):1675-86 [21469105] Cell Immunol. 2011;271(1):184-91 [21802073] Nat Rev Immunol. 2011 Nov;11(11):762-74 [21984070] J Exp Med. 2001 Jan 1;193(1):51-60 [11136820] Blood. 2001 Nov 15;98(10):3022-9 [11698286] Blood. 2002 Feb 15;99(4):1109-16 [11830455] Immunity. 2002 May;16(5):649-60 [12049717] Nat Immunol. 2002 Jul;3(7):643-51 [12055628] Nat Immunol. 2002 Dec;3(12):1135-41 [12415265] J Immunol. 2003 May 15;170(10):5295-301 [12734379] J Exp Med. 2003 Aug 18;198(4):615-21 [12925677] Immunity. 2004 Aug;21(2):279-88 [15308107] Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10598-603 [16027362] Science. 2006 Jan 6;311(5757):83-7 [16322423] J Immunol. 2006 Nov 15;177(10):7346-54 [17082654] Genes Dev. 2007 May 1;21(9):1050-63 [17437993] Cell. 2007 May 18;129(4):823-37 [17512414] Immunology. 2007 Dec;122(4):596-606 [17635610] J Immunol. 2007 Dec 1;179(11):7577-84 [18025203] Nat Rev Immunol. 2008 May;8(5):362-71 [18379575] J Exp Med. 2008 Jul 7;205(7):1621-34 [18591406] Immunity. 2009 Jan 16;30(1):155-67 [19144320] Cell. 2009 Mar 20;136(6):1122-35 [19303854] Protein J. 2009 Feb;28(2):57-65 [19184382] Immunity. 2009 Sep 18;31(3):513-25 [19733489] Nat Med. 2010 Jan;16(1):98-105 [20037595] Mucosal Immunol. 2012 Jan;5(1):53-65 [22012243] Annu Rev Immunol. 2012;30:707-31 [22224760] Annu Rev Immunol. 2012;30:243-70 [22224777] Chromosoma. 2012 Jun;121(3):221-34 [22349693] J Exp Med. 2012 Jun 4;209(6):1135-52 [22615127] J Exp Med. 2012 Jun 4;209(6):1153-65 [22615130] Nat Immunol. 2012 Sep;13(9):888-99 [22797772] Nature. 2012 Sep 6;489(7414):57-74 [22955616] Breast Cancer Res. 2012;14(1):R14 [22251626] J Immunol. 2012 Oct 1;189(7):3368-77 [22933627] Nat Immunol. 2012 Dec;13(12):1145-54 [23160217] Immunity. 2012 Dec 14;37(6):1076-90 [23219392] Mucosal Immunol. 2013 Jul;6(4):678-91 [23168837] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4049/jimmunol.1401104 ER - TY - JOUR T1 - DNA recombination. Recombination initiation maps of individual human genomes. AN - 1625345774; 25395542 AB - DNA double-strand breaks (DSBs) are introduced in meiosis to initiate recombination and generate crossovers, the reciprocal exchanges of genetic material between parental chromosomes. Here, we present high-resolution maps of meiotic DSBs in individual human genomes. Comparing DSB maps between individuals shows that along with DNA binding by PRDM9, additional factors may dictate the efficiency of DSB formation. We find evidence for both GC-biased gene conversion and mutagenesis around meiotic DSB hotspots, while frequent colocalization of DSB hotspots with chromosome rearrangement breakpoints implicates the aberrant repair of meiotic DSBs in genomic disorders. Furthermore, our data indicate that DSB frequency is a major determinant of crossover rate. These maps provide new insights into the regulation of meiotic recombination and the impact of meiotic recombination on genome function. Copyright © 2014, American Association for the Advancement of Science. JF - Science (New York, N.Y.) AU - Pratto, Florencia AU - Brick, Kevin AU - Khil, Pavel AU - Smagulova, Fatima AU - Petukhova, Galina V AU - Camerini-Otero, R Daniel AD - National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD, USA. ; Department of Biochemistry and Molecular Biology, Uniformed Services University of Health Sciences, Bethesda, MD, USA. ; Department of Biochemistry and Molecular Biology, Uniformed Services University of Health Sciences, Bethesda, MD, USA. rdcamerini@mail.nih.gov galina.petukhova@usuhs.edu. ; National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD, USA. rdcamerini@mail.nih.gov galina.petukhova@usuhs.edu. Y1 - 2014/11/14/ PY - 2014 DA - 2014 Nov 14 SP - 1256442 VL - 346 IS - 6211 KW - Histone-Lysine N-Methyltransferase KW - EC 2.1.1.43 KW - PRDM9 protein, human KW - Index Medicus KW - Histone-Lysine N-Methyltransferase -- genetics KW - Alleles KW - Humans KW - Telomere -- genetics KW - Protein Binding KW - Histone-Lysine N-Methyltransferase -- metabolism KW - Spermatocytes KW - Male KW - Homologous Recombination KW - Genomic Instability KW - Meiosis -- genetics KW - Genome, Human -- genetics KW - DNA Breaks, Double-Stranded KW - Chromosome Mapping UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1625345774?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=DNA+recombination.+Recombination+initiation+maps+of+individual+human+genomes.&rft.au=Pratto%2C+Florencia%3BBrick%2C+Kevin%3BKhil%2C+Pavel%3BSmagulova%2C+Fatima%3BPetukhova%2C+Galina+V%3BCamerini-Otero%2C+R+Daniel&rft.aulast=Pratto&rft.aufirst=Florencia&rft.date=2014-11-14&rft.volume=346&rft.issue=6211&rft.spage=1256442&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=1095-9203&rft_id=info:doi/10.1126%2Fscience.1256442 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-04 N1 - Date created - 2014-11-14 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE59836; GEO N1 - SuppNotes - Comment In: Science. 2014 Nov 14;346(6211):808-9 [25395519] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1126/science.1256442 ER - TY - JOUR T1 - Dual effects of a targeted small-molecule inhibitor (cabozantinib) on immune-mediated killing of tumor cells and immune tumor microenvironment permissiveness when combined with a cancer vaccine. AN - 1676341169; 25388653 AB - Growing awareness of the complexity of carcinogenesis has made multimodal therapies for cancer increasingly compelling and relevant. In recent years, immunotherapy has gained acceptance as an active therapeutic approach to cancer treatment, even though cancer is widely considered an immunosuppressive disease. Combining immunotherapy with targeted agents that have immunomodulatory capabilities could significantly improve its efficacy. We evaluated the ability of cabozantinib, a receptor tyrosine kinase inhibitor, to modulate the immune system in vivo as well as alter the phenotype of tumor cells in vitro in order to determine if this inhibitor could act synergistically with a cancer vaccine. Our studies indicated that cabozantinib altered the phenotype of MC38-CEA murine tumor cells, rendering them more sensitive to immune-mediated killing. Cabozantinib also altered the frequency of immune sub-populations in the periphery as well as in the tumor microenvironment, which generated a more permissive immune environment. When cabozantinib was combined with a poxviral-based cancer vaccine targeting a self-antigen, the combination significantly reduced the function of regulatory T cells and increased cytokine production from effector T cells in response to the antigen. These alterations to the immune landscape, along with direct modification of tumor cells, led to markedly improved antitumor efficacy. These studies support the clinical combination of cabozantinib with immunotherapy for the treatment of cancer. JF - Journal of translational medicine AU - Kwilas, Anna R AU - Ardiani, Andressa AU - Donahue, Renee N AU - Aftab, Dana T AU - Hodge, James 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. anna.kwilas@nih.gov. ; 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. smith.andressa.a@gmail.com. ; 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. renee.donahue@nih.gov. ; Exelixis, Inc., South San Francisco, CA, USA. daftab@exelixis.com. ; 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 - 2014/11/13/ PY - 2014 DA - 2014 Nov 13 SP - 294 VL - 12 KW - Anilides KW - 0 KW - Biomarkers, Tumor KW - Cancer Vaccines KW - Pyridines KW - Small Molecule Libraries KW - cabozantinib KW - 1C39JW444G KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Animals KW - Combined Modality Therapy KW - Immunotherapy KW - Lymphocyte Subsets -- drug effects KW - Cell Line, Tumor KW - Mice, Transgenic KW - Biomarkers, Tumor -- metabolism KW - Phenotype KW - Mice, Inbred C57BL KW - Lymphocyte Subsets -- immunology KW - T-Lymphocytes -- drug effects KW - T-Lymphocytes -- immunology KW - Female KW - Neoplasms -- drug therapy KW - Small Molecule Libraries -- therapeutic use KW - Pyridines -- therapeutic use KW - Tumor Microenvironment -- drug effects KW - Anilides -- pharmacology KW - Cancer Vaccines -- immunology KW - Anilides -- therapeutic use KW - Neoplasms -- blood supply KW - Neoplasms -- pathology KW - Small Molecule Libraries -- pharmacology KW - Cytotoxicity, Immunologic -- drug effects KW - Pyridines -- pharmacology KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676341169?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+translational+medicine&rft.atitle=Dual+effects+of+a+targeted+small-molecule+inhibitor+%28cabozantinib%29+on+immune-mediated+killing+of+tumor+cells+and+immune+tumor+microenvironment+permissiveness+when+combined+with+a+cancer+vaccine.&rft.au=Kwilas%2C+Anna+R%3BArdiani%2C+Andressa%3BDonahue%2C+Renee+N%3BAftab%2C+Dana+T%3BHodge%2C+James+W&rft.aulast=Kwilas&rft.aufirst=Anna&rft.date=2014-11-13&rft.volume=12&rft.issue=&rft.spage=294&rft.isbn=&rft.btitle=&rft.title=Journal+of+translational+medicine&rft.issn=1479-5876&rft_id=info:doi/10.1186%2Fs12967-014-0294-y LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-14 N1 - Date created - 2015-04-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Oncol. 2011 Jul 1;29(19):2660-6 [21606412] J Biomed Biotechnol. 2011;2011:165214 [21687596] Cancer Immunol Immunother. 2011 Sep;60(9):1227-42 [21544650] Mol Cancer Ther. 2011 Dec;10(12):2298-308 [21926191] Histol Histopathol. 2012 Feb;27(2):197-207 [22207554] Cancer Biother Radiopharm. 2012 Feb;27(1):23-35 [22316209] Int J Cancer. 2012 Apr 15;130(8):1948-59 [21633954] Cancer Discov. 2012 Mar;2(3):270-87 [22585997] Semin Oncol. 2012 Jun;39(3):323-39 [22595055] Oncologist. 2012;17(8):1039-50 [22773560] J Immunol. 2012 Oct 15;189(8):3789-93 [23042723] Proc Natl Acad Sci U S A. 2012 Oct 23;109(43):17561-6 [23045683] J Clin Oncol. 2013 Feb 1;31(4):412-9 [23169517] PLoS One. 2013;8(7):e70417 [23894654] Future Oncol. 2013 Aug;9(8):1083-92 [23902240] J Clin Oncol. 2013 Oct 10;31(29):3639-46 [24002501] Clin Cancer Res. 2013 Nov 15;19(22):6205-18 [24048332] Oncotarget. 2014 Jan 30;5(2):403-16 [24480782] Clin Cancer Res. 2014 Jun 1;20(11):2959-70 [24700742] J Immunol. 2014 Jun 15;192(12):5451-8 [24907378] Ann Oncol. 2014 Aug;25(8):1603-8 [24827131] Lancet. 2014 Sep 20;384(9948):1109-17 [25034862] Clin Cancer Res. 2003 May;9(5):1837-49 [12738742] J Immunol. 2003 Jun 15;170(12):6338-47 [12794167] Cancer Res. 2003 Nov 15;63(22):7942-9 [14633725] Nat Rev Mol Cell Biol. 2003 Dec;4(12):915-25 [14685170] Cancer Res. 2004 Jun 15;64(12):4328-37 [15205348] Cancer Res. 1991 Jul 15;51(14):3657-62 [1712245] Cancer Res. 1998 Apr 1;58(7):1469-77 [9537250] Int J Cancer. 2005 Feb 10;113(4):678-82 [15455388] J Chemother. 2004 Nov;16 Suppl 4:59-63 [15688612] Curr Opin Immunol. 2005 Apr;17(2):187-94 [15766680] Clin Cancer Res. 2005 Mar 15;11(6):2416-26 [15788693] J Immunol. 2005 Oct 1;175(7):4745-53 [16177122] Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18538-43 [16344461] Cancer Res. 2006 Jun 1;66(11):5527-36 [16740684] Clin Breast Cancer. 2006 Jun;7(2):176-9 [16800982] Nat Rev Cancer. 2006 Aug;6(8):637-45 [16862193] Annu Rev Immunol. 2007;25:267-96 [17134371] Curr Med Chem. 2007;14(23):2495-516 [17979703] Handb Exp Pharmacol. 2008;(181):131-50 [18071944] Cancer. 2009 Aug 15;115(16):3670-9 [19536890] Gastroenterology. 2009 Oct;137(4):1270-9 [19577568] Anticancer Res. 2009 Nov;29(11):4807-11 [20032439] Cancer Immunol Immunother. 2010 Mar;59(3):397-408 [19756595] J Clin Oncol. 2010 Mar 1;28(7):1099-105 [20100959] Int J Cancer. 2010 Oct 1;127(7):1603-13 [20091862] N Engl J Med. 2010 Aug 19;363(8):711-23 [20525992] PLoS One. 2010;5(11):e15384 [21072211] Cancer Res. 2010 Dec 15;70(24):10090-100 [20952508] Int J Biochem Cell Biol. 2011 Aug;43(8):1134-46 [21536148] Cancer Res. 2011 Jul 15;71(14):4758-68 [21613405] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12967-014-0294-y ER - TY - JOUR T1 - PPARβ/δ promotes HRAS-induced senescence and tumor suppression by potentiating p-ERK and repressing p-AKT signaling. AN - 1625342356; 24213576 AB - Peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) inhibits skin tumorigenesis through mechanisms that may be dependent on HRAS signaling. The present study examined the hypothesis that PPARβ/δ promotes HRAS-induced senescence resulting in suppression of tumorigenesis. PPARβ/δ expression increased p-ERK and decreased p-AKT activity. Increased p-ERK activity results from the dampened HRAS-induced negative feedback response mediated in part through transcriptional upregulation of RAS guanyl-releasing protein 1 (RASGRP1) by PPARβ/δ. Decreased p-AKT activity results from repression of integrin-linked kinase (ILK) and phosphoinositide-dependent protein kinase-1 (PDPK1) expression. Decreased p-AKT activity in turn promotes cellular senescence through upregulation of p53 and p27 expression. Both over-expression of RASGRP1 and shRNA-mediated knockdown of ILK partially restore cellular senescence in Pparβ/δ-null cells. Higher PPARβ/δ expression is also correlated with increased senescence observed in human benign neurofibromas and colon adenoma lesions in vivo. These results demonstrate that PPARβ/δ promotes senescence to inhibit tumorigenesis and provide new mechanistic insights into HRAS-induced cellular senescence. JF - Oncogene AU - Zhu, B AU - Ferry, C H AU - Blazanin, N AU - Bility, M T AU - Khozoie, C AU - Kang, B-H AU - Glick, A B AU - Gonzalez, F J AU - Peters, J M AD - Department of Veterinary and Biomedical Sciences, The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA, USA. ; Preclinical Research Center, Chemon, Yongin-Si, Korea. ; Laboratory of Metabolism, National Cancer Institute, Bethesda, MD, USA. Y1 - 2014/11/13/ PY - 2014 DA - 2014 Nov 13 SP - 5348 EP - 5359 VL - 33 IS - 46 KW - PPAR delta KW - 0 KW - PPAR-beta KW - Proto-Oncogene Proteins c-akt KW - EC 2.7.11.1 KW - Mitogen-Activated Protein Kinase 1 KW - EC 2.7.11.24 KW - Mitogen-Activated Protein Kinase 3 KW - ras Proteins KW - EC 3.6.5.2 KW - Index Medicus KW - Aging -- metabolism KW - Animals KW - Carcinogenesis -- metabolism KW - HEK293 Cells KW - Humans KW - Skin Neoplasms -- pathology KW - Mice KW - Reverse Transcriptase Polymerase Chain Reaction KW - Skin Neoplasms -- metabolism KW - Cell Aging -- genetics KW - NIH 3T3 Cells KW - Mice, Knockout KW - Skin Neoplasms -- genetics KW - Blotting, Western KW - Carcinogenesis -- genetics KW - Phosphorylation KW - Cells, Cultured KW - Keratinocytes -- cytology KW - Keratinocytes -- metabolism KW - RNA Interference KW - Signal Transduction KW - Aging -- genetics KW - Female KW - Mitogen-Activated Protein Kinase 3 -- metabolism KW - ras Proteins -- genetics KW - Proto-Oncogene Proteins c-akt -- metabolism KW - PPAR-beta -- metabolism KW - PPAR delta -- genetics KW - Mitogen-Activated Protein Kinase 1 -- metabolism KW - PPAR-beta -- genetics KW - ras Proteins -- metabolism KW - PPAR delta -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1625342356?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=PPAR%CE%B2%2F%CE%B4+promotes+HRAS-induced+senescence+and+tumor+suppression+by+potentiating+p-ERK+and+repressing+p-AKT+signaling.&rft.au=Zhu%2C+B%3BFerry%2C+C+H%3BBlazanin%2C+N%3BBility%2C+M+T%3BKhozoie%2C+C%3BKang%2C+B-H%3BGlick%2C+A+B%3BGonzalez%2C+F+J%3BPeters%2C+J+M&rft.aulast=Zhu&rft.aufirst=B&rft.date=2014-11-13&rft.volume=33&rft.issue=46&rft.spage=5348&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2013.477 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-28 N1 - Date created - 2014-11-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 2011 Sep 23;286(38):33447-56 [21795702] Cell Signal. 2011 Dec;23(12):2039-50 [21843636] Mol Carcinog. 2011 Nov;50(11):884-900 [21400612] Cancer Metastasis Rev. 2011 Dec;30(3-4):619-40 [22037942] Nat Rev Cancer. 2012 Mar;12(3):181-95 [22318237] Mol Cell Biol. 2012 Jun;32(11):2065-82 [22473992] Nat Biotechnol. 2010 Dec;28(12):1248-50 [21139605] Gastroenterology. 2000 Oct;119(4):929-42 [11040180] Cancer Res. 2001 Apr 1;61(7):3124-30 [11306497] Mol Cell Biol. 2001 Jun;21(11):3616-31 [11340156] J Biol Chem. 2001 Jul 20;276(29):27462-9 [11313365] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):2613-8 [11867749] J Biol Chem. 2002 Jun 14;277(24):21843-50 [11923280] Cancer Res. 2003 Jul 1;63(13):3447-52 [12839923] Clin Cancer Res. 2003 Oct 1;9(12):4409-14 [14555513] J Biol Chem. 2004 May 28;279(22):23719-27 [15033975] Mol Cell Biol. 2004 Jun;24(12):5459-74 [15169907] J Biol Chem. 2004 Aug 13;279(33):34411-20 [15190076] Nature. 1986 Jul 3-9;322(6074):78-80 [3014349] Nature. 1986 Oct 30-Nov 5;323(6091):822-4 [2430189] Environ Health Perspect. 1986 Sep;68:91-104 [3780637] Proc Natl Acad Sci U S A. 1990 Jan;87(2):538-42 [2105486] Cancer Res. 1992 Jun 1;52(11):3145-56 [1375535] Methods Enzymol. 1995;254:3-20 [8531694] Cell. 1997 Mar 7;88(5):593-602 [9054499] Curr Biol. 1997 Apr 1;7(4):261-9 [9094314] J Biol Chem. 1997 Apr 25;272(17):11426-33 [9111053] Genes Dev. 1998 Oct 1;12(19):2997-3007 [9765202] Nature. 2005 Aug 4;436(7051):642 [16079833] Cell Signal. 2006 Jan;18(1):9-20 [16109478] Oncogene. 2005 Nov 14;24(50):7410-25 [16288288] Cancer Res. 2006 Apr 15;66(8):4394-401 [16618765] Cancer Cell. 2006 Dec;10(6):459-72 [17157787] Cell. 2007 Jan 26;128(2):295-308 [17254968] Nat Rev Cancer. 2007 Apr;7(4):295-308 [17384584] Cell Signal. 2007 Jun;19(6):1163-71 [17254750] Cell. 2007 Jun 15;129(6):1065-79 [17574021] Cell. 2007 Jun 29;129(7):1261-74 [17604717] Mol Cancer Res. 2007 Dec;5(12):1263-75 [18171984] Genome Biol. 2007;8(7):R131 [17615082] Oncogene. 2008 May 1;27(20):2801-9 [18193093] Curr Opin Investig Drugs. 2008 May;9(5):463-9 [18465655] Biochem Biophys Res Commun. 2008 Jul 4;371(3):456-61 [18442472] Cell. 2008 Jun 13;133(6):1019-31 [18555778] Clin Sci (Lond). 2008 Aug;115(4):107-27 [18616431] Cancer Cell. 2008 Aug 12;14(2):146-55 [18691549] Mol Pharmacol. 2008 Nov;74(5):1429-42 [18687807] N Engl J Med. 2008 Oct 23;359(17):1757-65 [18946061] Toxicology. 2008 Dec 5;254(1-2):112-7 [18950674] Carcinogenesis. 2008 Dec;29(12):2406-14 [18799709] Cancer Res. 2009 Aug 1;69(15):6299-306 [19602588] Biochim Biophys Acta. 2009 Dec;1796(2):230-41 [19505534] Nat Protoc. 2009;4(12):1798-806 [20010931] Toxicol Sci. 2010 Jan;113(1):27-36 [19748995] EMBO Mol Med. 2009 Jul;1(4):236-48 [20049725] Oncogene. 2010 Jan 28;29(4):516-26 [19935699] Gastroenterology. 2010 Feb;138(2):636-48, 648.e1-12 [19818784] Clin Exp Metastasis. 2010 Feb;27(2):83-90 [20143136] Nature. 2010 Mar 18;464(7287):374-9 [20237562] J Biol Chem. 2010 May 21;285(21):15724-30 [20308057] Curr Opin Lipidol. 2010 Jun;21(3):186-91 [20480546] Mol Pharmacol. 2010 Sep;78(3):419-30 [20516370] PLoS One. 2010;5(10). pii: e13091. doi: 10.1371/journal.pone.0013091 [20957034] Mol Pharmacol. 2010 Nov;78(5):961-70 [20736318] Proc Natl Acad Sci U S A. 2010 Oct 19;107(42):18061-6 [20921405] Cancer Res. 2010 Nov 1;70(21):8526-36 [20959475] Mol Cancer Ther. 2010 Dec;9(12):3267-77 [21159610] Virchows Arch. 2011 Jan;458(1):99-107 [21136077] PLoS One. 2011;6(1):e16344 [21283829] Mol Cell. 2011 Apr 8;42(1):36-49 [21474066] Clin Cancer Res. 2011 Jun 1;17(11):3760-70 [21531809] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/onc.2013.477 ER - TY - JOUR T1 - Cell cycle restriction is more important than apoptosis induction for RASSF1A protein tumor suppression. AN - 1622066495; 25225292 AB - The Ras association domain family protein 1A (RASSF1A) is arguably one of the most frequently inactivated tumor suppressors in human cancer. RASSF1A modulates apoptosis via the Hippo and Bax pathways but also modulates the cell cycle. In part, cell cycle regulation appears to be dependent upon the ability of RASSF1A to complex with microtubules and regulate their dynamics. Which property of RASSF1A, apoptosis induction or microtubule regulation, is responsible for its tumor suppressor function is not known. We have identified a short conserved motif that is essential for the binding of RASSF family proteins with microtubule-associated proteins. By making a single point mutation in the motif, we were able to generate a RASSF1A variant that retains wild-type apoptotic properties but completely loses the ability to bind microtubule-associated proteins and complex with microtubules. Comparison of this mutant to wild-type RASSF1A showed that, despite retaining its proapoptotic properties, the mutant was completely unable to induce cell cycle arrest or suppress the tumorigenic phenotype. Therefore, it appears that the cell cycle/microtubule effects of RASSF1A are key to its tumor suppressor function rather than its apoptotic effects. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Donninger, Howard AU - Clark, Jennifer A AU - Monaghan, Megan K AU - Schmidt, M Lee AU - Vos, Michele AU - Clark, Geoffrey J AD - From the Departments of Medicine. ; Biochemistry and Molecular Biology, and. ; the Cell and Cancer Biology Branch, NCI, National Institutes of Health, Rockville, Maryland 20850. ; Pharmacology and Toxicology, James Graham Brown Cancer Center, Molecular Targets Program, University of Louisville, Louisville, Kentucky 40202 and gjclar01@louisville.edu. Y1 - 2014/11/07/ PY - 2014 DA - 2014 Nov 07 SP - 31287 EP - 31295 VL - 289 IS - 45 KW - RASSF1 protein, human KW - 0 KW - Tumor Suppressor Proteins KW - Green Fluorescent Proteins KW - 147336-22-9 KW - ras Proteins KW - EC 3.6.5.2 KW - Index Medicus KW - Ras KW - Oncogene KW - Ras Protein KW - Tumor Suppressor KW - Apoptosis KW - Cell Cycle KW - Microtubule-associated Protein (MAP) KW - Animals KW - COS Cells KW - HEK293 Cells KW - Humans KW - Amino Acid Sequence KW - Cell Line, Tumor KW - Phenotype KW - Amino Acid Motifs KW - Cercopithecus aethiops KW - Point Mutation KW - Molecular Sequence Data KW - ras Proteins -- metabolism KW - Sequence Homology, Amino Acid KW - Green Fluorescent Proteins -- metabolism KW - Mutation KW - Tumor Suppressor Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622066495?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cell+cycle+restriction+is+more+important+than+apoptosis+induction+for+RASSF1A+protein+tumor+suppression.&rft.au=Donninger%2C+Howard%3BClark%2C+Jennifer+A%3BMonaghan%2C+Megan+K%3BSchmidt%2C+M+Lee%3BVos%2C+Michele%3BClark%2C+Geoffrey+J&rft.aulast=Donninger&rft.aufirst=Howard&rft.date=2014-11-07&rft.volume=289&rft.issue=45&rft.spage=31287&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.609537 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-17 N1 - Date created - 2014-11-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncogene. 2002 Feb 21;21(9):1381-90 [11857081] Methods Enzymol. 2001;332:3-36 [11305105] Nat Cell Biol. 2004 Feb;6(2):129-37 [14743218] Cancer Res. 2004 Jun 15;64(12):4112-6 [15205320] J Natl Cancer Inst. 2001 May 2;93(9):691-9 [11333291] Cancer Res. 2004 Jun 15;64(12):4244-50 [15205337] Front Biosci. 1998 Aug 6;3:d887-912 [9696882] Oncogene. 2004 Oct 28;23(50):8216-30 [15378022] J Biol Chem. 1995 Sep 15;270(37):21695-700 [7665586] J Biol Chem. 1997 Nov 28;272(48):30362-70 [9374526] Histol Histopathol. 2005 Apr;20(2):645-63 [15736067] Cancer Res. 2005 Mar 1;65(5):1830-8 [15753381] Cancer Res. 2005 May 1;65(9):3497-508 [15867337] Biochem Biophys Res Commun. 2005 Jul 8;332(3):670-6 [15907802] Mol Cell. 2005 Jun 10;18(6):637-50 [15949439] Exp Cell Res. 2005 Aug 15;308(2):446-58 [15936015] J Biol Chem. 2006 Feb 24;281(8):4557-63 [16344548] Methods Enzymol. 2006;407:290-310 [16757333] Cancer Res. 2007 Jan 15;67(2):492-500 [17234756] Curr Biol. 2007 Apr 17;17(8):700-5 [17379520] Biochim Biophys Acta. 2007 Sep;1776(1):58-85 [17692468] J Cell Sci. 2007 Sep 15;120(Pt 18):3163-72 [17878233] Mol Cell. 2007 Sep 21;27(6):962-75 [17889669] Oncogene. 2007 Dec 6;26(55):7700-8 [17563743] Biol Chem. 2008 Jan;389(1):57-67 [18095870] EMBO J. 2008 Jul 23;27(14):1995-2005 [18596699] Mol Cell Neurosci. 2009 Jan;40(1):111-9 [19013529] Mol Cell Biol. 2009 Mar;29(5):1338-53 [19114553] Cancer Res. 2009 Mar 1;69(5):1748-57 [19223555] Oncogene. 2009 Aug 20;28(33):2988-98 [19525978] Oncogene. 2010 Oct 21;29(42):5729-40 [20697344] J Biol Chem. 2011 May 27;286(21):18483-91 [21489991] Mol Cell. 2011 Dec 23;44(6):893-906 [22195963] Mol Biol Cell. 2014 Mar;25(6):800-10 [24478455] Nat Genet. 2000 Jul;25(3):315-9 [10888881] J Biol Chem. 2000 Nov 17;275(46):35669-72 [10998413] J Biol Chem. 2000 Dec 29;275(52):41251-7 [11007785] Oncogene. 2003 Nov 6;22(50):8125-36 [14603253] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.609537 ER - TY - JOUR T1 - Substrate-induced DNA polymerase β activation. AN - 1622065096; 25261471 AB - DNA polymerases and substrates undergo conformational changes upon forming protein-ligand complexes. These conformational adjustments can hasten or deter DNA synthesis and influence substrate discrimination. From structural comparison of binary DNA and ternary DNA-dNTP complexes of DNA polymerase β, several side chains have been implicated in facilitating formation of an active ternary complex poised for chemistry. Site-directed mutagenesis of these highly conserved residues (Asp-192, Arg-258, Phe-272, Glu-295, and Tyr-296) and kinetic characterization provides insight into the role these residues play during correct and incorrect insertion as well as their role in conformational activation. The catalytic efficiencies for correct nucleotide insertion for alanine mutants were wild type ∼ R258A > F272A ∼ Y296A > E295A > D192A. Because the efficiencies for incorrect insertion were affected to about the same extent for each mutant, the effects on fidelity were modest (<5-fold). The R258A mutant exhibited an increase in the single-turnover rate of correct nucleotide insertion. This suggests that the wild-type Arg-258 side chain generates a population of non-productive ternary complexes. Structures of binary and ternary substrate complexes of the R258A mutant and a mutant associated with gastric carcinomas, E295K, provide molecular insight into intermediate structural conformations not appreciated previously. Although the R258A mutant crystal structures were similar to wild-type enzyme, the open ternary complex structure of E295K indicates that Arg-258 stabilizes a non-productive conformation of the primer terminus that would decrease catalysis. Significantly, the open E295K ternary complex binds two metal ions indicating that metal binding cannot overcome the modified interactions that have interrupted the closure of the N-subdomain. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Beard, William A AU - Shock, David D AU - Batra, Vinod K AU - Prasad, Rajendra AU - Wilson, Samuel H AD - From the Laboratory of Structural Biology, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709. ; From the Laboratory of Structural Biology, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709 wilson5@niehs.nih.gov. Y1 - 2014/11/07/ PY - 2014 DA - 2014 Nov 07 SP - 31411 EP - 31422 VL - 289 IS - 45 KW - Nucleotides KW - 0 KW - DNA Polymerase beta KW - EC 2.7.7.- KW - Lysine KW - K3Z4F929H6 KW - Alanine KW - OF5P57N2ZX KW - Index Medicus KW - Enzyme Mechanism KW - X-ray Crystallography KW - Conformational Change KW - DNA Polymerase KW - Mutagenesis KW - Mutagenesis, Site-Directed KW - Lysine -- chemistry KW - Humans KW - Catalytic Domain KW - Nucleotides -- chemistry KW - Crystallography, X-Ray KW - Alanine -- chemistry KW - Substrate Specificity KW - Protein Binding KW - Mutation KW - Hydrogen Bonding KW - Catalysis KW - DNA Polymerase beta -- genetics KW - DNA Polymerase beta -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622065096?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Substrate-induced+DNA+polymerase+%CE%B2+activation.&rft.au=Beard%2C+William+A%3BShock%2C+David+D%3BBatra%2C+Vinod+K%3BPrasad%2C+Rajendra%3BWilson%2C+Samuel+H&rft.aulast=Beard&rft.aufirst=William&rft.date=2014-11-07&rft.volume=289&rft.issue=45&rft.spage=31411&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.607432 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-17 N1 - Date created - 2014-11-08 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4R63; PDB; 4R65; 4R64; 4R66 N1 - SuppNotes - Cited By: Biochemistry. 1997 Feb 4;36(5):1100-7 [9033400] Nat Struct Mol Biol. 2014 Mar;21(3):253-60 [24487959] Structure. 1999 Feb 15;7(2):R31-5 [10368292] Biochemistry. 1999 Apr 13;38(15):4800-8 [10200168] J Biol Chem. 1999 Jul 23;274(30):20749-52 [10409611] Nat Struct Mol Biol. 2005 Jan;12(1):97-8 [15608652] Biochemistry. 2005 Apr 5;44(13):5177-87 [15794655] Chem Rev. 2006 Feb;106(2):361-82 [16464010] Chem Rev. 2014 Mar 12;114(5):2759-74 [24359247] Biochemistry. 2014 May 6;53(17):2768-80 [24717170] DNA Repair (Amst). 2014 Jun;18:1-9 [24666693] J Biol Chem. 2014 Jun 6;289(23):16541-50 [24764311] Nucleic Acids Res. 2014 Jul;42(13):8755-66 [24966350] DNA Repair (Amst). 2014 Oct;22:77-88 [25112931] Biochemistry. 2007 May 8;46(18):5463-72 [17419590] Structure. 2006 Apr;14(4):757-66 [16615916] Biochemistry. 2006 Aug 15;45(32):9675-87 [16893169] Biochemistry. 2006 Dec 26;45(51):15142-56 [17176036] Biochemistry. 2007 Jan 16;46(2):461-71 [17209556] Nucleic Acids Res. 2007 Jul;35(Web Server issue):W375-83 [17452350] Mol Cell Biol. 2007 Aug;27(15):5587-96 [17526740] DNA Repair (Amst). 2007 Dec 1;6(12):1709-25 [17631059] Mol Cell. 2008 May 9;30(3):315-24 [18471977] J Biol Chem. 2008 Sep 26;283(39):26297-301 [18544537] Biochemistry. 2009 Apr 14;48(14):3197-208 [19231836] J Biol Chem. 2009 Nov 13;284(46):31680-9 [19759017] Proc Natl Acad Sci U S A. 2010 Jan 12;107(2):715-20 [20080740] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702] J Biol Chem. 2010 Aug 6;285(32):24457-65 [20519499] Nucleic Acids Res. 2010 Sep;38(16):5419-31 [20435673] Mutat Res. 2010 Nov 28;703(1):18-23 [20696268] Mutat Res. 1999 Oct 22;435(2):121-8 [10556592] Protein Expr Purif. 2000 Feb;18(1):100-10 [10648175] J Biol Chem. 2000 Sep 8;275(36):28033-8 [10851238] J Biol Chem. 2001 Feb 2;276(5):3408-16 [11024043] J Biol Chem. 2002 Mar 8;277(10):8235-42 [11756435] J Mol Biol. 2002 Apr 12;317(5):651-71 [11955015] Biochemistry. 2002 Sep 17;41(37):11226-35 [12220188] J Biol Chem. 2002 Dec 6;277(49):47393-8 [12370169] J Biol Chem. 2003 Feb 14;278(7):5072-81 [12458221] Biophys J. 2004 Jun;86(6):3392-408 [15189842] Biochemistry. 2004 Jul 20;43(28):8911-22 [15248749] J Biol Chem. 2004 Jul 23;279(30):31921-9 [15145936] J Comput Chem. 2004 Oct;25(13):1605-12 [15264254] Acta Crystallogr A. 1991 Mar 1;47 ( Pt 2):110-9 [2025413] Biochemistry. 1991 May 28;30(21):5286-92 [2036395] Science. 1994 Jun 24;264(5167):1930-5 [7516581] Biochemistry. 1995 Dec 12;34(49):15934-42 [8519750] Methods Enzymol. 1995;262:98-107 [8594388] J Biol Chem. 1996 May 24;271(21):12141-4 [8647805] Nucleic Acids Res. 2012 Apr;40(7):2974-83 [22169953] J Mol Biol. 2012 Jun 8;419(3-4):171-82 [22446382] J Biol Chem. 2012 Jul 6;287(28):23830-9 [22577134] Structure. 2012 Nov 7;20(11):1829-37 [22959623] Cell. 2013 Jul 3;154(1):157-68 [23827680] J Mol Biol. 2013 Nov 15;425(22):4334-52 [23856622] J Biol Chem. 2013 Nov 29;288(48):34850-60 [24133209] Biochemistry. 1997 Sep 16;36(37):11205-15 [9287163] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.607432 ER - TY - JOUR T1 - Epidemiology of Dengue Disease in the Philippines (2000-2011): A Systematic Literature Review AN - 1642617607; 21084600 AB - This literature analysis describes the available dengue epidemiology data in the Philippines between 2000 and 2011. Of 253 relevant data sources identified, 34, including additional epidemiology data provided by the National Epidemiology Center, Department of Health, Philippines, were reviewed. There were 14 publications in peer reviewed journals, and 17 surveillance reports/sources, which provided variable information from the passive reporting system and show broad trends in dengue incidence, including age group predominance and disease severity. The peer reviewed studies focused on clinical severity of cases, some revealed data on circulating serotypes and genotypes and on the seroepidemiology of dengue including incidence rates for infection and apparent disease. Gaps in the data were identified, and include the absence incidence rates stratified by age, dengue serotype and genotype distribution, disease severity data, sex distribution data, and seroprevalence data. Dengue disease is a tropical and subtropical mosquito-borne viral illness and is a major health concern in the Philippines. To determine the dengue disease burden in the Philippines and identify gaps and future research needs, we conducted a literature analysis and review to describe the epidemiology of dengue disease. We used well-defined methods to search and identify relevant research conducted between 2000 and 2011. This long-term review highlights an increase in the reported incidence of dengue disease in the Philippines. The rising incidence of dengue disease may be related to a growing population, increasing urbanization, improvements in surveillance, and the limited success of vector control measures. Gaps in the epidemiological information available in the Philippines during the period 2000-2011 include comprehensive national and regional data that describe the proportion of severe dengue disease, including hospitalizations and mortality, and incidence data per 100,000 population. More comprehensive data are also needed for age, serotype, and seroprevalence on both national and regional levels. The data presented enable the observation of epidemiological characteristics, both within and across years. Such assessments are essential at national and regional levels to improve both preparedness and response activities relating to dengue disease outbreaks. JF - PLoS Neglected Tropical Diseases AU - Bravo, Lulu AU - Roque, Vito G AU - Brett, Jeremy AU - Dizon, Ruby AU - L'Azou, Maina AD - National Institutes of Health, University of the Philippines Manila (UPM), Manila, Philippines Y1 - 2014/11/06/ PY - 2014 DA - 2014 Nov 06 PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States VL - 8 IS - 11 SN - 1935-2727, 1935-2727 KW - Virology & AIDS Abstracts; Health & Safety Science Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources KW - Philippines KW - Age KW - Human diseases KW - Serotypes KW - Urbanization KW - Genotypes KW - Infection KW - Public health KW - Disease transmission KW - ISEW, Philippines KW - Dengue KW - Seroepidemiology KW - Sex KW - Mortality KW - Data processing KW - Surveillance and enforcement KW - Vectors KW - Literature reviews KW - Epidemiology KW - Viral diseases KW - Reviews KW - Outbreaks KW - Mortality causes KW - V 22410:Animal Diseases KW - Q1 08604:Stock assessment and management KW - H 12000:Epidemiology and Public Health KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1642617607?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+Neglected+Tropical+Diseases&rft.atitle=Epidemiology+of+Dengue+Disease+in+the+Philippines+%282000-2011%29%3A+A+Systematic+Literature+Review&rft.au=Bravo%2C+Lulu%3BRoque%2C+Vito+G%3BBrett%2C+Jeremy%3BDizon%2C+Ruby%3BL%27Azou%2C+Maina&rft.aulast=Bravo&rft.aufirst=Lulu&rft.date=2014-11-06&rft.volume=8&rft.issue=11&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0003027 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Human diseases; Viral diseases; Urbanization; Epidemiology; Surveillance and enforcement; Genotypes; Mortality causes; Disease transmission; Public health; Mortality; Age; Data processing; Serotypes; Vectors; Infection; Literature reviews; Dengue; Reviews; Seroepidemiology; Sex; Outbreaks; Philippines; ISEW, Philippines DO - http://dx.doi.org/10.1371/journal.pntd.0003027 ER - TY - JOUR T1 - Coincident Helminth Infection Modulates Systemic Inflammation and Immune Activation in Active Pulmonary Tuberculosis AN - 1639474579; 21084608 AB - Helminth-induced changes in the immune system are thought to influence the outcome of secondary infections. Approximately 50-100 million people are thought to have infection by worms known as Strongyloides stercoralis, while more than 2 billion people worldwide are infected with the bacterium, Mycobacterium tuberculosis. Interestingly, there is a great degree of overlap in the geographical spread of both infections. We and others have previously shown that helminth infections induce modulation of innate and adaptive immune responses in tuberculosis. In this study, we examined whether concomitant helminth infection has a secondary effect on systemic markers of disease severity/activity in pulmonary tuberculosis. We show that helminth infection have profound effect on lowering most of the circulating parameters associated with tuberculosis pathology. We therefore, conclude that helminth infections have both beneficial and detrimental effects on the progression of tuberculosis, with the beneficial effect manifest upon development of pathology. JF - PLoS Neglected Tropical Diseases AU - George, Parakkal Jovvian AU - Kumar, Nathella Pavan AU - Sridhar, Rathinam AU - Hanna, Luke E AU - Nair, Dina AU - Banurekha, Vaithilingam V AU - Nutman, Thomas B AU - Babu, Subash AD - National Institutes of Health-NIRT-International Center for Excellence in Research, Chennai, India Y1 - 2014/11/06/ PY - 2014 DA - 2014 Nov 06 PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States VL - 8 IS - 11 SN - 1935-2727, 1935-2727 KW - Microbiology Abstracts B: Bacteriology KW - Strongyloides stercoralis KW - Lung KW - Immune system KW - Tuberculosis KW - Immune response KW - Secondary infection KW - Mycobacterium tuberculosis KW - Inflammation KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639474579?accountid=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+Neglected+Tropical+Diseases&rft.atitle=Coincident+Helminth+Infection+Modulates+Systemic+Inflammation+and+Immune+Activation+in+Active+Pulmonary+Tuberculosis&rft.au=George%2C+Parakkal+Jovvian%3BKumar%2C+Nathella+Pavan%3BSridhar%2C+Rathinam%3BHanna%2C+Luke+E%3BNair%2C+Dina%3BBanurekha%2C+Vaithilingam+V%3BNutman%2C+Thomas+B%3BBabu%2C+Subash&rft.aulast=George&rft.aufirst=Parakkal&rft.date=2014-11-06&rft.volume=8&rft.issue=11&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0003289 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Lung; Immune system; Tuberculosis; Secondary infection; Immune response; Inflammation; Strongyloides stercoralis; Mycobacterium tuberculosis DO - http://dx.doi.org/10.1371/journal.pntd.0003289 ER - TY - JOUR T1 - Broad and potent HIV-1 neutralization by a human antibody that binds the gp41-gp120 interface. AN - 1622059203; 25186731 AB - The isolation of human monoclonal antibodies is providing important insights into the specificities that underlie broad neutralization of HIV-1 (reviewed in ref. 1). Here we report a broad and extremely potent HIV-specific monoclonal antibody, termed 35O22, which binds a novel HIV-1 envelope glycoprotein (Env) epitope. 35O22 neutralized 62% of 181 pseudoviruses with a half-maximum inhibitory concentration (IC50) <50 μg ml(-1). The median IC50 of neutralized viruses was 0.033 μg ml(-1), among the most potent thus far described. 35O22 did not bind monomeric forms of Env tested, but did bind the trimeric BG505 SOSIP.664. Mutagenesis and a reconstruction by negative-stain electron microscopy of the Fab in complex with trimer revealed that it bound to a conserved epitope, which stretched across gp120 and gp41. The specificity of 35O22 represents a novel site of vulnerability on HIV Env, which serum analysis indicates to be commonly elicited by natural infection. Binding to this new site of vulnerability may thus be an important complement to current monoclonal-antibody-based approaches to immunotherapies, prophylaxis and vaccine design. JF - Nature AU - Huang, Jinghe AU - Kang, Byong H AU - Pancera, Marie AU - Lee, Jeong Hyun AU - Tong, Tommy AU - Feng, Yu AU - Imamichi, Hiromi AU - Georgiev, Ivelin S AU - Chuang, Gwo-Yu AU - Druz, Aliaksandr AU - Doria-Rose, Nicole A AU - Laub, Leo AU - Sliepen, Kwinten AU - van Gils, Marit J AU - de la Peña, Alba Torrents AU - Derking, Ronald AU - Klasse, Per-Johan AU - Migueles, Stephen A AU - Bailer, Robert T AU - Alam, Munir AU - Pugach, Pavel AU - Haynes, Barton F AU - Wyatt, Richard T AU - Sanders, Rogier W AU - Binley, James M AU - Ward, Andrew B AU - Mascola, John R AU - Kwong, Peter D AU - Connors, Mark AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] The Scripps Center for HIV/AIDS Vaccine Immunology and Immunogen Discovery, The Scripps Research Institute, La Jolla, California 92037, USA [2] International AIDS Vaccine Initiative (IAVI) Neutralizing Antibody Center, The Scripps Research Institute, La Jolla, California 92037, USA. ; San Diego Biomedical Research Institute, San Diego, California 92121, USA. ; International AIDS Vaccine Initiative (IAVI) Neutralizing Antibody Center, The Scripps Research Institute, La Jolla, California 92037, USA. ; Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, Amsterdam 1100 DD, The Netherlands. ; Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York, New York 10065, USA. ; Duke Human Vaccine Institute, Duke University, Durham, North Carolina 27710, USA. ; 1] Department of Medical Microbiology, Academic Medical Center, University of Amsterdam, Amsterdam 1100 DD, The Netherlands [2] Department of Microbiology and Immunology, Weill Medical College of Cornell University, New York, New York 10065, USA. Y1 - 2014/11/06/ PY - 2014 DA - 2014 Nov 06 SP - 138 EP - 142 VL - 515 IS - 7525 KW - AIDS Vaccines KW - 0 KW - Antibodies, Monoclonal KW - Antibodies, Neutralizing KW - Antigens, CD4 KW - Epitopes KW - HIV Antibodies KW - HIV Envelope Protein gp120 KW - HIV Envelope Protein gp41 KW - Immunoglobulin Fab Fragments KW - Receptors, CCR5 KW - Index Medicus KW - HIV-1 -- immunology KW - AIDS Vaccines -- chemistry KW - Antibodies, Monoclonal -- genetics KW - Humans KW - Immunoglobulin Fab Fragments -- genetics KW - Immunoglobulin Fab Fragments -- ultrastructure KW - Antibodies, Monoclonal -- pharmacology KW - Antigens, CD4 -- metabolism KW - Antibodies, Monoclonal -- immunology KW - Antibody Specificity KW - Molecular Sequence Data KW - Immunoglobulin Fab Fragments -- immunology KW - Epitopes -- chemistry KW - Inhibitory Concentration 50 KW - Immunoglobulin Fab Fragments -- chemistry KW - Leukocytes, Mononuclear KW - Cell Membrane -- virology KW - AIDS Vaccines -- immunology KW - Models, Molecular KW - Antibodies, Monoclonal -- chemistry KW - Conserved Sequence KW - Epitopes -- immunology KW - Epitope Mapping KW - HIV-1 -- drug effects KW - Receptors, CCR5 -- metabolism KW - Cell Line KW - Virus Internalization -- drug effects KW - HIV Envelope Protein gp120 -- chemistry KW - HIV Envelope Protein gp41 -- immunology KW - HIV Antibodies -- genetics KW - Antibody Affinity KW - HIV Envelope Protein gp120 -- immunology KW - HIV Antibodies -- immunology KW - Antibodies, Neutralizing -- genetics KW - Antibodies, Neutralizing -- chemistry KW - Antibodies, Neutralizing -- immunology KW - HIV Antibodies -- chemistry KW - Antibodies, Neutralizing -- pharmacology KW - HIV Antibodies -- pharmacology KW - HIV Envelope Protein gp41 -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622059203?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Broad+and+potent+HIV-1+neutralization+by+a+human+antibody+that+binds+the+gp41-gp120+interface.&rft.au=Huang%2C+Jinghe%3BKang%2C+Byong+H%3BPancera%2C+Marie%3BLee%2C+Jeong+Hyun%3BTong%2C+Tommy%3BFeng%2C+Yu%3BImamichi%2C+Hiromi%3BGeorgiev%2C+Ivelin+S%3BChuang%2C+Gwo-Yu%3BDruz%2C+Aliaksandr%3BDoria-Rose%2C+Nicole+A%3BLaub%2C+Leo%3BSliepen%2C+Kwinten%3Bvan+Gils%2C+Marit+J%3Bde+la+Pe%C3%B1a%2C+Alba+Torrents%3BDerking%2C+Ronald%3BKlasse%2C+Per-Johan%3BMigueles%2C+Stephen+A%3BBailer%2C+Robert+T%3BAlam%2C+Munir%3BPugach%2C+Pavel%3BHaynes%2C+Barton+F%3BWyatt%2C+Richard+T%3BSanders%2C+Rogier+W%3BBinley%2C+James+M%3BWard%2C+Andrew+B%3BMascola%2C+John+R%3BKwong%2C+Peter+D%3BConnors%2C+Mark&rft.aulast=Huang&rft.aufirst=Jinghe&rft.date=2014-11-06&rft.volume=515&rft.issue=7525&rft.spage=138&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=1476-4687&rft_id=info:doi/10.1038%2Fnature13601 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-22 N1 - Date created - 2014-11-06 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4TOY; PDB; KM516890; GENBANK; KM516894; KM516893; KM516892; KM516891; KM516897; KM516896; KM516895; KM516888; KM516889; KM001887; KM001883; KM001884; KM001885; KM001886; KM001880; KM001881; KM001882; KM516887; KM516886; KM001878; KM001879; KM001876; KM001877; KM001874; KM001875; KM001872; KM001873 N1 - SuppNotes - Cited By: Nucleic Acids Res. 2007 Jul;35(Web Server issue):W375-83 [17452350] Retrovirology. 2014;11:41 [24884783] Nature. 2008 Sep 4;455(7209):109-13 [18668044] J Virol. 2009 Jan;83(2):757-69 [18987148] Nature. 2009 Apr 2;458(7238):636-40 [19287373] J Virol. 2009 Jul;83(14):7337-48 [19439467] J Virol. 2003 May;77(10):5678-84 [12719560] J Virol. 1993 Nov;67(11):6642-7 [7692082] Science. 1994 Nov 11;266(5187):1024-7 [7973652] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] Virology. 2005 Feb 5;332(1):145-56 [15661147] J Virol. 2009 Sep;83(17):8925-37 [19553335] Science. 2005 Jun 24;308(5730):1906-8 [15860590] J Virol. 2005 Aug;79(15):9954-69 [16014956] J Virol. 2005 Aug;79(16):10108-25 [16051804] Hum Antibodies. 2005;14(3-4):101-13 [16720980] Science. 2009 Oct 9;326(5950):285-9 [19729618] J Virol. 2010 Feb;84(3):1631-6 [19923174] PLoS Pathog. 2010;6(8):e1001028 [20700449] Science. 2010 Aug 13;329(5993):856-61 [20616233] J Virol. 2010 Oct;84(20):10510-21 [20686044] Nature. 2010 Sep 30;467(7315):591-5 [20882016] Acta Crystallogr D Biol Crystallogr. 2011 Apr;67(Pt 4):235-42 [21460441] J Virol. 2011 Aug;85(16):8217-26 [21653673] Science. 2011 Sep 16;333(6049):1633-7 [21764753] Nature. 2011 Sep 22;477(7365):466-70 [21849977] Nature. 2011 Dec 15;480(7377):336-43 [22113616] J Virol. 2012 Apr;86(7):3574-87 [22301141] J Virol. 2012 Apr;86(8):4688-92 [22301150] PLoS One. 2012;7(9):e44241 [22970187] Immunity. 2012 Sep 21;37(3):412-25 [22999947] Nature. 2012 Nov 15;491(7424):406-12 [23151583] Cell. 2013 Mar 28;153(1):126-38 [23540694] Science. 2013 May 10;340(6133):751-6 [23661761] Nat Struct Mol Biol. 2013 Jul;20(7):796-803 [23708606] J Virol. 2013 Sep;87(18):10047-58 [23843642] Nat Protoc. 2013 Oct;8(10):1907-15 [24030440] PLoS Pathog. 2013 Sep;9(9):e1003618 [24068931] J Clin Invest. 2013 Oct;123(10):4405-9 [23999429] Proc Natl Acad Sci U S A. 2013 Nov 5;110(45):18256-61 [24145402] Science. 2013 Dec 20;342(6165):1477-83 [24179159] Cell Rep. 2014 May 8;7(3):785-95 [24767986] Immunity. 2014 May 15;40(5):657-68 [24768347] Immunity. 2014 May 15;40(5):669-80 [24768348] J Immunol Methods. 2008 Jan 1;329(1-2):112-24 [17996249] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nature13601 ER - TY - JOUR T1 - The National Library of Medicine's (NLM) Hazardous Substances Data Bank (HSDB): background, recent enhancements and future plans. AN - 1612286862; 25223694 AB - The National Library of Medicine's (NLM) Division of Specialized Information Services (SIS) Toxicology and Environmental Health Information Program is responsible for the management of the online Hazardous Substances Data Bank (HSDB). HSDB, a part of NLM's Toxicology Data Network (TOXNET(®)), is a file of chemical/substance information with one record for each specific chemical or substance, or for a category of chemicals or substances. Like the rest of TOXNET's databases and other resources, HSDB is available online at no cost to global users. HSDB has approximately 5600 chemicals and substances, with a focus on toxicology information and also on human exposure, industrial hygiene, emergency handling procedures, environmental fate, regulatory requirements, and related areas of likely interest to HSDB users. All data are from a core set of books, government documents, technical reports, selected primary journal literature, and other online sources of information, with a goal of linking the HSDB content to as much publicly available information as possible. HSDB's content is peer-reviewed by the Scientific Review Panel, a group of experts in the areas covering the scope of HSDB content. Recent enhancements include the addition of chemical structures to HSDB records, the addition of new subfields such as age groups for human data, more occupational exposure standards, and the addition of information on numerous nanomaterials. Examples of future plans include providing more exposure-related information, e.g., uses of a chemical or substance in consumer products; the addition of information summaries aimed towards consumers and other members of the public wanting to learn about a chemical or substance; more visual content such as diagrams (images) of the pathways of metabolism of a substance; and enhanced search features and navigation. Published by Elsevier Ireland Ltd. JF - Toxicology AU - Fonger, George Charles AU - Hakkinen, Pertti AU - Jordan, Shannon AU - Publicker, Stephanie AD - National Library of Medicine, Division of Specialized Information Services, Bethesda, MD 20894, USA. Electronic address: fongerg@mail.nlm.nih.gov. ; National Library of Medicine, Division of Specialized Information Services, Bethesda, MD 20894, USA. Y1 - 2014/11/05/ PY - 2014 DA - 2014 Nov 05 SP - 209 EP - 216 VL - 325 KW - Hazardous Substances KW - 0 KW - Index Medicus KW - Information KW - Databases KW - Online KW - National Library of Medicine KW - United States KW - Animals KW - History, 21st Century KW - History, 20th Century KW - Access to Information KW - Humans KW - Information Dissemination KW - Forecasting KW - Internet KW - Risk Assessment KW - Databases, Factual -- trends KW - Hazardous Substances -- classification KW - Environmental Health -- trends KW - National Library of Medicine (U.S.) -- trends KW - Toxicology -- trends KW - Toxicology -- history KW - Environmental Health -- history KW - Databases, Factual -- history KW - National Library of Medicine (U.S.) -- history KW - Hazardous Substances -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1612286862?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+National+Library+of+Medicine%27s+%28NLM%29+Hazardous+Substances+Data+Bank+%28HSDB%29%3A+background%2C+recent+enhancements+and+future+plans.&rft.au=Fonger%2C+George+Charles%3BHakkinen%2C+Pertti%3BJordan%2C+Shannon%3BPublicker%2C+Stephanie&rft.aulast=Fonger&rft.aufirst=George&rft.date=2014-11-05&rft.volume=325&rft.issue=&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=1879-3185&rft_id=info:doi/10.1016%2Fj.tox.2014.09.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-18 N1 - Date created - 2014-10-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.tox.2014.09.003 ER - TY - JOUR T1 - Estimation of the Probability of Exposure to Machining Fluids in a Population-Based Case-Control Study AN - 1808729120; PQ0003494068 AB - We describe an approach for estimating the probability that study subjects were exposed to metalworking fluids (MWFs) in a population-based case-control study of bladder cancer. Study subject reports on the frequency of machining and use of specific MWFs (straight, soluble, and synthetic/semi-synthetic) were used to estimate exposure probability when available. Those reports also were used to develop estimates for job groups, which were then applied to jobs without MWF reports. Estimates using both cases and controls and controls only were developed. The prevalence of machining varied substantially across job groups (0.1->0.9%), with the greatest percentage of jobs that machined being reported by machinists and tool and die workers. Reports of straight and soluble MWF use were fairly consistent across job groups (generally 50-70%). Synthetic MWF use was lower (13-45%). There was little difference in reports by cases and controls vs. controls only. Approximately, 1% of the entire study population was assessed as definitely exposed to straight or soluble fluids in contrast to 0.2% definitely exposed to synthetic/semi-synthetics. A comparison between the reported use of the MWFs and U.S. production levels found high correlations (r generally >0.7). Overall, the method described here is likely to have provided a systematic and reliable ranking that better reflects the variability of exposure to three types of MWFs than approaches applied in the past. [Supplementary materials are available for this article. Go to the publisher's online edition of Journal of Occupational and Environmental Hygiene for the following free supplemental resources: a list of keywords in the occupational histories that were used to link study subjects to the metalworking fluids (MWFs) modules; recommendations from the literature on selection of MWFs based on type of machining operation, the metal being machined and decade; popular additives to MWFs; the number and proportion of controls who reported various MWF responses by job group; the number and proportion of controls assigned to the MWF types by job group and exposure category; and the distribution of cases and controls assigned various levels of probability by MWF type.] JF - Journal of Occupational and Environmental Hygiene AU - Park, Dong-Uk AU - Colt, Joanne S AU - Baris, Dalsu AU - Schwenn, Molly AU - Karagas, Margaret R AU - Armenti, Karla R AU - Johnson, Alison AU - Silverman, Debra T AU - Stewart, Patricia A AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland Y1 - 2014/11/02/ PY - 2014 DA - 2014 Nov 02 SP - 757 EP - 770 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 11 IS - 11 SN - 1545-9624, 1545-9624 KW - Toxicology Abstracts; Environment Abstracts; Health & Safety Science Abstracts KW - Historical account KW - Metals KW - Urinary bladder KW - Population studies KW - Metal-working fluids KW - Cancer KW - Workers KW - Hygiene KW - Additives KW - Internet KW - Occupational exposure KW - Environmental hygiene KW - H 1000:Occupational Safety and Health KW - X 24360:Metals KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808729120?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Occupational+and+Environmental+Hygiene&rft.atitle=Estimation+of+the+Probability+of+Exposure+to+Machining+Fluids+in+a+Population-Based+Case-Control+Study&rft.au=Park%2C+Dong-Uk%3BColt%2C+Joanne+S%3BBaris%2C+Dalsu%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BArmenti%2C+Karla+R%3BJohnson%2C+Alison%3BSilverman%2C+Debra+T%3BStewart%2C+Patricia+A&rft.aulast=Park&rft.aufirst=Dong-Uk&rft.date=2014-11-02&rft.volume=11&rft.issue=11&rft.spage=757&rft.isbn=&rft.btitle=&rft.title=Journal+of+Occupational+and+Environmental+Hygiene&rft.issn=15459624&rft_id=info:doi/10.1080%2F15459624.2014.918984 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Workers; Metals; Urinary bladder; Population studies; Cancer; Occupational exposure; Internet; Environmental hygiene; Historical account; Hygiene; Additives; Metal-working fluids DO - http://dx.doi.org/10.1080/15459624.2014.918984 ER - TY - JOUR T1 - Spoiling and Sustainability: Technology, Water Insecurity, and Visibility in Arctic Alaska AN - 1622612928; 20825382 AB - One third of households in Alaska Native villages lack running water and sewer services. Historically, this public health need drove policies to improve access to treated water and sanitation. However, despite public health being a stated priority of water infrastructure development, current policies require demonstrated economic sustainability in ways that render suffering from water insecurity invisible. In this article, I situate the introduction of water treatment technologies within the history of domination coproduced with vulnerability. These processes are reflected in local narratives describing the relationships between technology, tradition, and suffering. By drawing attention to the role of the state in creating vulnerability, village leaders are trying to historicize and insert their health concerns into the sustainability conversation using narratives that both fit within and challenge the ideology of sustainability. These narratives are thus central to Inupiat struggles for visibility. JF - Medical Anthropology AU - Eichelberger, Laura AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology & Genetics, National Cancer Institute, Bethesda, Maryland, USA Y1 - 2014/11/02/ PY - 2014 DA - 2014 Nov 02 SP - 478 EP - 496 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 33 IS - 6 SN - 0145-9740, 0145-9740 KW - Health & Safety Science Abstracts; Sustainability Science Abstracts KW - USA, Alaska KW - Historical account KW - Anthropology KW - Polar environments KW - Traditions KW - Sustainability KW - Public health KW - PN, Arctic KW - Sanitation KW - Water treatment KW - Villages KW - Households KW - Economics KW - Visibility KW - Vulnerability KW - Technology KW - M3 1010:Issues in Sustainable Development KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622612928?accountid=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=Medical+Anthropology&rft.atitle=Spoiling+and+Sustainability%3A+Technology%2C+Water+Insecurity%2C+and+Visibility+in+Arctic+Alaska&rft.au=Eichelberger%2C+Laura&rft.aulast=Eichelberger&rft.aufirst=Laura&rft.date=2014-11-02&rft.volume=33&rft.issue=6&rft.spage=478&rft.isbn=&rft.btitle=&rft.title=Medical+Anthropology&rft.issn=01459740&rft_id=info:doi/10.1080%2F01459740.2014.917374 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2014-11-26 N1 - SubjectsTermNotLitGenreText - Historical account; Anthropology; Traditions; Polar environments; Sustainability; Public health; Sanitation; Villages; Water treatment; Households; Economics; Visibility; Vulnerability; Technology; USA, Alaska; PN, Arctic DO - http://dx.doi.org/10.1080/01459740.2014.917374 ER - TY - JOUR T1 - Is CD4 Monitoring Needed Among Ugandan Clients Achieving a Virologic and Immunologic Response to Treatment? AN - 1827882746; PQ0003681045 AB - It is unclear whether ongoing CD4 monitoring is needed following immunologic and virologic response to antiretroviral therapy (ART). We investigated the proportion of clients who achieved a virologic and immunologic response and then had a subsequent CD4 count <200 cells/ mu L despite continued virologic suppression. Included in this analysis were clients receiving ART through the Rakai Health Sciences Program between June 2004-May 2013 who achieved a CD4 greater than or equal to 200 cells/ mu L and VL less than or equal to 400 copies/mL and who had three sets of CD4 and VL measurements (defined as a sequence) within a 390 day period. A CD4 decline was defined as any drop in CD4 count to <200 cells/ mu L during a period of viral suppression. A total of 1553 clients were included, 68% females, mean age of 35.5 years (SD 8.3), median baseline CD4 count 183 cells/ mu L (IQR 106-224). 43 (2.8%) clients developed CD4 declines, the majority, 32/43 (74%), among individuals whose initial CD4 was <300 cells/ mu L. Of the 43 clients with CD4 declines, 24 had an additional CD4 measurement and 20/24 (83%) achieved a CD4 greater than or equal to 200 cell/ mu L on their next measurement (median 285 cells/ mu L; IQR 220-365). CD4 declines were significantly greater among those with lower CD4 at sequence initiation [adjusted hazard ratio (AHR) 4.3 (95% CI 2.1, 9.0) CD4 200-249 versus greater than or equal to 350 cells/ mu L]. Clients who achieved an immunologic and virologic response to ART were unlikely to experience a subsequent CD4 count decline to <200 cells/ mu L, and among those experiencing a decline, the majority were transient in nature. Thus, ongoing CD4 monitoring could be omitted. JF - AIDS Patient Care and STDs AU - Reynolds, Steven J AU - Sempa, Joseph B AU - Kiragga, Agnes N AU - Newell, Kevin AU - Nakigozi, Gertrude AU - Galiwango, Ronald AU - Gray, Ron AU - Quinn, Thomas C AU - Serwadda, David AU - Chang, Larry AD - Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 575 EP - 578 PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538 United States VL - 28 IS - 11 SN - 1087-2914, 1087-2914 KW - Immunology Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Acquired immune deficiency syndrome KW - CD4 antigen KW - Age KW - antiretroviral therapy KW - Antiretroviral agents KW - Sexually transmitted diseases KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1827882746?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Patient+Care+and+STDs&rft.atitle=Is+CD4+Monitoring+Needed+Among+Ugandan+Clients+Achieving+a+Virologic+and+Immunologic+Response+to+Treatment%3F&rft.au=Reynolds%2C+Steven+J%3BSempa%2C+Joseph+B%3BKiragga%2C+Agnes+N%3BNewell%2C+Kevin%3BNakigozi%2C+Gertrude%3BGaliwango%2C+Ronald%3BGray%2C+Ron%3BQuinn%2C+Thomas+C%3BSerwadda%2C+David%3BChang%2C+Larry&rft.aulast=Reynolds&rft.aufirst=Steven&rft.date=2014-11-01&rft.volume=28&rft.issue=11&rft.spage=575&rft.isbn=&rft.btitle=&rft.title=AIDS+Patient+Care+and+STDs&rft.issn=10872914&rft_id=info:doi/10.1089%2Fapc.2014.0086 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Number of references - 17 N1 - Last updated - 2016-10-26 N1 - SubjectsTermNotLitGenreText - Age; CD4 antigen; antiretroviral therapy; Acquired immune deficiency syndrome; Antiretroviral agents; Sexually transmitted diseases DO - http://dx.doi.org/10.1089/apc.2014.0086 ER - TY - JOUR T1 - Predictive prognostic role of miR-181a with discrepancy in the liver and serum of genotype 4 hepatitis C virus patients. AN - 1826615268; 25279157 AB - microRNA (miRNA) expression in organs does not always represent their quantity in serum. A disparity in the expression of miR-181a has been reported in the tissues and serum of hepatocellular carcinoma (HCC) patients. Since hepatitis C virus (HCV) is a major cause of HCC and miR-181a has never been studied in HCV, the present study aimed to investigate the miR-181a expression profile in genotype 4 (GT4)-HCV patients to evaluate whether this pattern is also apparent in HCV. RNA was extracted from liver tissues, peripheral mononuclear cells (PBMCs) and serum samples from GT4-HCV-infected patients and healthy donors to evaluate the relative miR-181a expression using quantitative reverse transcription-polymerase chain reaction. miR-181a was significantly higher in the serum of naïve patients compared to controls, and an inverse correlation with the viral load and liver enzymes was apparent. By contrast, no difference in miR-181a expression was observed in the liver tissues and PBMCs of patients compared to controls. This expression observed in HCV is conflicting to that previously reported in HCC. The study also demonstrates a significant upregulation of miR-181a post-interferon/ribavirin treatment in the serum of sustained virological responders (SVRs) compared to non-responders and treatment-naïve SVRs. In conclusion, miR-181a may be considered to be a possible prognostic marker in GT4-HCV infection. JF - Biomedical reports AU - Elhelw, Dalia Sherif AU - Mekky, Radwa Yehia AU - El-Ekiaby, Nada AU - Ahmed, Rasha AU - Eldin, Mohammad Ahmed Mohey AU - El-Sayed, Mohammad AU - Abouelkhair, Mahmoud Mohammad AU - Salah, Ayman AU - Zekri, Abdel Rahman AU - Esmat, Gamal AU - Abdelaziz, Ahmed Ihab AD - The Molecular Pathology Research Group, Department of Pharmacology and Toxicology, German University in Cairo, New Cairo 11835, Egypt. ; Department of Endemic Medicine and Hepatology, Cairo University, Cairo 11562, Egypt. ; Department of Surgery, Cairo University, Cairo 11562, Egypt. ; Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo 11976, Egypt. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 843 EP - 848 VL - 2 IS - 6 SN - 2049-9434, 2049-9434 KW - genotype 4 KW - treatment response KW - microRNA-181a KW - hepatitis C virus KW - sustained virological responders KW - prognosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826615268?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomedical+reports&rft.atitle=Predictive+prognostic+role+of+miR-181a+with+discrepancy+in+the+liver+and+serum+of+genotype+4+hepatitis+C+virus+patients.&rft.au=Elhelw%2C+Dalia+Sherif%3BMekky%2C+Radwa+Yehia%3BEl-Ekiaby%2C+Nada%3BAhmed%2C+Rasha%3BEldin%2C+Mohammad+Ahmed+Mohey%3BEl-Sayed%2C+Mohammad%3BAbouelkhair%2C+Mahmoud+Mohammad%3BSalah%2C+Ayman%3BZekri%2C+Abdel+Rahman%3BEsmat%2C+Gamal%3BAbdelaziz%2C+Ahmed+Ihab&rft.aulast=Elhelw&rft.aufirst=Dalia&rft.date=2014-11-01&rft.volume=2&rft.issue=6&rft.spage=843&rft.isbn=&rft.btitle=&rft.title=Biomedical+reports&rft.issn=20499434&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2014-10-03 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - HIV-1 Envelope Glycoprotein Trimer Immunogenicity Elicited in the Presence of Human CD4 Alters the Neutralization Profile AN - 1768582376; PQ0002687106 AB - The HIV-1 envelope glycoproteins (Env) gp120 and gp41 are the sole virally derived components on the surface of the virus. These glycoproteins mediate receptor binding and entry and are targets for neutralizing antibodies. The most highly validated protein region on Env that is a target for broadly neutralizing antibodies is the conserved CD4 binding site. Mimetics of Env have been used in attempts to elicit antibodies to the CD4 binding site. Some trimers, such as the soluble foldon trimers used here, elicit 5-10% of the Env-directed B cell response to this conserved region. As these trimers, or other Env versions, advance into clinical development, there is both considerable interest and concern as to whether binding to the abundant CD4 present on the surface of T cells and macrophages may blunt potentially protective antibody responses to this site. Here, we utilized rabbits transgenic for human CD4 to evaluate the role of CD4:Env interaction in vivo relative to the elicitation of Env-directed antibodies following immunization. We analyzed responses to trimers both capable and incapable of recognizing human CD4 with high affinity. We demonstrated that the presence of human CD4 in vivo did not significantly affect the overall elicitation of Env binding or CD4bs-directed antibodies. However, the presence of CD4 did reduce the capacity of elicited serum antibodies to neutralize the clade C isolate, MW965. Reduction of HXBc2 neutralization was associated with the CD4 binding-incompetent trimers. These results highlight an important consideration regarding CD4 binding-competent trimeric Env immunogens as they enter the clinic for human vaccine trials. JF - AIDS Research and Human Retroviruses AU - Forsell, Mattias NE AU - McKee, Krisha AU - Feng, Yu AU - Mascola, John R AU - Wyatt, Richard T AD - Vaccine Research Center, NIAID, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 1089 EP - 1098 PB - Mary Ann Liebert, Inc., 140 Huguenot Street New Rochelle NY 10801 United States VL - 30 IS - 11 SN - 0889-2229, 0889-2229 KW - Immunology Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Macrophages KW - Acquired immune deficiency syndrome KW - glycoprotein gp41 KW - Lymphocytes B KW - Clinical trials KW - Immunization KW - Glycoprotein gp120 KW - CD4 antigen KW - Antibodies KW - Retrovirus KW - Envelopes KW - Immunogenicity KW - Human immunodeficiency virus 1 KW - Lymphocytes T KW - Proteins KW - Glycoproteins KW - Vaccines KW - Neutralization KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22360:AIDS and HIV KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768582376?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Research+and+Human+Retroviruses&rft.atitle=HIV-1+Envelope+Glycoprotein+Trimer+Immunogenicity+Elicited+in+the+Presence+of+Human+CD4+Alters+the+Neutralization+Profile&rft.au=Forsell%2C+Mattias+NE%3BMcKee%2C+Krisha%3BFeng%2C+Yu%3BMascola%2C+John+R%3BWyatt%2C+Richard+T&rft.aulast=Forsell&rft.aufirst=Mattias&rft.date=2014-11-01&rft.volume=30&rft.issue=11&rft.spage=1089&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/10.1089%2Faid.2014.0104 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 34 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Macrophages; Glycoprotein gp120; Antibodies; CD4 antigen; Envelopes; glycoprotein gp41; Lymphocytes B; Immunogenicity; Lymphocytes T; Vaccines; Clinical trials; Immunization; Acquired immune deficiency syndrome; Proteins; Glycoproteins; Neutralization; Retrovirus; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1089/aid.2014.0104 ER - TY - JOUR T1 - Do newspaper reports of suicides comply with standard suicide reporting guidelines? A study from Bangalore, India AN - 1695153284 AB - Background: Several countries have prescribed standard guidelines for media professionals on suicide reporting. However, the implementation of these guidelines has been varied. Suicide rates in South Asia are one of the highest in the world, and it is known that media guidelines for suicide reporting are not followed adequately. However, there are no published reports available from this region. Aim: This study aimed at assessing newspaper reports of suicide for quality of reporting based on standard reporting guidelines and to study differences between English and vernacular (Kannada) newspapers in Bangalore, South India. Methods: A total of 341 newspaper reports of suicide from 550 newspapers (3 English and 3 Kannada) over 3 months were systematically assessed for compliance with reporting guidelines. Each report was evaluated on 2 domains and 36 parameters. Data were analyzed for frequency of inappropriate reporting and patterns compared between vernacular and English newspapers. Results: In all, 87% of the reports were those of completed suicide. Non-compliant reporting – method of suicide was reported in 89% and 32% of reports were in prominent pages of the newspaper, 95% mentioned gender, 90% reported the name, 80% reported age and suicide location, 75% reported life events related to suicide, 70% reported occupation, 69% had headline explicity on suicide and 61% reported monocausality. Only 16% reported mental disorder related to suicide, and less than 3% included information on suicide prevention and helplines. Vernacular papers showed significantly better compliance in 16 of the 20 areas. However, protective characteristics were better reported in English newspapers. Conclusion: Majority of reports on suicides in newspapers from Bangalore did not comply with standard guidelines of reporting. There is a strong need to evolve local guidelines and mechanisms for ensuring responsible reporting which have important implications in prevention of suicide.                                                JF - The International Journal of Social Psychiatry AU - Chandra, Prabha S AU - Doraiswamy, Padmavathy AU - Padmanabh, Anuroopa AU - Philip, Mariamma AD - NIMHANS Centre for Well-Being, National Institute of Mental Health and Neurosciences, Bangalore, India ; NIMHANS Centre for Well-Being, Department of Nursing, National Institute of Mental Health and Neurosciences, Bangalore, India ; Department of Biostatistics, National Institute of Mental Health and Neurosciences, Bangalore, India ; NIMHANS Centre for Well-Being, National Institute of Mental Health and Neurosciences, Bangalore, India Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 687 EP - 694 CY - London PB - SAGE PUBLICATIONS, INC. VL - 60 IS - 7 SN - 0020-7640 KW - Medical Sciences--Psychiatry And Neurology KW - Suicide KW - media KW - suicide reporting KW - India UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1695153284?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+International+Journal+of+Social+Psychiatry&rft.atitle=Do+newspaper+reports+of+suicides+comply+with+standard+suicide+reporting+guidelines%3F+A+study+from+Bangalore%2C+India&rft.au=Chandra%2C+Prabha+S%3BDoraiswamy%2C+Padmavathy%3BPadmanabh%2C+Anuroopa%3BPhilip%2C+Mariamma&rft.aulast=Chandra&rft.aufirst=Prabha&rft.date=2014-11-01&rft.volume=60&rft.issue=7&rft.spage=687&rft.isbn=&rft.btitle=&rft.title=The+International+Journal+of+Social+Psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764013513438 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-06-18 N1 - Last updated - 2016-09-08 N1 - SubjectsTermNotLitGenreText - India DO - http://dx.doi.org/10.1177/0020764013513438 ER - TY - JOUR T1 - Concerns about unintended negative consequences of informing the public about multifactorial risks may be premature for young adult smokers AN - 1665160477 AB - Background Many health risks are associated with both genetic and behavioural factors. Concerns have been raised that learning about such multifactorial risks might have detrimental effects on health-related beliefs, cognitions, and affect. However, experimental evidence is sparse. Objective To explore the effects of reading an online news article about the discovery of a genetic basis for nicotine addiction. Methods Smokers ( N = 333) were recruited from the psychology subject pools of two major universities. Participants were randomly assigned to read one of three news articles: one describing a genetic basis for nicotine addiction and lung cancer obtained from a national news source, one altered to indicate no genetic basis for nicotine addiction and lung cancer, or one unrelated attention control. Participants then completed an online questionnaire, which assessed smoking-related cognitions and affect, and beliefs about nicotine addiction, quitting smoking, and whether the harms of tobacco use are delayed. Results There was no statistically significant influence of experimental condition on smoking-related cognitions/affect ( ps > .05, η2 < .002), beliefs about addiction and quitting (Wilksʼ λ = .98, p = .66, η2 = .01), or delayed harm ( ps > .05, η2 < .002). Conclusion Reading an online news article about the presence or absence of a genetic basis for nicotine addiction was not found to change smoking-related cognitions/affect or beliefs among young adult smokers. Concerns about negative effects of multifactorial risk information on health beliefs may be premature. Nevertheless, to effectively translate basic genomics research into effective public health practice, further research should investigate these issues in different populations, via different communication modalities, and for different health outcomes. Statement of contribution What is already known on this subject? * Information about the health implications of the interaction between genetics and behaviour is becoming prevalent. * Learning about these interactions may reduce perceived risk and intentions to engage in health behaviours. What does this study add?* Informing young adult smokers about the genetic basis for nicotine addiction does not affect health beliefs negatively. * Responses are not moderated by endorsing the idea of genetic causation or current/experimenter smoking status. JF - British Journal of Health Psychology AU - Waters, Erika A AU - Kincaid, Caroline AU - Kaufman, Annette R AU - Stock, Michelle L AU - Peterson, Laurel M AU - Muscanell, Nicole L AU - Guadagno, Rosanna E AD - Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, Saint Louis, Missouri, USA. ; Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, Maryland, USA. ; Department of Psychology, George Washington University, Washington, District of Columbia, USA. ; Department of Psychiatry, University of Pittsburgh, Pennsylvania, USA. ; Department of Psychology, The University of Alabama, Tuscaloosa, Alabama, USA. ; Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, Saint Louis, Missouri, USA. Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 720 EP - 736 CY - Leicester PB - British Psychological Society VL - 19 IS - 4 SN - 1359-107X KW - Psychology KW - Addiction KW - Adults KW - Articles KW - Causality KW - Health behaviour KW - Health status KW - Internet KW - Learning KW - Lung cancer KW - Medical research KW - Moderated KW - Negative events KW - News KW - Nicotine KW - Premature KW - Public health KW - Basis KW - Behaviour KW - Beliefs KW - Cancer KW - Cessation KW - Cognition KW - Communication KW - Consequences KW - Delayed KW - Discovery KW - Genetic factors KW - Health KW - Health beliefs KW - Health risks UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665160477?accountid=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=British+Journal+of+Health+Psychology&rft.atitle=Concerns+about+unintended+negative+consequences+of+informing+the+public+about+multifactorial+risks+may+be+premature+for+young+adult+smokers&rft.au=Waters%2C+Erika+A%3BKincaid%2C+Caroline%3BKaufman%2C+Annette+R%3BStock%2C+Michelle+L%3BPeterson%2C+Laurel+M%3BMuscanell%2C+Nicole+L%3BGuadagno%2C+Rosanna+E&rft.aulast=Waters&rft.aufirst=Erika&rft.date=2014-11-01&rft.volume=19&rft.issue=4&rft.spage=720&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Health+Psychology&rft.issn=1359107X&rft_id=info:doi/10.1111%2Fbjhp.12069 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-24 DO - http://dx.doi.org/10.1111/bjhp.12069 ER - TY - JOUR T1 - Symptoms of Attention-Deficit/Hyperactivity Disorder and Peer Functioning: a Transactional Model of Development AN - 1665155814 AB - The goals of this short-term longitudinal study were to investigate differential, independent effects of inattention and hyperactivity/impulsivity on children’s peer relationships and the dynamic, transactional interplay between ADHD symptoms and indices of peer functioning over time. This study used a community sample that included 739 preadolescents (239 fourth graders and 500 fifth graders; 52.23 % boys) from northern Taiwan, who were assessed every six months at three time points. Children’s ADHD symptoms were measured using the parent report on the Swanson, Nolan, and Pelham, version IV scale. Positive and negative facets of peer functioning, including peer rejection, peer acceptance, and the number of friendships, were assessed via peer nomination. Results of cross-lagged models indicated that inattention, but not hyperactivity/impulsivity, predicted subsequent peer impairment (i.e., lower peer acceptance and fewer dyadic friendships). Findings also showed a vicious cycle in which inattentive symptoms predicted later peer impairment, which in turn led to increases in both inattention and hyperactivity/impulsivity. These findings did not differ across gender, and the majority of the findings remained significant even after controlling for age and physical aggression. Taken together, this study demonstrated the detrimental effect of inattention on children’s peer functioning and the transactional and dynamic interplay between inattention and peer impairment in a Chinese culture. JF - Journal of Abnormal Child Psychology AU - Tseng, Wan-Ling AU - Kawabata, Yoshito AU - Gau, Susan Shur-Fen AU - Crick, Nicki R AD - Institute of Child Development, University of Minnesota, Minneapolis, USA wan-ling.tseng@nih.gov wan-ling.tseng@nih.gov wan-ling.tseng@nih.gov; Department of Psychiatry, National Taiwan University Hospital and College of Medicine, 7 Chung-Shan Road, Taipei, 10002, Taiwan gaushufe@ntu.edu.tw; Institute of Child Development, University of Minnesota, Minneapolis, USA Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 1353 EP - 1365 CY - New York PB - Springer Science & Business Media VL - 42 IS - 8 SN - 0091-0627 KW - Medical Sciences--Physical Medicine And Rehabilitation KW - Acceptance KW - Aggressive young boys KW - Aggression KW - Attention deficit hyperactivity disorder KW - Attention deficits KW - Boys KW - Children KW - Friendships KW - Gender KW - Hyperactivity KW - Impulsivity KW - Peer acceptance KW - Peer rejection KW - Peer relationships KW - Rejection KW - Short term KW - Taiwan UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665155814?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Abnormal+Child+Psychology&rft.atitle=Symptoms+of+Attention-Deficit%2FHyperactivity+Disorder+and+Peer+Functioning%3A+a+Transactional+Model+of+Development&rft.au=Tseng%2C+Wan-Ling%3BKawabata%2C+Yoshito%3BGau%2C+Susan+Shur-Fen%3BCrick%2C+Nicki+R&rft.aulast=Tseng&rft.aufirst=Wan-Ling&rft.date=2014-11-01&rft.volume=42&rft.issue=8&rft.spage=1353&rft.isbn=&rft.btitle=&rft.title=Journal+of+Abnormal+Child+Psychology&rft.issn=00910627&rft_id=info:doi/10.1007%2Fs10802-014-9883-8 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-12 N1 - SubjectsTermNotLitGenreText - Taiwan DO - http://dx.doi.org/10.1007/s10802-014-9883-8 ER - TY - JOUR T1 - Exploring psychological responses to genetic testing for Lynch Syndrome within the family context AN - 1665154316 AB - Objective Genetic testing for hereditary cancer susceptibility syndromes is a family-centered process. Nonetheless, little research has explored how the family context affects psychological responses to genetic testing. We examine how personal test results and the test results of immediate and extended family members shape responses to genetic testing. Methods Individuals at risk of carrying a mutation associated with an inherited cancer susceptibility syndrome (Lynch syndrome) received genetic testing. Six months after receiving their results, participants reported on cancer distress, cancer worry, and depressive symptoms. Results Among mutation carriers for Lynch syndrome, the higher the proportion of carriers in their immediate family, the less cancer worry and distress they reported. In contrast, mutation carriers and non-carriers with a high proportion of carriers in their immediate family and mutation carriers with a high proportion of carriers in their extended family were at elevated risk for clinically significant levels of depressive symptoms. Conclusion Personal test results alone are not highly predictive of psychological outcomes. Instead, the interaction between personal and family test results, or in some cases, family test results alone, predict key psychological outcomes. The current research has important implications for genetic counseling and intervention efforts. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - Psycho-Oncology AU - Eliezer, Dina AU - Hadley, Donald W AU - Koehly, Laura M AD - National Human Genome Research Institute, Bethesda, MD, USA. ; National Human Genome Research Institute, Bethesda, MD, USA. Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 1292 EP - 1299 CY - Chichester PB - Wiley Subscription Services, Inc. VL - 23 IS - 11 SN - 1057-9249 KW - Medical Sciences--Psychiatry And Neurology KW - At risk KW - Cancer KW - Carriers KW - Counselling KW - Depression KW - Genetic counselling KW - Genetic screening KW - Psychological distress KW - Public domain KW - Relatives KW - Susceptibility KW - Symptoms KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665154316?accountid=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=Exploring+psychological+responses+to+genetic+testing+for+Lynch+Syndrome+within+the+family+context&rft.au=Eliezer%2C+Dina%3BHadley%2C+Donald+W%3BKoehly%2C+Laura+M&rft.aulast=Eliezer&rft.aufirst=Dina&rft.date=2014-11-01&rft.volume=23&rft.issue=11&rft.spage=1292&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3551 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1002/pon.3551 ER - TY - JOUR T1 - Reliability and validity of expert assessment based on airborne and urinary measures of nickel and chromium exposure in the electroplating industry AN - 1664212763; PQ0001187959 AB - The reliability and validity of six experts' exposure ratings were evaluated for 64 nickel-exposed and 72 chromium-exposed workers from six Shanghai electroplating plants based on airborne and urinary nickel and chromium measurements. Three industrial hygienists and three occupational physicians independently ranked the exposure intensity of each metal on an ordinal scale (1-4) for each worker's job in two rounds: the first round was based on responses to an occupational history questionnaire and the second round also included responses to an electroplating industry-specific questionnaire. The Spearman correlation (r sub(s)) was used to compare each rating's validity to its corresponding subject-specific arithmetic mean of four airborne or four urinary measurements. Reliability was moderately high (weighted kappa range=0.60-0.64). Validity was poor to moderate (r sub(s)=-0.37-0.46) for both airborne and urinary concentrations of both metals. For airborne nickel concentrations, validity differed by plant. For dichotomized metrics, sensitivity and specificity were higher based on urinary measurements (47-78%) than airborne measurements (16-50%). Few patterns were observed by metal, assessment round, or expert type. These results suggest that, for electroplating exposures, experts can achieve moderately high agreement and (reasonably) distinguish between low and high exposures when reviewing responses to in-depth questionnaires used in population-based case-control studies. JF - Journal of Exposure Science and Environmental Epidemiology AU - Chen, Yu-Cheng AU - Coble, Joseph B AU - Deziel, Nicole C AU - Ji, Bu-Tian AU - Xue, Shouzheng AU - Lu, Wei AU - Stewart, Patricia A AU - Friesen, Melissa C AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 622 EP - 628 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 24 IS - 6 SN - 1559-0631, 1559-0631 KW - Toxicology Abstracts; Health & Safety Science Abstracts; Environment Abstracts KW - Metals KW - Historical account KW - Sensitivity KW - Inventories KW - Chromium KW - Heavy metals KW - Nickel KW - Mathematics KW - Urine KW - Metal finishing industry KW - China, People's Rep., Shanghai KW - Occupational exposure KW - H 1000:Occupational Safety and Health KW - X 24360:Metals KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664212763?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.atitle=Reliability+and+validity+of+expert+assessment+based+on+airborne+and+urinary+measures+of+nickel+and+chromium+exposure+in+the+electroplating+industry&rft.au=Chen%2C+Yu-Cheng%3BCoble%2C+Joseph+B%3BDeziel%2C+Nicole+C%3BJi%2C+Bu-Tian%3BXue%2C+Shouzheng%3BLu%2C+Wei%3BStewart%2C+Patricia+A%3BFriesen%2C+Melissa+C&rft.aulast=Chen&rft.aufirst=Yu-Cheng&rft.date=2014-11-01&rft.volume=24&rft.issue=6&rft.spage=622&rft.isbn=&rft.btitle=&rft.title=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.issn=15590631&rft_id=info:doi/10.1038%2Fjes.2014.22 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-03-30 N1 - SubjectsTermNotLitGenreText - Inventories; Chromium; Heavy metals; Nickel; Occupational exposure; Mathematics; Sensitivity; Historical account; Metals; Urine; Metal finishing industry; China, People's Rep., Shanghai DO - http://dx.doi.org/10.1038/jes.2014.22 ER - TY - JOUR T1 - A Research on the Relationship between Exercise Behavior of the Elderly and Medical Frequency as well as Quality of Life AN - 1660394907; PQ0001022306 AB - Purpose: To understand the impact of exercise frequency (per week of the elderly) on medical inspection frequency and quality of life. Method: Conduct an investigation through questionnaire survey method, aiming at people over 65. Descriptive statistics, t-test, and one-way ANOVA were used to analyze the data including 898 valid questionnaires. Result: 1. Elderly whose exercise more than 5 days a week get higher score in Physical Component Summary (PCS) and Mental Component Summary (MCS), and the inspection frequency was low. 2. The significant differences on medical inspection frequency exist in variables such as exercise frequency, gender, age, hospitalized or not, suffer from chronic diseases or not, and work or not. 3. The medical inspection frequency show sudden deterioration after the age of 75, which means that the age of 75 is a key age point. Conclusion: Elders whose exercise more than 3 days a week only perform better in MCS. However, if the number of days of doing exercise reaches 5 days a week, it will get better scores in not only MCS and PCS, but also reduce the number of medical inspection frequency. We suggest the elderly people should exercise more than five days a week to reduce the medical visits, and enhance the quality of life. JF - Tiyu Keyan/Sports Science Research AU - Kao, Hsingkuei AU - Liu, Zhimin AD - Taipei Municipal Nei-Hu Junior High School, Taipei, China Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 17 EP - 22 PB - Shanghai Research Institute of Sports Science, 87 Wu Xing Rd. Shanghai 200030 China, [mailto:shtyky@online.sh.cn], [URL:http://www.shriss.cn] VL - 35 IS - 6 SN - 1006-1207, 1006-1207 KW - Physical Education Index KW - Age KW - Statistics KW - Research (statistical design) KW - Gerontology KW - Surveys KW - Lifestyle KW - scoring KW - Exercise (frequency) KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660394907?accountid=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=Tiyu+Keyan%2FSports+Science+Research&rft.atitle=A+Research+on+the+Relationship+between+Exercise+Behavior+of+the+Elderly+and+Medical+Frequency+as+well+as+Quality+of+Life&rft.au=Kao%2C+Hsingkuei%3BLiu%2C+Zhimin&rft.aulast=Kao&rft.aufirst=Hsingkuei&rft.date=2014-11-01&rft.volume=35&rft.issue=6&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Tiyu+Keyan%2FSports+Science+Research&rft.issn=10061207&rft_id=info:doi/ LA - Chinese DB - Physical Education Index N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Age; Statistics; Research (statistical design); Gerontology; Surveys; Exercise (frequency); scoring; Lifestyle ER - TY - JOUR T1 - A bilingual-monolingual comparison of young children's vocabulary size: Evidence from comprehension and production AN - 1660012214; 201501679 AB - It is often assumed that young bilinguals are lexically delayed in comparison to monolinguals. A comprehensive comparison of comprehension and production vocabulary in 31 firstborn bilingual and 30 matched monolingual children fails to find empirical foundation for this assumption. Several raters completed Dutch and French adaptations of the MacArthur Communicative Development Inventories for children aged 13 and 20 months. At 13 months, bilinguals understood more words than did monolinguals; at 20 months, monolinguals knew more Dutch words than did bilinguals (combining comprehension and production). There were no group differences for word production or for Dutch word comprehension. Both groups understood and produced the same number of lexicalized meanings; ratios of word comprehension to word production did not differ; interindividual variation was similar. This study underscores the importance of conducting bilingual-monolingual comparisons with matched groups and suggests that if individual bilingual children appear to be slow in early vocabulary development, reasons other than their bilingualism should be investigated. Adapted from the source document JF - Applied Psycholinguistics AU - De Houwer, Annick AU - Bornstein, Marc H AU - Putnick, Diane L AD - Erfurt University and Eunice Kennedy Shriver National Institute of Child Health and Human Development annick.dehouwer@uni-erfurt.de Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 1189 EP - 1211 VL - 35 IS - 6 SN - 0142-7164, 0142-7164 KW - Vocabulary Size (94862) KW - Dutch (20100) KW - Language Acquisition (41600) KW - Bilingualism (08850) KW - French (25750) KW - Comprehension (13950) KW - Monolingualism (54850) KW - Children (11850) KW - article KW - 4026: psycholinguistics; bilingual language processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660012214?accountid=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=Applied+Psycholinguistics&rft.atitle=A+bilingual-monolingual+comparison+of+young+children%27s+vocabulary+size%3A+Evidence+from+comprehension+and+production&rft.au=De+Houwer%2C+Annick%3BBornstein%2C+Marc+H%3BPutnick%2C+Diane+L&rft.aulast=De+Houwer&rft.aufirst=Annick&rft.date=2014-11-01&rft.volume=35&rft.issue=6&rft.spage=1189&rft.isbn=&rft.btitle=&rft.title=Applied+Psycholinguistics&rft.issn=01427164&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-09-27 N1 - CODEN - APPSDZ N1 - SubjectsTermNotLitGenreText - Bilingualism (08850); Comprehension (13950); Children (11850); Dutch (20100); Monolingualism (54850); Vocabulary Size (94862); French (25750); Language Acquisition (41600) ER - TY - JOUR T1 - Improving the specificity and efficacy of CRISPR/CAS9 and gRNA through target specific DNA reporter AN - 1647013778; 21276148 AB - Genomic engineering by the guide RNA (gRNA)-directed CRISPR/CAS9 is rapidly becoming a method of choice for various biological systems. However, pressing concerns remain regarding its off-target activities and wide variations in efficacies. While next generation sequencing (NGS) has been primarily used to evaluate the efficacies and off-target activities of gRNAs, it only detects the imperfectly repaired double strand DNA breaks (DSB) by the error-prone non-homologous end joining (NHEJ) mechanism and may not faithfully represent the DSB activities because the efficiency of NHEJ-mediated repair varies depending on the local chromatin environment. Here we describe a reporter system for unbiased detection and comparison of DSB activities that promises to improve the chance of success in genomic engineering and to facilitate large-scale screening of CAS9 activities and gRNA libraries. Additionally, we demonstrated that the tolerances to mismatches between a gRNA and the corresponding target DNA can occur at any position of the gRNA, and depend on both specific gRNA sequences and CAS9 constructs used. JF - Journal of Biotechnology AU - Zhang, Jian-Hua AU - Pandey, Mritunjay AU - Kahler, John F AU - Loshakov, Anna AU - Harris, Benjamin AU - Dagur, Pradeep K AU - Mo, Yin-Yuan AU - Simonds, William F AD - Metabolic Diseases Branch, Bldg. 10, Room 8C-101, National Institute of Diabetes and Digestive and Kidney Diseases, United States Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 1 EP - 8 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 189 SN - 0168-1656, 0168-1656 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - CRISPR KW - CAS9 KW - gRNA KW - EGFP reporter KW - Specificity KW - CRISPR clustered regularly interspaced short palindromic repeats KW - CAS9 CRISPR associated protein KW - gRNA guide RNA KW - NHEJ none homologous end joining KW - DSB double strand DNA break KW - NGS next generation sequencing KW - DNA damage KW - Non-homologous end joining KW - RNA KW - Chromatin KW - Nucleotide sequence KW - genomics KW - W 30925:Genetic Engineering KW - N 14820:DNA Metabolism & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647013778?accountid=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+Biotechnology&rft.atitle=Improving+the+specificity+and+efficacy+of+CRISPR%2FCAS9+and+gRNA+through+target+specific+DNA+reporter&rft.au=Zhang%2C+Jian-Hua%3BPandey%2C+Mritunjay%3BKahler%2C+John+F%3BLoshakov%2C+Anna%3BHarris%2C+Benjamin%3BDagur%2C+Pradeep+K%3BMo%2C+Yin-Yuan%3BSimonds%2C+William+F&rft.aulast=Zhang&rft.aufirst=Jian-Hua&rft.date=2014-11-01&rft.volume=189&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biotechnology&rft.issn=01681656&rft_id=info:doi/10.1016%2Fj.jbiotec.2014.08.033 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-07-20 N1 - SubjectsTermNotLitGenreText - DNA damage; Chromatin; RNA; Non-homologous end joining; Nucleotide sequence; genomics; gRNA DO - http://dx.doi.org/10.1016/j.jbiotec.2014.08.033 ER - TY - JOUR T1 - The First US Domestic Report of Disseminated Mycobacterium avium Complex and Anti-Interferon- gamma Autoantibodies AN - 1635034209; 21030520 AB - Introduction: Anti-interferon- gamma (IFN gamma ) autoantibodies have been associated with disseminated mycobacterial infections, mostly in patients from Southeast Asia. Purpose: We studied an American-born, Caucasian female with M. avium complex infection of the subglottic mucosa and brain for underlying etiologies of infection. Methods: Plasma was screened for anticytokine autoantibodies using a Luminex-based approach. The ability of patient plasma to block IFN gamma -induced STAT1 phosphorylation in normal blood cells was evaluated by flow cytometry with intracellular staining. Plasma inhibition of IFN gamma production and IFN gamma -induced cytokines in normal and patient blood cells washed of autologous plasma was also evaluated. Results: Patient plasma contained high-titer IgG anti-IFN gamma autoantibodies, primarily of the IgG sub(1) subclass. Patient but not control plasma prevented IFN gamma -induced STAT1 phosphorylation and expression of the IFN gamma -inducible cytokines tumor necrosis factor (TNF) alpha and interleukin (IL)-12 in normal blood cells. Patient blood cells washed free of autologous plasma demonstrated normal IFN gamma production and response. Conclusions: Disseminated nontuberculous mycobacterial infections should always prompt immune evaluation. This first case of disseminated nontuberculous mycobacterial infection and anti-IFN gamma autoantibodies in an American-born Caucasian suggests that anti-cytokine autoantibodies are not racially or regionally restricted. JF - Journal of Clinical Immunology AU - O'Connell, Elise AU - Rosen, Lindsey B AU - LaRue, Richard W AU - Fabre, Valeria AU - Melia, Michael T AU - Auwaerter, Paul G AU - Holland, Steven M AU - Browne, Sarah K AD - Laboratory of Parasitic Diseases, NIAID, NIH, CRC B3-4141, MSC 1684, Bethesda, MD, 20892-1684, USA, brownesa@niaid.nih.gov Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 928 EP - 932 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 34 IS - 8 SN - 0271-9142, 0271-9142 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Etiology KW - Mycobacterium avium KW - Tumor necrosis factor KW - Mucosa KW - Brain KW - Interleukins KW - Infection KW - Flow cytometry KW - Autoantibodies KW - Phosphorylation KW - Stat1 protein KW - Immunoglobulin G KW - Blood cells KW - F 06930:Autoimmunity KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635034209?accountid=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=The+First+US+Domestic+Report+of+Disseminated+Mycobacterium+avium+Complex+and+Anti-Interferon-+gamma+Autoantibodies&rft.au=O%27Connell%2C+Elise%3BRosen%2C+Lindsey+B%3BLaRue%2C+Richard+W%3BFabre%2C+Valeria%3BMelia%2C+Michael+T%3BAuwaerter%2C+Paul+G%3BHolland%2C+Steven+M%3BBrowne%2C+Sarah+K&rft.aulast=O%27Connell&rft.aufirst=Elise&rft.date=2014-11-01&rft.volume=34&rft.issue=8&rft.spage=928&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Immunology&rft.issn=02719142&rft_id=info:doi/10.1007%2Fs10875-014-0073-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Number of references - 25 N1 - Last updated - 2015-03-04 N1 - SubjectsTermNotLitGenreText - Flow cytometry; Etiology; Phosphorylation; Autoantibodies; Stat1 protein; Tumor necrosis factor; Mucosa; Interleukins; Brain; Immunoglobulin G; Blood cells; Infection; Mycobacterium avium DO - http://dx.doi.org/10.1007/s10875-014-0073-9 ER - TY - JOUR T1 - Antigen Reversal Identifies Targets of Opsonizing IgGs against Pregnancy-Associated Malaria AN - 1635034065; 20999613 AB - Clinical immunity to pregnancy associated-malaria (PAM) in multigravida women has been attributed to antibodies that recognize VAR2CSA on the infected erythrocyte (IE) surface. The size and complexity of VAR2CSA have focused efforts on selecting one or more of its six Duffy binding-like (DBL) domains for vaccine development. Presently, however, there is no consensus as to which DBL domain(s) would be most effective in eliciting immunity. This is because antibodies to a number of the DBL domains have been found to block the adhesion of VAR2CSA-expressing erythrocytes to chondroitin sulfate A (CSA)-a major criterion for evaluating vaccine candidacy. Opsonization of IEs by cytophilic antibodies that recognize VAR2CSA represents an important yet understudied effector mechanism in acquired immunity to PAM. To date, no studies have sought to determine the targets of those antibodies. In this study, we found that IgGs from multigravida Malian women showed (i) higher reactivity to recombinant DBL domains by enzyme-linked immunosorbent assay (ELISA), (ii) more binding to VAR2CSA-expressing IEs, and (iii) greater opsonization of these IEs by human monocytic cells than IgGs from malaria-exposed Malian men and malaria-naive American adults. Preincubation of IgGs from multigravida women with recombinant DBL2 chi , DBL3 chi , or DBL5 epsilon domains significantly diminished opsonization of VAR2CSA-expressing IEs by human monocytes. These data identify the DBL2 chi , DBL3 chi , and DBL5 epsilon domains as the primary targets of opsonizing IgGs for the first time. Our study introduces a new approach to determining the antigenic targets of opsonizing IgGs in phagocytosis assays. JF - Infection and Immunity AU - Lambert, Lester H AU - Bullock, Jeanee L AU - Cook, Sharma T AU - Miura, Kazutoyo AU - Garboczi, David N AU - Diakite, Mahamadou AU - Fairhurst, Rick M AU - Singh, Kavita AU - Long, Carole A AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, USA, clong@niaid.nih.gov. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 4842 EP - 4853 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 82 IS - 11 SN - 0019-9567, 0019-9567 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts KW - Enzyme-linked immunosorbent assay KW - Human diseases KW - Chondroitin sulfate KW - Data processing KW - Erythrocytes KW - Disease control KW - Malaria KW - Immunity KW - Adhesion KW - Pregnancy KW - Recombinants KW - Antibodies KW - Antigens KW - Immunoglobulin G KW - Monocytes KW - Vaccines KW - Phagocytosis KW - Opsonization KW - K 03300:Methods KW - Q1 08485:Species interactions: pests and control 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/1635034065?accountid=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=Infection+and+Immunity&rft.atitle=Antigen+Reversal+Identifies+Targets+of+Opsonizing+IgGs+against+Pregnancy-Associated+Malaria&rft.au=Lambert%2C+Lester+H%3BBullock%2C+Jeanee+L%3BCook%2C+Sharma+T%3BMiura%2C+Kazutoyo%3BGarboczi%2C+David+N%3BDiakite%2C+Mahamadou%3BFairhurst%2C+Rick+M%3BSingh%2C+Kavita%3BLong%2C+Carole+A&rft.aulast=Lambert&rft.aufirst=Lester&rft.date=2014-11-01&rft.volume=82&rft.issue=11&rft.spage=4842&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.02097-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Number of references - 62 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Recombinants; Human diseases; Antibodies; Erythrocytes; Disease control; Malaria; Vaccines; Immunity; Adhesion; Enzyme-linked immunosorbent assay; Data processing; Chondroitin sulfate; Pregnancy; Antigens; Immunoglobulin G; Monocytes; Phagocytosis; Opsonization DO - http://dx.doi.org/10.1128/IAI.02097-14 ER - TY - JOUR T1 - Mono-anionic phosphopeptides produced by unexpected histidine alkylation exhibit high plk1 polo-box domain-binding affinities and enhanced antiproliferative effects in hela cells AN - 1635025032; 21033297 AB - Binding of polo-like kinase 1 (Plk1) polo-box domains (PBDs) to phosphothreonine (pThr)/phosphoserine (pSer)-containing sequences is critical for the proper function of Plk1. Although high-affinity synthetic pThr-containing peptides provide starting points for developing PBD-directed inhibitors, to date the efficacy of such peptides in whole cell assays has been poor. This potentially reflects limited cell membrane permeability arising, in part, from the di-anionic nature of the phosphoryl group or its mimetics. In our current article we report the unanticipated on-resin N( tau )-alkylation of histidine residues already bearing a N( pi )- alkyl group. This resulted in cationic imidazolium-containing pThr peptides, several of which exhibit single-digit nanomolar PBD-binding affinities in extracellular assays and improved antimitotic efficacies in intact cells. We enhanced the cellular efficacies of these peptides further by applying bio-reversible pivaloyloxymethyl (POM) phosphoryl protection. New structural insights presented in our current study, including the potential utility of intramolecular charge masking, may be useful for the further development of PBD-binding peptides and peptide mimetics. copyright 2014 Wiley Periodicals, Inc. Biopolymers (Pept Sci) 102: 444-455, 2014. JF - Biopolymers AU - Qian, Wen-Jian AU - Park, Jung-Eun AU - Lim, Dan AU - Lai, Christopher C AU - Kelley, James A AU - Park, Suk-Youl AU - Lee, Ki Won AU - Yaffe, Michael B AU - Lee, Kyung S AU - Burke, Terrence R AD - Chemical Biology Laboratory, Center for Cancer Research, National Institutes of Health, NCI at Frederick, Frederick, MD, 21702. Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 444 EP - 455 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 102 IS - 6 SN - 0006-3525, 0006-3525 KW - Biotechnology and Bioengineering Abstracts KW - Cell membranes KW - Histidine KW - polo-like kinase 1 KW - Biopolymers KW - Membrane permeability KW - phosphoserine KW - Alkylation KW - W 30935:Food Biotechnology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635025032?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biopolymers&rft.atitle=Mono-anionic+phosphopeptides+produced+by+unexpected+histidine+alkylation+exhibit+high+plk1+polo-box+domain-binding+affinities+and+enhanced+antiproliferative+effects+in+hela+cells&rft.au=Qian%2C+Wen-Jian%3BPark%2C+Jung-Eun%3BLim%2C+Dan%3BLai%2C+Christopher+C%3BKelley%2C+James+A%3BPark%2C+Suk-Youl%3BLee%2C+Ki+Won%3BYaffe%2C+Michael+B%3BLee%2C+Kyung+S%3BBurke%2C+Terrence+R&rft.aulast=Qian&rft.aufirst=Wen-Jian&rft.date=2014-11-01&rft.volume=102&rft.issue=6&rft.spage=444&rft.isbn=&rft.btitle=&rft.title=Biopolymers&rft.issn=00063525&rft_id=info:doi/10.1002%2Fbip.22569 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Cell membranes; Histidine; Biopolymers; polo-like kinase 1; Membrane permeability; phosphoserine; Alkylation DO - http://dx.doi.org/10.1002/bip.22569 ER - TY - JOUR T1 - Effect of Suberoylanilide Hydroxamic Acid (SAHA) Administration on the Residual Virus Pool in a Model of Combination Antiretroviral Therapy-Mediated Suppression in SIVmac239-Infected Indian Rhesus Macaques AN - 1635016632; 20999487 AB - Nonhuman primate models are needed for evaluations of proposed strategies targeting residual virus that persists in HIV-1-infected individuals receiving suppressive combination antiretroviral therapy (cART). However, relevant nonhuman primate (NHP) models of cART-mediated suppression have proven challenging to develop. We used a novel three-class, six-drug cART regimen to achieve durable 4.0- to 5.5-log reductions in plasma viremia levels and declines in cell-associated viral RNA and DNA in blood and tissues of simian immunodeficiency virus SIVmac239-infected Indian-origin rhesus macaques, then evaluated the impact of treatment with the histone deacetylase inhibitor (HDACi) suberoylanilide hydroxamic acid (SAHA; Vorinostat) on the residual virus pool. Ex vivo SAHA treatment of CD4+ T cells obtained from cART-suppressed animals increased histone acetylation and viral RNA levels in culture supernatants. cART-suppressed animals each received 84 total doses of oral SAHA. We observed SAHA dose-dependent increases in acetylated histones with evidence for sustained modulation as well as refractoriness following prolonged administration. In vivo virologic activity was demonstrated based on the ratio of viral RNA to viral DNA in peripheral blood mononuclear cells, a presumptive measure of viral transcription, which significantly increased in SAHA-treated animals. However, residual virus was readily detected at the end of treatment, suggesting that SAHA alone may be insufficient for viral eradication in the setting of suppressive cART. The effects observed were similar to emerging data for repeat-dose SAHA treatment of HIV-infected individuals on cART, demonstrating the feasibility, utility, and relevance of NHP models of cART-mediated suppression for in vivo assessments of AIDS virus functional cure/eradication approaches. JF - Antimicrobial Agents & Chemotherapy AU - Del Prete, Gregory Q AU - Shoemaker, Rebecca AU - Oswald, Kelli AU - Lara, Abigail AU - Trubey, Charles M AU - Fast, Randy AU - Schneider, Douglas K AU - Kiser, Rebecca AU - Coalter, Vicky AU - Wiles, Adam AD - AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA, lifsonj@mail.nih.gov. Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 6790 EP - 6806 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 58 IS - 11 SN - 0066-4804, 0066-4804 KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Histone deacetylase KW - Acquired immune deficiency syndrome KW - Data processing KW - antiretroviral therapy KW - Transcription KW - Cell culture KW - Primates KW - Hydroxamic acid KW - Acetylation KW - CD4 antigen KW - Peripheral blood mononuclear cells KW - Antiviral agents KW - RNA KW - Human immunodeficiency virus KW - DNA KW - Lymphocytes T KW - Macaca mulatta KW - Viremia KW - Simian 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/1635016632?accountid=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=Effect+of+Suberoylanilide+Hydroxamic+Acid+%28SAHA%29+Administration+on+the+Residual+Virus+Pool+in+a+Model+of+Combination+Antiretroviral+Therapy-Mediated+Suppression+in+SIVmac239-Infected+Indian+Rhesus+Macaques&rft.au=Del+Prete%2C+Gregory+Q%3BShoemaker%2C+Rebecca%3BOswald%2C+Kelli%3BLara%2C+Abigail%3BTrubey%2C+Charles+M%3BFast%2C+Randy%3BSchneider%2C+Douglas+K%3BKiser%2C+Rebecca%3BCoalter%2C+Vicky%3BWiles%2C+Adam&rft.aulast=Del+Prete&rft.aufirst=Gregory&rft.date=2014-11-01&rft.volume=58&rft.issue=11&rft.spage=6790&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.03746-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Number of references - 78 N1 - Last updated - 2015-03-04 N1 - SubjectsTermNotLitGenreText - Histone deacetylase; Acquired immune deficiency syndrome; Data processing; antiretroviral therapy; Transcription; Cell culture; Hydroxamic acid; Acetylation; Peripheral blood mononuclear cells; CD4 antigen; RNA; Antiviral agents; Lymphocytes T; DNA; Viremia; Human immunodeficiency virus; Macaca mulatta; Primates; Simian immunodeficiency virus DO - http://dx.doi.org/10.1128/AAC.03746-14 ER - TY - JOUR T1 - Respiratory Flexibility in Response to Inhibition of Cytochrome c Oxidase in Mycobacterium tuberculosis AN - 1635016562; 20999456 AB - We report here a series of five chemically diverse scaffolds that have in vitro activities on replicating and hypoxic nonreplicating bacilli by targeting the respiratory bc1 complex in Mycobacterium tuberculosis in a strain-dependent manner. Deletion of the cytochrome bd oxidase generated a hypersusceptible mutant in which resistance was acquired by a mutation in qcrB. These results highlight the promiscuity of the bc1 complex and the risk of targeting energy metabolism with new drugs. JF - Antimicrobial Agents & Chemotherapy AU - Arora, Kriti AU - Ochoa-Montano, Bernardo AU - Tsang, Patricia S AU - Blundell, Tom L AU - Dawes, Stephanie S AU - Mizrahi, Valerie AU - Bayliss, Tracy AU - Mackenzie, Claire J AU - Cleghorn, Laura AT AU - Ray, Peter C AD - Tuberculosis Research Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, USA, hboshoff@niaid.nih.gov. Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 6962 EP - 6965 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 58 IS - 11 SN - 0066-4804, 0066-4804 KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Bacilli KW - Gene deletion KW - Energy metabolism KW - Drug metabolism KW - Hypoxia KW - Cytochrome-c oxidase KW - cytochrome bd KW - Mutation KW - scaffolds KW - Mycobacterium tuberculosis KW - A 01340:Antibiotics & Antimicrobials KW - J 02320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635016562?accountid=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=Respiratory+Flexibility+in+Response+to+Inhibition+of+Cytochrome+c+Oxidase+in+Mycobacterium+tuberculosis&rft.au=Arora%2C+Kriti%3BOchoa-Montano%2C+Bernardo%3BTsang%2C+Patricia+S%3BBlundell%2C+Tom+L%3BDawes%2C+Stephanie+S%3BMizrahi%2C+Valerie%3BBayliss%2C+Tracy%3BMackenzie%2C+Claire+J%3BCleghorn%2C+Laura+AT%3BRay%2C+Peter+C&rft.aulast=Arora&rft.aufirst=Kriti&rft.date=2014-11-01&rft.volume=58&rft.issue=11&rft.spage=6962&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.03486-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Number of references - 19 N1 - Last updated - 2015-03-04 N1 - SubjectsTermNotLitGenreText - Bacilli; Gene deletion; Energy metabolism; Hypoxia; Drug metabolism; cytochrome bd; Cytochrome-c oxidase; Mutation; scaffolds; Mycobacterium tuberculosis DO - http://dx.doi.org/10.1128/AAC.03486-14 ER - TY - JOUR T1 - Structural characterization of the virulence factor nuclease A from Streptococcus agalactiae AN - 1635014773; 20933097 AB - The group B pathogen Streptococcus agalactiae commonly populates the human gut and urogenital tract, and is a major cause of infection-based mortality in neonatal infants and in elderly or immunocompromised adults. Nuclease A (GBS_NucA), a secreted DNA/RNA nuclease, serves as a virulence factor for S. agalactiae, facilitating bacterial evasion of the human innate immune response. GBS_NucA efficiently degrades the DNA matrix component of neutrophil extracellular traps (NETs), which attempt to kill and clear invading bacteria during the early stages of infection. In order to better understand the mechanisms of DNA substrate binding and catalysis of GBS_NucA, the high-resolution structure of a catalytically inactive mutant (H148G) was solved by X-ray crystallography. Several mutants on the surface of GBS_NucA which might influence DNA substrate binding and catalysis were generated and evaluated using an imidazole chemical rescue technique. While several of these mutants severely inhibited nuclease activity, two mutants (K146R and Q183A) exhibited significantly increased activity. These structural and biochemical studies have greatly increased our understanding of the mechanism of action of GBS_NucA in bacterial virulence and may serve as a foundation for the structure-based drug design of antibacterial compounds targeted to S. agalactiae. JF - Acta Crystallographica Section D AU - Moon, Andrea F AU - Gaudu, Philippe AU - Pedersen, Lars C AD - Laboratory of Structural Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA Y1 - 2014/11/01/ PY - 2014 DA - 2014 Nov 01 SP - 2937 EP - 2949 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 70 IS - 11 SN - 1399-0047, 1399-0047 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Mortality KW - imidazole KW - virulence factors KW - Leukocytes (neutrophilic) KW - Nuclease KW - Drug development KW - Pathogens KW - Infection KW - X-ray crystallography KW - Digestive tract KW - RNA KW - Streptococcus agalactiae KW - Geriatrics KW - DNA KW - Immune response KW - Neonates KW - Catalysis KW - Infants KW - N 14830:RNA KW - J 02340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635014773?accountid=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=Structural+characterization+of+the+virulence+factor+nuclease+A+from+Streptococcus+agalactiae&rft.au=Moon%2C+Andrea+F%3BGaudu%2C+Philippe%3BPedersen%2C+Lars+C&rft.aulast=Moon&rft.aufirst=Andrea&rft.date=2014-11-01&rft.volume=70&rft.issue=11&rft.spage=2937&rft.isbn=&rft.btitle=&rft.title=Acta+Crystallographica+Section+D&rft.issn=13990047&rft_id=info:doi/10.1107%2FS1399004714019725 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Document feature - figure 0 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Mortality; imidazole; virulence factors; Leukocytes (neutrophilic); Nuclease; Drug development; Pathogens; Infection; X-ray crystallography; Digestive tract; RNA; DNA; Geriatrics; Neonates; Immune response; Infants; Catalysis; Streptococcus agalactiae DO - http://dx.doi.org/10.1107/S1399004714019725 ER - TY - JOUR T1 - Optimizing dosing of oncology drugs. AN - 1635012184; 25105705 AB - The purpose of this article is to acknowledge the challenges in optimizing the dosing of oncology drugs and to propose potential approaches to address these challenges in order to optimize effectiveness, minimize toxicity, and promote adherence in patients. These approaches could provide better opportunities to understand the sources of variability in drug exposure and clinical outcomes during the development and premarketing evaluation of investigational new drugs. JF - Clinical pharmacology and therapeutics AU - Minasian, L AU - Rosen, O AU - Auclair, D AU - Rahman, A AU - Pazdur, R AU - Schilsky, R L AD - Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland, USA. ; Millennium: The Takeda Oncology Company, Cambridge, Massachusetts, USA. ; Multiple Myeloma Research Foundation, Norwalk, Connecticut, USA. ; Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, Maryland, USA. ; American Society of Clinical Oncology, Alexandria, Virginia, USA. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 572 EP - 579 VL - 96 IS - 5 KW - Antineoplastic Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Medication Adherence KW - Dose-Response Relationship, Drug KW - Humans KW - Time Factors KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635012184?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmacology+and+therapeutics&rft.atitle=Optimizing+dosing+of+oncology+drugs.&rft.au=Minasian%2C+L%3BRosen%2C+O%3BAuclair%2C+D%3BRahman%2C+A%3BPazdur%2C+R%3BSchilsky%2C+R+L&rft.aulast=Minasian&rft.aufirst=L&rft.date=2014-11-01&rft.volume=96&rft.issue=5&rft.spage=572&rft.isbn=&rft.btitle=&rft.title=Clinical+pharmacology+and+therapeutics&rft.issn=1532-6535&rft_id=info:doi/10.1038%2Fclpt.2014.153 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-23 N1 - Date created - 2014-10-22 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/clpt.2014.153 ER - TY - JOUR T1 - A wedge-based approach to estimating health co-benefits of climate change mitigation activities in the United States AN - 1627985248; 20926036 AB - While it has been recognized that actions reducing greenhouse gas (GHG) emissions can have significant positive and negative impacts on human health through reductions in ambient fine particulate matter (PM sub(2.5)) concentrations, these impacts are rarely taken into account when analyzing specific policies. This study presents a new framework for estimating the change in health outcomes resulting from implementation of specific carbon dioxide (CO sub(2)) reduction activities, allowing comparison of different sectors and options for climate mitigation activities. Our estimates suggest that in the year 2020, the reductions in adverse health outcomes from lessened exposure to PM sub(2.5) would yield economic benefits in the range of $6 to $30 billion (in 2008 USD), depending on the specific activity. This equates to between $40 and $198 per metric ton of CO sub(2) in health benefits. Specific climate interventions will vary in the health co-benefits they provide as well as in potential harms that may result from their implementation. Rigorous assessment of these health impacts is essential for guiding policy decisions as efforts to reduce GHG emissions increase in scope and intensity. JF - Climatic Change AU - Balbus, John M AU - Greenblatt, Jeffery B AU - Chari, Ramya AU - Millstein, Dev AU - Ebi, Kristie L AD - National Institute of Environmental Health Sciences, 31 Center Drive, Room B1C02, Bethesda, MD, 20892-2256, USA, john.balbus@nih.gov Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 199 EP - 210 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 127 IS - 2 SN - 0165-0009, 0165-0009 KW - ASFA 3: Aquatic Pollution & Environmental Quality; Health & Safety Science Abstracts; Environment Abstracts; Pollution Abstracts; Sustainability Science Abstracts; Meteorological & Geoastrophysical Abstracts KW - Mitigation KW - Climate change KW - Intervention KW - Particulates KW - Public health KW - Particulate matter in atmosphere KW - Economics KW - Particle size KW - Policies KW - Atmospheric pollution KW - Climate KW - Greenhouse effect KW - Suspended particulate matter KW - USA KW - Particulate matter emissions KW - Greenhouse gases KW - Carbon dioxide KW - Environment management KW - Economic benefits KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - M2 551.583:Variations (551.583) KW - P 0000:AIR POLLUTION KW - M3 1010:Issues in Sustainable Development KW - Q5 08504:Effects on organisms KW - ENA 01:Air Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627985248?accountid=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=Climatic+Change&rft.atitle=A+wedge-based+approach+to+estimating+health+co-benefits+of+climate+change+mitigation+activities+in+the+United+States&rft.au=Balbus%2C+John+M%3BGreenblatt%2C+Jeffery+B%3BChari%2C+Ramya%3BMillstein%2C+Dev%3BEbi%2C+Kristie+L&rft.aulast=Balbus&rft.aufirst=John&rft.date=2014-11-01&rft.volume=127&rft.issue=2&rft.spage=199&rft.isbn=&rft.btitle=&rft.title=Climatic+Change&rft.issn=01650009&rft_id=info:doi/10.1007%2Fs10584-014-1262-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Number of references - 21 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Policies; Climate change; Greenhouse effect; Suspended particulate matter; Carbon dioxide; Environment management; Economic benefits; Public health; Particulate matter in atmosphere; Atmospheric pollution; Particulate matter emissions; Greenhouse gases; Particle size; Mitigation; Climate; Economics; Intervention; Particulates; USA DO - http://dx.doi.org/10.1007/s10584-014-1262-5 ER - TY - JOUR T1 - Gcn5 and PCAF negatively regulate interferon-β production through HAT-independent inhibition of TBK1. AN - 1622060911; 25269644 AB - Viral infection triggers innate immune signaling, which in turn induces interferon-β (IFN-β) production to establish innate antiviral immunity. Previous studies showed that Gcn5 (Kat2a), a histone acetyltransferase (HAT) with partial functional redundancy with PCAF (Kat2b), and Gcn5/PCAF-mediated histone H3K9 acetylation (H3K9ac) are enriched on the active IFNB gene promoter. However, whether Gcn5/PCAF and H3K9ac regulate IFN-β production is unknown. Here, we show that Gcn5/PCAF-mediated H3K9ac correlates well with, but is surprisingly dispensable for, the expression of endogenous IFNB and the vast majority of active genes in fibroblasts. Instead, Gcn5/PCAF repress IFN-β production and innate antiviral immunity in several cell types in a HAT-independent and non-transcriptional manner: by inhibiting the innate immune signaling kinase TBK1 in the cytoplasm. Our results thus identify Gcn5 and PCAF as negative regulators of IFN-β production and innate immune signaling. © 2014 The Authors. JF - EMBO reports AU - Jin, Qihuang AU - Zhuang, Lenan AU - Lai, Binbin AU - Wang, Chaochen AU - Li, Wenqian AU - Dolan, Brian AU - Lu, Yue AU - Wang, Zhibin AU - Zhao, Keji AU - Peng, Weiqun AU - Dent, Sharon Y R AU - Ge, Kai AD - Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA Department of Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA. ; Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA. ; Department of Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA. ; Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD, USA. ; Systems Biology Center, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD, USA. ; Department of Physics, The George Washington University, Washington, DC, USA. ; Department of Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas MD Anderson Cancer Center, Smithville, TX, USA sroth@mdanderson.org kaig@niddk.nih.gov. ; Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA sroth@mdanderson.org kaig@niddk.nih.gov. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 1192 EP - 1201 VL - 15 IS - 11 KW - Histones KW - 0 KW - Interferon-beta KW - 77238-31-4 KW - p300-CBP Transcription Factors KW - EC 2.3.1.48 KW - p300-CBP-associated factor KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - TBK1 protein, human KW - Index Medicus KW - H3K9ac KW - TBK1 KW - interferon‐β KW - Gcn5/PCAF KW - innate immune signaling KW - Fibroblasts -- immunology KW - Acetylation KW - Humans KW - Histones -- metabolism KW - HEK293 Cells KW - Immunity, Innate KW - Protein Binding KW - Fibroblasts -- metabolism KW - Protein-Serine-Threonine Kinases -- metabolism KW - Interferon-beta -- metabolism KW - p300-CBP Transcription Factors -- metabolism KW - p300-CBP Transcription Factors -- genetics KW - Protein-Serine-Threonine Kinases -- genetics KW - Interferon-beta -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622060911?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=EMBO+reports&rft.atitle=Gcn5+and+PCAF+negatively+regulate+interferon-%CE%B2+production+through+HAT-independent+inhibition+of+TBK1.&rft.au=Jin%2C+Qihuang%3BZhuang%2C+Lenan%3BLai%2C+Binbin%3BWang%2C+Chaochen%3BLi%2C+Wenqian%3BDolan%2C+Brian%3BLu%2C+Yue%3BWang%2C+Zhibin%3BZhao%2C+Keji%3BPeng%2C+Weiqun%3BDent%2C+Sharon+Y+R%3BGe%2C+Kai&rft.aulast=Jin&rft.aufirst=Qihuang&rft.date=2014-11-01&rft.volume=15&rft.issue=11&rft.spage=1192&rft.isbn=&rft.btitle=&rft.title=EMBO+reports&rft.issn=1469-3178&rft_id=info:doi/10.15252%2Fembr.201438990 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-08 N1 - Date created - 2014-11-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2002 Apr 19;277(16):13840-7 [11839743] Elife. 2013;2:e01503 [24368734] Nucleic Acids Res. 2003 Aug 1;31(15):4285-92 [12888487] J Virol. 2004 Oct;78(19):10636-49 [15367631] Proc Natl Acad Sci U S A. 1981 Dec;78(12):7426-30 [6174973] Mol Cell Biol. 1998 May;18(5):2986-96 [9566918] Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9319-24 [9689078] Immunity. 2006 Sep;25(3):349-60 [16979567] Immunity. 2006 Sep;25(3):383-92 [16979570] Mol Cell Biol. 2007 May;27(9):3405-16 [17325035] J Biol Chem. 2007 May 25;282(21):15325-9 [17395583] Oncogene. 2007 Aug 13;26(37):5341-57 [17694077] Nat Genet. 2008 Jul;40(7):897-903 [18552846] Genes Dev. 2009 Apr 1;23(7):849-61 [19339690] J Biol Chem. 2009 May 22;284(21):14136-46 [19307177] Bioinformatics. 2009 Aug 1;25(15):1952-8 [19505939] Mol Cell. 2009 Aug 14;35(3):352-64 [19683498] Cell. 2010 Feb 5;140(3):436-436.e2 [20144765] Cell. 2010 Aug 6;142(3):480-93 [20691906] Immunity. 2010 Dec 14;33(6):878-89 [21145761] EMBO J. 2011 Jan 19;30(2):249-62 [21131905] Mol Cell. 2011 Feb 18;41(4):458-70 [21329883] Cell. 2012 Oct 26;151(3):476-82 [23101621] Cell. 2002 Nov 1;111(3):381-92 [12419248] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.15252/embr.201438990 ER - TY - JOUR T1 - Safety of in utero and neonatal antiretroviral exposure: cognitive and academic outcomes in HIV-exposed, uninfected children 5-13 years of age. AN - 1619318519; 25361407 AB - Long-term effects of in utero and neonatal antiretroviral (ARV) exposure on cognitive and academic development in HIV-exposed, uninfected school-age children are unknown. HIV-exposed, uninfected children, ages 5-13 years, in Pediatric HIV/AIDS Cohort Study Surveillance Monitoring for Antiretroviral Treatment Toxicities, a US-based multisite cohort study, completed age-appropriate Wechsler intelligence and academic scales (WPPSI-III, WASI, WIAT-II-A). Associations between cognitive and academic outcomes and in utero ARV exposure by regimen, class and individual ARVs were evaluated, adjusting for potential confounders. Children completing WPPSI-IIIs (n = 350) were 49% male, 74% Black, 25% Hispanic; WASI (n = 337) and WIAT-II-A (n = 415) cohorts were similar. The percentage exposed to combination ARV (cARV) was 84% (WPPSI-III), 64% (WASI) and 67% (WIAT-II-A). Among ARV-exposed children, there were no significant associations between any ARV regimen or class and any cognitive or academic outcome. In addition, in both unadjusted models and after adjustment for caregiver IQ, sociodemographic factors and maternal health and substance use during pregnancy, no individual ARV drug was associated with significantly lower cognitive or academic scores. Factors typically associated with lower cognitive and academic scores in the general population, such as prematurity, small for gestational age, maternal alcohol use and lower maternal cognitive status, were also associated with lower scores in this study. Overall, the safety of prenatal and neonatal ARV use was supported. JF - The Pediatric infectious disease journal AU - Nozyce, Molly L AU - Huo, Yanling AU - Williams, Paige L AU - Kapetanovic, Suad AU - Hazra, Rohan AU - Nichols, Sharon AU - Hunter, Scott AU - Smith, Renee AU - Seage, George R AU - Sirois, Patricia A AU - Pediatric HIVAIDS Cohort Study AD - From the *Jacobi Medical Center, Albert Einstein College of Medicine, New York, NY; †Harvard School of Public Health, Boston, MA; ‡National Institute of Mental Health, Bethesda; §Eunice Kennedy Shriver National Institute of Child Health and Human Development, Rockville, MD; ¶University of California, San Diego, CA; ‖University of Chicago; **University of Illinois, Chicago, IL; ††Tulane University School of Medicine, New Orleans, LA. ; Pediatric HIVAIDS Cohort Study Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 1128 EP - 1133 VL - 33 IS - 11 KW - Anti-Retroviral Agents KW - 0 KW - Index Medicus KW - Wechsler Scales KW - Drug Therapy, Combination KW - Educational Status KW - Humans KW - Infant, Newborn KW - Child Development KW - Child KW - Adolescent KW - Male KW - Female KW - Pregnancy KW - Child, Preschool KW - Infectious Disease Transmission, Vertical -- prevention & control KW - Intelligence -- drug effects KW - HIV Infections -- transmission KW - HIV Infections -- drug therapy KW - Anti-Retroviral Agents -- adverse effects KW - Pregnancy Complications, Infectious -- drug therapy KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619318519?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Pediatric+infectious+disease+journal&rft.atitle=Safety+of+in+utero+and+neonatal+antiretroviral+exposure%3A+cognitive+and+academic+outcomes+in+HIV-exposed%2C+uninfected+children+5-13+years+of+age.&rft.au=Nozyce%2C+Molly+L%3BHuo%2C+Yanling%3BWilliams%2C+Paige+L%3BKapetanovic%2C+Suad%3BHazra%2C+Rohan%3BNichols%2C+Sharon%3BHunter%2C+Scott%3BSmith%2C+Renee%3BSeage%2C+George+R%3BSirois%2C+Patricia+A%3BPediatric+HIVAIDS+Cohort+Study&rft.aulast=Nozyce&rft.aufirst=Molly&rft.date=2014-11-01&rft.volume=33&rft.issue=11&rft.spage=1128&rft.isbn=&rft.btitle=&rft.title=The+Pediatric+infectious+disease+journal&rft.issn=1532-0987&rft_id=info:doi/10.1097%2FINF.0000000000000410 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-28 N1 - Date created - 2014-11-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Neurosci Lett. 2002 Nov 22;333(2):111-4 [12419493] AIDS. 2002 Jan 25;16(2):299-300 [11807320] Annu Rev Psychol. 2002;53:371-99 [11752490] Am J Epidemiol. 2001 Oct 15;154(8):711-7 [11590083] Pediatr Infect Dis J. 2013 Oct;32(10):e406-13 [24067563] J Pediatr. 2013 Aug;163(2):447-53 [23453550] Pediatr Infect Dis J. 2013 Jun;32(6):648-55 [23340561] Pediatrics. 2012 Nov;130(5):e1326-44 [23118140] Pediatr Infect Dis J. 2012 Jun;31(6):592-8 [22592486] AIDS Patient Care STDS. 2011 Jul;25(7):385-94 [21992592] J Acquir Immune Defic Syndr. 2011 Aug 1;57(4):290-6 [21602695] J Acquir Immune Defic Syndr. 2011 Jul 1;57(3):218-22 [21372725] Lancet. 1999 Sep 25;354(9184):1084-9 [10509500] Neurotoxicol Teratol. 2005 Jan-Feb;27(1):169-73 [15681130] Environ Health Perspect. 2005 Jul;113(7):894-9 [16002379] Pediatrics. 2006 Oct;118(4):e1139-45 [16940166] Pediatrics. 2007 Mar;119(3):e681-93 [17296781] Drug Saf. 2007;30(3):203-13 [17343429] AIDS. 2007 May 11;21(8):929-38 [17457086] Toxicol Sci. 2007 Sep;99(1):203-13 [17545213] Curr Opin Pediatr. 2008 Apr;20(2):172-7 [18332714] AIDS. 2008 Nov 12;22(17):2359-69 [18981776] AIDS Patient Care STDS. 2009 Jun;23(6):415-21 [19415986] Curr HIV Res. 2009 Nov;7(6):620-5 [19929798] Pediatrics. 2010 Feb;125(2):e250-60 [20083530] Toxicol Sci. 2010 Nov;118(1):191-201 [20702595] Am Psychol. 1998 Feb;53(2):185-204 [9491747] JAMA. 1999 Jan 13;281(2):151-7 [9917118] J Infect Dis. 2011 Aug 15;204(4):506-14 [21791651] Future Child. 1997 Summer-Fall;7(2):55-71 [9299837] Toxicol Appl Pharmacol. 2004 Sep 1;199(2):151-61 [15313587] AIDS Res Hum Retroviruses. 2004 Jan;20(1):91-100 [15000702] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/INF.0000000000000410 ER - TY - JOUR T1 - Preclinical activity of the liposomal cisplatin lipoplatin in ovarian cancer. AN - 1619318046; 25231401 AB - Cisplatin and its platinum derivatives are first-line chemotherapeutic agents in the treatment of ovarian cancer; however, treatment is associated with tumor resistance and significant toxicity. Here we investigated the antitumoral activity of lipoplatin, one of the most promising liposomal platinum drug formulations under clinical investigation. In vitro effects of lipoplatin were tested on a panel of ovarian cancer cell lines, sensitive and resistant to cisplatin, using both two-dimensional (2D) and 3D cell models. We evaluated in vivo the lipoplatin anticancer activity using tumor xenografts. Lipoplatin exhibited a potent antitumoral activity in all ovarian cancer cell lines tested, induced apoptosis, and activated caspase-9, -8, and -3, downregulating Bcl-2 and upregulating Bax. Lipoplatin inhibited thioredoxin reductase enzymatic activity and increased reactive oxygen species accumulation and reduced EGF receptor (EGFR) expression and inhibited cell invasion. Lipoplatin demonstrated a synergistic effect when used in combination with doxorubicin, widely used in relapsed ovarian cancer treatment, and with the albumin-bound paclitaxel, Abraxane. Lipoplatin decreased both ALDH and CD133 expression, markers of ovarian cancer stem cells. Multicellular aggregates/spheroids are present in ascites of patients and most contribute to the spreading to secondary sites. Lipoplatin decreased spheroids growth, vitality, and cell migration out of preformed spheroids. Finally, lipoplatin inhibited more than 90% tumor xenograft growth with minimal systemic toxicity, and after the treatment suspension, no tumor progression was observed. These preclinical data suggest that lipoplatin has potential for clinical assessment in aggressive cisplatin-resistant patients with ovarian cancer. ©2014 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Casagrande, Naike AU - Celegato, Marta AU - Borghese, Cinzia AU - Mongiat, Maurizio AU - Colombatti, Alfonso AU - Aldinucci, Donatella AD - Experimental Oncology 2, CRO Aviano National Cancer Institute, Aviano, Italy. ; Experimental Oncology 2, CRO Aviano National Cancer Institute, Aviano, Italy. Department of Medical and Biological Science Technology and MATI (Microgravity Ageing Training Immobility) Excellence Center, University of Udine, Udine, Italy. ; Experimental Oncology 2, CRO Aviano National Cancer Institute, Aviano, Italy. daldinucci@cro.it. Y1 - 2014/11/01/ PY - 2014 DA - 2014 Nov 01 SP - 5496 EP - 5506 VL - 20 IS - 21 SN - 1078-0432, 1078-0432 KW - AC133 Antigen KW - 0 KW - Albumin-Bound Paclitaxel KW - Albumins KW - Antigens, CD KW - Antineoplastic Agents KW - Glycoproteins KW - Liposomes KW - PROM1 protein, human KW - Peptides KW - Proto-Oncogene Proteins c-bcl-2 KW - Reactive Oxygen Species KW - bcl-2-Associated X Protein KW - lipoplatin KW - Doxorubicin KW - 80168379AG KW - EGFR protein, human KW - EC 2.7.10.1 KW - Receptor, Epidermal Growth Factor KW - Caspases KW - EC 3.4.22.- KW - Paclitaxel KW - P88XT4IS4D KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Spheroids, Cellular -- metabolism KW - Reactive Oxygen Species -- metabolism KW - Humans KW - Antigens, CD -- genetics KW - Paclitaxel -- pharmacology KW - Caspases -- genetics KW - Neoplasm Invasiveness -- genetics KW - Caspases -- metabolism KW - bcl-2-Associated X Protein -- genetics KW - Doxorubicin -- pharmacology KW - Spheroids, Cellular -- drug effects KW - Drug Resistance, Neoplasm -- genetics KW - Up-Regulation -- drug effects KW - Cell Movement -- drug effects KW - Down-Regulation -- drug effects KW - Receptor, Epidermal Growth Factor -- metabolism KW - Albumins -- pharmacology KW - Peptides -- metabolism KW - Up-Regulation -- genetics KW - Cell Line, Tumor KW - Cell Movement -- genetics KW - Glycoproteins -- genetics KW - bcl-2-Associated X Protein -- metabolism KW - Receptor, Epidermal Growth Factor -- genetics KW - Down-Regulation -- genetics KW - Glycoproteins -- metabolism KW - Proto-Oncogene Proteins c-bcl-2 -- metabolism KW - Antigens, CD -- metabolism KW - Peptides -- genetics KW - Proto-Oncogene Proteins c-bcl-2 -- genetics KW - Antineoplastic Agents -- pharmacology KW - Female KW - Drug Resistance, Neoplasm -- drug effects KW - Ovarian Neoplasms -- metabolism KW - Ovarian Neoplasms -- genetics KW - Cisplatin -- pharmacology KW - Liposomes -- pharmacology KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619318046?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preclinical+activity+of+the+liposomal+cisplatin+lipoplatin+in+ovarian+cancer.&rft.au=Casagrande%2C+Naike%3BCelegato%2C+Marta%3BBorghese%2C+Cinzia%3BMongiat%2C+Maurizio%3BColombatti%2C+Alfonso%3BAldinucci%2C+Donatella&rft.aulast=Casagrande&rft.aufirst=Naike&rft.date=2014-11-01&rft.volume=20&rft.issue=21&rft.spage=5496&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-0713 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-01 N1 - Date created - 2014-11-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-0713 ER - TY - JOUR T1 - RECQ helicase RECQL4 participates in non-homologous end joining and interacts with the Ku complex. AN - 1619317860; 24942867 AB - RECQL4, a member of the RecQ helicase family, is a multifunctional participant in DNA metabolism. RECQL4 protein participates in several functions both in the nucleus and in the cytoplasm of the cell, and mutations in human RECQL4 are associated with three genetic disorders: Rothmund-Thomson, RAPADILINO and Baller-Gerold syndromes. We previously reported that RECQL4 is recruited to laser-induced DNA double-strand breaks (DSB). Here, we have characterized the functional roles of RECQL4 in the non-homologous end joining (NHEJ) pathway of DSB repair. In an in vitro NHEJ assay that depends on the activity of DNA-dependent protein kinase (DNA-PK), extracts from RECQL4 knockdown cells display reduced end-joining activity on DNA substrates with cohesive and non-cohesive ends. Depletion of RECQL4 also reduced the end joining activity on a GFP reporter plasmid in vivo. Knockdown of RECQL4 increased the sensitivity of cells to γ-irradiation and resulted in accumulation of 53BP1 foci after irradiation, indicating defects in the processing of DSB. We find that RECQL4 interacts with the Ku70/Ku80 heterodimer, part of the DNA-PK complex, via its N-terminal domain. Further, RECQL4 stimulates higher order DNA binding of Ku70/Ku80 to a blunt end DNA substrate. Taken together, these results implicate that RECQL4 participates in the NHEJ pathway of DSB repair via a functional interaction with the Ku70/Ku80 complex. This is the first study to provide both in vitro and in vivo evidence for a role of a RecQ helicase in NHEJ. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Shamanna, Raghavendra A AU - Singh, Dharmendra Kumar AU - Lu, Huiming AU - Mirey, Gladys AU - Keijzers, Guido AU - Salles, Bernard AU - Croteau, Deborah L AU - Bohr, Vilhelm A AD - Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, NIH, 251 Bayview Boulevard, Baltimore, MD 21224, USA, INRA, Université de Toulouse, UMR1331, Toxalim, Research Centre in Food Toxicology, F-31027 Toulouse, France and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, 2200 Copenhagen, Denmark. ; INRA, Université de Toulouse, UMR1331, Toxalim, Research Centre in Food Toxicology, F-31027 Toulouse, France and. ; Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, 2200 Copenhagen, Denmark. ; Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, NIH, 251 Bayview Boulevard, Baltimore, MD 21224, USA, INRA, Université de Toulouse, UMR1331, Toxalim, Research Centre in Food Toxicology, F-31027 Toulouse, France and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, 2200 Copenhagen, Denmark vbohr@nih.gov. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 2415 EP - 2424 VL - 35 IS - 11 KW - Antigens, Nuclear KW - 0 KW - DNA-Binding Proteins KW - Intracellular Signaling Peptides and Proteins KW - TP53BP1 protein, human KW - Tumor Suppressor p53-Binding Protein 1 KW - DNA-Activated Protein Kinase KW - EC 2.7.11.1 KW - RECQL4 protein, human KW - EC 3.6.1.- KW - RecQ Helicases KW - EC 3.6.4.12 KW - Xrcc6 protein, human KW - Ku Autoantigen KW - EC 4.2.99.- KW - Index Medicus KW - Intracellular Signaling Peptides and Proteins -- genetics KW - DNA-Activated Protein Kinase -- genetics KW - Gene Knockdown Techniques KW - Gamma Rays KW - HeLa Cells KW - Humans KW - DNA Breaks, Double-Stranded -- radiation effects KW - Radiation Tolerance -- genetics KW - Rothmund-Thomson Syndrome -- genetics KW - DNA-Binding Proteins -- genetics KW - RecQ Helicases -- genetics KW - DNA End-Joining Repair -- genetics KW - Antigens, Nuclear -- genetics KW - RecQ Helicases -- antagonists & inhibitors KW - Rothmund-Thomson Syndrome -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619317860?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=RECQ+helicase+RECQL4+participates+in+non-homologous+end+joining+and+interacts+with+the+Ku+complex.&rft.au=Shamanna%2C+Raghavendra+A%3BSingh%2C+Dharmendra+Kumar%3BLu%2C+Huiming%3BMirey%2C+Gladys%3BKeijzers%2C+Guido%3BSalles%2C+Bernard%3BCroteau%2C+Deborah+L%3BBohr%2C+Vilhelm+A&rft.aulast=Shamanna&rft.aufirst=Raghavendra&rft.date=2014-11-01&rft.volume=35&rft.issue=11&rft.spage=2415&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu137 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-13 N1 - Date created - 2014-11-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: DNA Repair (Amst). 2010 Dec 10;9(12):1307-14 [21030321] Nat Struct Mol Biol. 2006 May;13(5):414-22 [16622405] Front Biosci (Landmark Ed). 2012;17:1362-88 [22201809] DNA Repair (Amst). 2012 Jul 1;11(7):624-35 [22633600] Nucleic Acids Res. 2012 Jul;40(13):5795-818 [22467216] Mutat Res. 2012 Aug 1;736(1-2):15-24 [21689668] Nucleic Acids Res. 2012 Aug;40(14):6632-48 [22544709] Biochim Biophys Acta. 2012 Nov;1822(11):1727-34 [22885111] Trends Genet. 2012 Dec;28(12):624-31 [22940096] Adv Exp Med Biol. 2013;767:161-84 [23161011] Aging (Albany NY). 2012 Nov;4(11):790-802 [23238538] Biophys Chem. 2013 Jul-Aug;177-178:34-9 [23624328] PLoS One. 2013;8(5):e62481 [23650516] Nat Rev Cancer. 2013 Jul;13(7):443-54 [23760025] PLoS One. 2013;8(7):e69607 [23874974] Oncogene. 2013 Sep 26;32(39):4593-601 [23318447] Oncologist. 2013;18(10):1063-73 [24072219] Carcinogenesis. 2014 Jan;35(1):34-45 [24067899] Nature. 2000 Mar 30;404(6777):510-4 [10761921] Genes Dev. 2000 Apr 15;14(8):907-12 [10783163] J Biol Chem. 2000 Sep 15;275(37):28349-52 [10880505] J Cell Biol. 2000 Dec 25;151(7):1381-90 [11134068] J Biol Chem. 2001 Mar 30;276(13):9896-902 [11152456] J Biol Chem. 2002 May 24;277(21):18291-302 [11889123] Nucleic Acids Res. 2002 Aug 15;30(16):3583-91 [12177300] Nucleic Acids Res. 2001 May 1;29(9):1926-34 [11328876] Nucleic Acids Res. 2003 Sep 15;31(18):5377-88 [12954774] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7624-9 [15123826] Proc Natl Acad Sci U S A. 1992 Aug 1;89(15):6958-62 [1495986] J Biol Chem. 1998 Jan 9;273(2):842-8 [9422740] Genomics. 1998 Dec 15;54(3):443-52 [9878247] J Biol Chem. 2005 Jun 17;280(24):23397-407 [15845538] J Cell Sci. 2005 Sep 15;118(Pt 18):4261-9 [16141230] J Cell Sci. 2005 Sep 15;118(Pt 18):4153-62 [16141234] Cancer Lett. 2006 Jan 28;232(1):107-20 [16271439] DNA Repair (Amst). 2006 Feb 3;5(2):172-80 [16214424] Cell. 2006 Jan 27;124(2):287-99 [16439204] Biochem Biophys Res Commun. 2006 Sep 15;348(1):62-9 [16876111] Biochim Biophys Acta. 2007 Apr;1773(4):556-64 [17320201] Cell Cycle. 2008 May 15;7(10):1321-5 [18418068] Biochemistry. 2008 Jul 15;47(28):7548-56 [18558713] Trends Biochem Sci. 2008 Dec;33(12):609-20 [18926708] Eur J Hum Genet. 2009 Feb;17(2):151-8 [18716613] Int J Biochem Cell Biol. 2009 Jun;41(6):1254-60 [19110069] Neoplasia. 2009 Mar;11(3):260-8, 3p following 268 [19242607] EMBO J. 2009 Mar 4;28(5):568-77 [19177149] Biogerontology. 2009 Jun;10(3):235-52 [19083132] Hum Mol Genet. 2009 Sep 15;18(18):3470-83 [19567405] Nat Rev Cancer. 2009 Sep;9(9):644-54 [19657341] Nature. 2009 Oct 22;461(7267):1071-8 [19847258] Nat Rev Mol Cell Biol. 2010 Mar;11(3):196-207 [20177395] Am J Med Genet A. 2010 Jun;152A(6):1575-9 [20503338] Annu Rev Biochem. 2010;79:181-211 [20192759] DNA Repair (Amst). 2010 Jul 1;9(7):796-804 [20451470] Aging Cell. 2010 Jun;9(3):358-71 [20222902] Annu Rev Genet. 2010;44:393-417 [21047263] Cancer Res. 2010 Nov 15;70(22):9207-17 [21045146] Mol Cell Biol. 2011 Dec;31(23):4832-43 [21969602] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu137 ER - TY - JOUR T1 - Definition of smad3 phosphorylation events that affect malignant and metastatic behaviors in breast cancer cells. AN - 1619317779; 25205100 AB - Smad3, a major intracellular mediator of TGFβ signaling, functions as both a positive and negative regulator in carcinogenesis. In response to TGFβ, the TGFβ receptor phosphorylates serine residues at the Smad3 C-tail. Cancer cells often contain high levels of the MAPK and CDK activities, which can lead to the Smad3 linker region becoming highly phosphorylated. Here, we report, for the first time, that mutation of the Smad3 linker phosphorylation sites markedly inhibited primary tumor growth, but significantly increased lung metastasis of breast cancer cell lines. In contrast, mutation of the Smad3 C-tail phosphorylation sites had the opposite effect. We show that mutation of the Smad3 linker phosphorylation sites greatly intensifies all TGFβ-induced responses, including growth arrest, apoptosis, reduction in the size of putative cancer stem cell population, epithelial-mesenchymal transition, and invasive activity. Moreover, all TGFβ responses were completely lost on mutation of the Smad3 C-tail phosphorylation sites. Our results demonstrate a critical role of the counterbalance between the Smad3 C-tail and linker phosphorylation in tumorigenesis and metastasis. Our findings have important implications for therapeutic intervention of breast cancer. ©2014 American Association for Cancer Research. JF - Cancer research AU - Bae, Eunjin AU - Sato, Misako AU - Kim, Ran-Ju AU - Kwak, Mi-Kyung AU - Naka, Kazuhito AU - Gim, Jungsoo AU - Kadota, Mitsutaka AU - Tang, Binwu AU - Flanders, Kathleen C AU - Kim, Tae-Aug AU - Leem, Sun-Hee AU - Park, Taesung AU - Liu, Fang AU - Wakefield, Lalage M AU - Kim, Seong-Jin AU - Ooshima, Akira AD - CHA Cancer Research Institute, CHA University, Seoul, Korea. ; Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, Maryland. ; Cancer Research Institute, Kanazawa University, Kanazawa, Ishikawa, Japan. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul, Korea. ; Genome Resource and Analysis Unit, RIKEN Center for Developmental Biology, Kobe, Japan. ; Department of Biology and Biomedical Science, Dong-A University, Busan, Korea. ; Interdisciplinary Program in Bioinformatics, Seoul National University, Seoul, Korea. Department of Statistics, Seoul National University, Seoul, Korea. ; Center for Advanced Biotechnology and Medicine, Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, Piscataway, New Jersey. ; CHA Cancer Research Institute, CHA University, Seoul, Korea. aooshima@cha.ac.kr kimsj@cha.ac.kr. ; CHA Cancer Research Institute, CHA University, Seoul, Korea. Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, Maryland. aooshima@cha.ac.kr kimsj@cha.ac.kr. Y1 - 2014/11/01/ PY - 2014 DA - 2014 Nov 01 SP - 6139 EP - 6149 VL - 74 IS - 21 KW - Receptors, Transforming Growth Factor beta KW - 0 KW - SMAD3 protein, human KW - Smad3 Protein KW - Transforming Growth Factor beta KW - Index Medicus KW - Receptors, Transforming Growth Factor beta -- genetics KW - Humans KW - Receptors, Transforming Growth Factor beta -- metabolism KW - Cell Line, Tumor KW - Gene Expression Regulation, Neoplastic KW - Neoplasm Metastasis -- genetics KW - Phosphorylation -- genetics KW - Signal Transduction -- genetics KW - Xenograft Model Antitumor Assays KW - Neoplasm Metastasis -- pathology KW - Transforming Growth Factor beta -- genetics KW - Transforming Growth Factor beta -- metabolism KW - Mutation KW - Female KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- pathology KW - Smad3 Protein -- metabolism KW - Epithelial-Mesenchymal Transition -- genetics KW - Cell Transformation, Neoplastic -- genetics KW - Smad3 Protein -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619317779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Definition+of+smad3+phosphorylation+events+that+affect+malignant+and+metastatic+behaviors+in+breast+cancer+cells.&rft.au=Bae%2C+Eunjin%3BSato%2C+Misako%3BKim%2C+Ran-Ju%3BKwak%2C+Mi-Kyung%3BNaka%2C+Kazuhito%3BGim%2C+Jungsoo%3BKadota%2C+Mitsutaka%3BTang%2C+Binwu%3BFlanders%2C+Kathleen+C%3BKim%2C+Tae-Aug%3BLeem%2C+Sun-Hee%3BPark%2C+Taesung%3BLiu%2C+Fang%3BWakefield%2C+Lalage+M%3BKim%2C+Seong-Jin%3BOoshima%2C+Akira&rft.aulast=Bae&rft.aufirst=Eunjin&rft.date=2014-11-01&rft.volume=74&rft.issue=21&rft.spage=6139&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-0803 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-05 N1 - Date created - 2014-11-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0803 ER - TY - JOUR T1 - Inhibition of NANOG/NANOGP8 downregulates MCL-1 in colorectal cancer cells and enhances the therapeutic efficacy of BH3 mimetics. AN - 1619317717; 25208882 AB - High levels of BCL-2 family members in colorectal carcinoma cause resistance to treatment. Inhibition of NANOG or its paralog NANOGP8 reduces the proliferation, stemness, and tumorigenicity of colorectal carcinoma cells. Our hypothesis was that inhibition of NANOG/NANOGP8 enhances the cytotoxic effect of BH3 mimetics targeting BCL-2 family members in colorectal carcinoma cells through reducing expression of MCL-1, a prosurvival BCL-2 protein. Lentiviral vector (LV) shRNA to NANOG (shNG-1) or NANOGP8 (shNp8-1) transduced colorectal carcinoma cells that were also exposed to the BH3 mimetics ABT-737 or ABT-199 in vivo in colorectal carcinoma xenografts and in vitro where proliferation, protein and gene expression, and apoptosis were measured. Clone A and CX-1 were sensitive to ABT-737 and ABT-199 at IC50s of 2 to 9 μmol/L but LS174T was resistant with IC50s of 18 to 30 μmol/L. Resistance was associated with high MCL-1 expression in LS174T. LVshNG-1 or LVshNp8-1 decreased MCL-1 expression, increased apoptosis, and decreased replating efficiency in colorectal carcinoma cells treated with either ABT-737 or ABT-199 compared with the effects of either BH3 mimetic alone. Inhibition or overexpression of MCL-1 alone replicated the effects of LVshNG-1 or LVshNp8-1 in increasing or decreasing the apoptosis caused with the BH3 mimetic. The combination therapy inhibited the growth of LS174T xenografts in vivo compared with untreated controls or treatment with only LV shRNA or ABT-737. Inhibition of NANOGP8 or NANOG enhances the cytotoxicity of BH3 mimetics that target BCL-2 family members. Gene therapy targeting the NANOGs may increase the efficacy of BH3 mimetics in colorectal carcinoma. ©2014 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Mattoo, Abid R AU - Zhang, Jingyu AU - Espinoza, Luis A AU - Jessup, J Milburn AD - Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Cancer Diagnosis Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, Maryland. jessupj@mail.nih.gov. Y1 - 2014/11/01/ PY - 2014 DA - 2014 Nov 01 SP - 5446 EP - 5455 VL - 20 IS - 21 SN - 1078-0432, 1078-0432 KW - ABT-737 KW - 0 KW - BH3 Interacting Domain Death Agonist Protein KW - Biphenyl Compounds KW - Bridged Bicyclo Compounds, Heterocyclic KW - Homeodomain Proteins KW - MCL1 protein, human KW - Myeloid Cell Leukemia Sequence 1 Protein KW - NANOG protein, human KW - Nanog Homeobox Protein KW - Nitrophenols KW - Piperazines KW - RNA, Small Interfering KW - Sulfonamides KW - venetoclax KW - N54AIC43PW KW - Index Medicus KW - Animals KW - Nitrophenols -- pharmacology KW - Mice, Inbred NOD KW - HEK293 Cells KW - Humans KW - Biphenyl Compounds -- pharmacology KW - RNA, Small Interfering -- genetics KW - Cell Line, Tumor KW - Mice KW - Piperazines -- pharmacology KW - Apoptosis -- genetics KW - Bridged Bicyclo Compounds, Heterocyclic -- pharmacology KW - Sulfonamides -- pharmacology KW - Apoptosis -- drug effects KW - Xenograft Model Antitumor Assays KW - HT29 Cells KW - Mice, SCID KW - Cell Line KW - Male KW - BH3 Interacting Domain Death Agonist Protein -- genetics KW - Down-Regulation -- genetics KW - Homeodomain Proteins -- antagonists & inhibitors KW - Myeloid Cell Leukemia Sequence 1 Protein -- genetics KW - Colorectal Neoplasms -- genetics KW - Down-Regulation -- drug effects KW - Colorectal Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619317717?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+NANOG%2FNANOGP8+downregulates+MCL-1+in+colorectal+cancer+cells+and+enhances+the+therapeutic+efficacy+of+BH3+mimetics.&rft.au=Mattoo%2C+Abid+R%3BZhang%2C+Jingyu%3BEspinoza%2C+Luis+A%3BJessup%2C+J+Milburn&rft.aulast=Mattoo&rft.aufirst=Abid&rft.date=2014-11-01&rft.volume=20&rft.issue=21&rft.spage=5446&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-1134 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-01 N1 - Date created - 2014-11-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-1134 ER - TY - JOUR T1 - A phase I/II trial of belinostat in combination with cisplatin, doxorubicin, and cyclophosphamide in thymic epithelial tumors: a clinical and translational study. AN - 1619317602; 25189481 AB - This phase I/II study sought to determine the safety and maximum tolerated dose (MTD) of a novel schedule of belinostat, a histone deacetylase inhibitor (HDAC) administered before and in combination with cisplatin (P), doxorubicin (A), and cyclophosphamide (C) in thymic epithelial tumors (TET). Antitumor activity, pharmacokinetics, and biomarkers of response were also assessed. Patients with advanced, unresectable TET received increasing doses of belinostat as a continuous intravenous infusion over 48 hours with chemotherapy in 3-week cycles. In phase II, belinostat at the MTD was used. Twenty-six patients were enrolled (thymoma, 12; thymic carcinoma, 14). Dose-limiting toxicities at 2,000 mg/m(2) belinostat were grade 3 nausea and diarrhea and grade 4 neutropenia and thrombocytopenia, respectively, in two patients. Twenty-four patients were treated at the MTD of 1,000 mg/m(2) with chemotherapy (P, 50 mg/m(2) on day 2; A, 25 mg/m(2) on days 2 and 3; C, 500 mg/m(2) on day 3). Objective response rates in thymoma and thymic carcinoma were 64% (95% confidence interval, 30.8%-89.1%) and 21% (4.7%-50.8%), respectively. Modulation of pharmacodynamic markers of HDAC inhibition and declines in regulatory T cell (Treg) and exhausted CD8(+) T-cell populations were observed. Decline in Tregs was associated with response (P = 0.0041) and progression-free survival (P = 0.021). Declines in TIM3(+) CD8(+) T cells were larger in responders than nonresponders (P = 0.049). This study identified the MTD of belinostat in combination with PAC and indicates that the combination is active and feasible in TETs. Immunomodulatory effects on Tregs and TIM3(+) CD8(+) T cells warrant further study. ©2014 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Thomas, Anish AU - Rajan, Arun AU - Szabo, Eva AU - Tomita, Yusuke AU - Carter, Corey A AU - Scepura, Barbara AU - Lopez-Chavez, Ariel AU - Lee, Min-Jung AU - Redon, Christophe E AU - Frosch, Ari AU - Peer, Cody J AU - Chen, Yuanbin AU - Piekarz, Richard AU - Steinberg, Seth M AU - Trepel, Jane B AU - Figg, William D AU - Schrump, David S AU - Giaccone, Giuseppe AD - Medical Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland. ; Division of Cancer Prevention, National Cancer Institute, NIH, Bethesda, Maryland. ; Department of Hematology and Oncology, Walter Reed National Military Medical Center, Bethesda, Maryland. ; Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, Maryland. ; Cancer Therapy Evaluation Program, National Cancer Institute, NIH, Bethesda, Maryland. ; Biostatistics and Data Management Section, National Cancer Institute, NIH, Bethesda, Maryland. ; Thoracic Surgery Section, Thoracic and Gastrointestinal Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland. ; Medical Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland. gg496@georgetown.edu. Y1 - 2014/11/01/ PY - 2014 DA - 2014 Nov 01 SP - 5392 EP - 5402 VL - 20 IS - 21 SN - 1078-0432, 1078-0432 KW - Biomarkers, Tumor KW - 0 KW - Hydroxamic Acids KW - Sulfonamides KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - belinostat KW - F4H96P17NZ KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Young Adult KW - CD8-Positive T-Lymphocytes -- drug effects KW - Humans KW - Aged KW - Translational Medical Research -- methods KW - Doxorubicin -- administration & dosage KW - Sulfonamides -- administration & dosage KW - Cisplatin -- administration & dosage KW - Biomarkers, Tumor -- metabolism KW - Hydroxamic Acids -- administration & dosage KW - Adult KW - Middle Aged KW - Maximum Tolerated Dose KW - Female KW - Male KW - Neoplasms, Glandular and Epithelial -- drug therapy KW - Neoplasms, Glandular and Epithelial -- metabolism KW - Thymus Neoplasms -- metabolism KW - Thymus Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619317602?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+phase+I%2FII+trial+of+belinostat+in+combination+with+cisplatin%2C+doxorubicin%2C+and+cyclophosphamide+in+thymic+epithelial+tumors%3A+a+clinical+and+translational+study.&rft.au=Thomas%2C+Anish%3BRajan%2C+Arun%3BSzabo%2C+Eva%3BTomita%2C+Yusuke%3BCarter%2C+Corey+A%3BScepura%2C+Barbara%3BLopez-Chavez%2C+Ariel%3BLee%2C+Min-Jung%3BRedon%2C+Christophe+E%3BFrosch%2C+Ari%3BPeer%2C+Cody+J%3BChen%2C+Yuanbin%3BPiekarz%2C+Richard%3BSteinberg%2C+Seth+M%3BTrepel%2C+Jane+B%3BFigg%2C+William+D%3BSchrump%2C+David+S%3BGiaccone%2C+Giuseppe&rft.aulast=Thomas&rft.aufirst=Anish&rft.date=2014-11-01&rft.volume=20&rft.issue=21&rft.spage=5392&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-0968 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-01 N1 - Date created - 2014-11-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Cancer. 2010 Jun 29;103(1):12-7 [20588278] Cell. 2010 Apr 2;141(1):69-80 [20371346] J Exp Med. 2010 Sep 27;207(10):2187-94 [20819927] PLoS One. 2010;5(11):e15544 [21124906] J Clin Oncol. 2011 May 20;29(15):2052-9 [21502553] Cancer Chemother Pharmacol. 2011 Jun;67(6):1273-9 [20706839] Cell Cycle. 2011 Sep 15;10(18):3119-28 [21900747] Expert Opin Investig Drugs. 2011 Dec;20(12):1723-32 [22046971] J Clin Oncol. 2011 Dec 20;29(36):4820-7 [22105817] Ann Hematol. 2012 Jan;91(1):33-8 [21538061] Immunol Cell Biol. 2012 Jan;90(1):85-94 [22124371] J Clin Oncol. 2012 Sep 20;30(27):3361-7 [22915658] J Thorac Oncol. 2013 Feb;8(2):246-9 [23328550] Cancer Res. 2013 Apr 15;73(8):2428-34 [23382048] Clin Cancer Res. 2001 Apr;7(4):759-60 [11309319] Cancer. 2002 Jul 15;95(2):420-9 [12124843] Mol Cancer Ther. 2001 Dec;1(2):121-31 [12467229] Int J Cancer. 2003 Jul 1;105(4):546-51 [12712448] Cancer Res. 2003 Nov 1;63(21):7291-300 [14612526] Ann Thorac Surg. 2003 Dec;76(6):1859-64; discussion 1864-5 [14667600] Lung Cancer. 2004 Jun;44(3):369-79 [15140551] Radiat Res. 2004 Jun;161(6):667-74 [15161353] J Chin Med Assoc. 2004 Apr;67(4):172-8 [15244015] Cancer. 1981 Dec 1;48(11):2485-92 [7296496] J Clin Oncol. 1990 Aug;8(8):1419-23 [2380761] J Clin Oncol. 1994 Jun;12(6):1164-8 [8201378] Ann Neurol. 2004 Dec;56(6):901-4 [15562414] Leuk Res. 2005 Nov;29(11):1237-8 [15946739] Cancer. 2005 Nov 15;104(10):2063-71 [16206298] J Thorac Oncol. 2007 Jan;2(1):73-8 [17410014] Nat Med. 2007 Nov;13(11):1299-307 [17922010] Clin Cancer Res. 2008 Feb 1;14(3):804-10 [18245542] Hematol Oncol Clin North Am. 2008 Jun;22(3):381-92 [18514122] Crit Rev Immunol. 2008;28(2):109-26 [18540827] PLoS One. 2008;3(6):e2445 [18560576] In Vivo. 2008 May-Jun;22(3):305-9 [18610740] Eur J Cancer. 2009 Jan;45(2):228-47 [19097774] J Exp Med. 2010 Sep 27;207(10):2175-86 [20819923] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-0968 ER - TY - JOUR T1 - Disruption of tumor suppressor gene Hint1 leads to remodeling of the lipid metabolic phenotype of mouse liver. AN - 1619317240; 25193995 AB - A lipidomic and metabolomic investigation of serum and liver from mice was performed to gain insight into the tumor suppressor gene Hint1. A major reprogramming of lipid homeostasis was found in both serum and liver of Hint1-null (Hint(-/-)) mice, with significant changes in the levels of many lipid molecules, as compared with gender-, age-, and strain-matched WT mice. In the Hint1(-/-) mice, serum total and esterified cholesterol were reduced 2.5-fold, and lysophosphatidylcholines (LPCs) and lysophosphatidic acids were 10-fold elevated in serum, with a corresponding fall in phosphatidylcholines (PCs). In the liver, MUFAs and PUFAs, including arachidonic acid (AA) and its metabolic precursors, were also raised, as was mRNA encoding enzymes involved in AA de novo synthesis. There was also a significant 50% increase in hepatic macrophages in the Hint1(-/-) mice. Several hepatic ceramides and acylcarnitines were decreased in the livers of Hint1(-/-) mice. The changes in serum LPCs and PCs were neither related to hepatic phospholipase A2 activity nor to mRNAs encoding lysophosphatidylcholine acetyltransferases 1-4. The lipidomic phenotype of the Hint1(-/-) mouse revealed decreased inflammatory eicosanoids with elevated proliferative mediators that, combined with decreased ceramide apoptosis signaling molecules, may contribute to the tumor suppressor activity of Hint1. Copyright © 2014 by the American Society for Biochemistry and Molecular Biology, Inc. JF - Journal of lipid research AU - Beyoğlu, Diren AU - Krausz, Kristopher W AU - Martin, Juliette AU - Maurhofer, Olivier AU - Dorow, Juliane AU - Ceglarek, Uta AU - Gonzalez, Frank J AU - Dufour, Jean-François AU - Idle, Jeffrey R AD - Hepatology Research Group, Department of Clinical Research, University of Bern, Switzerland. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD. ; Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, University Hospital Leipzig, Leipzig, Germany. ; Hepatology Research Group, Department of Clinical Research, University of Bern, Switzerland Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 2309 EP - 2319 VL - 55 IS - 11 KW - Hint1 protein, mouse KW - 0 KW - Lipids KW - Nerve Tissue Proteins KW - Index Medicus KW - lipidomics KW - proliferation KW - phospholipids KW - eicosanoids KW - carcinogenesis KW - mass spectrometry KW - apoptosis KW - cholesterol KW - metabolomics KW - Lipids -- blood KW - Gene Knockout Techniques KW - Animals KW - Mice KW - Male KW - Phenotype KW - Nerve Tissue Proteins -- deficiency KW - Genes, Tumor Suppressor KW - Liver -- metabolism KW - Lipid Metabolism -- genetics KW - Nerve Tissue Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619317240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+lipid+research&rft.atitle=Disruption+of+tumor+suppressor+gene+Hint1+leads+to+remodeling+of+the+lipid+metabolic+phenotype+of+mouse+liver.&rft.au=Beyo%C4%9Flu%2C+Diren%3BKrausz%2C+Kristopher+W%3BMartin%2C+Juliette%3BMaurhofer%2C+Olivier%3BDorow%2C+Juliane%3BCeglarek%2C+Uta%3BGonzalez%2C+Frank+J%3BDufour%2C+Jean-Fran%C3%A7ois%3BIdle%2C+Jeffrey+R&rft.aulast=Beyo%C4%9Flu&rft.aufirst=Diren&rft.date=2014-11-01&rft.volume=55&rft.issue=11&rft.spage=2309&rft.isbn=&rft.btitle=&rft.title=Journal+of+lipid+research&rft.issn=1539-7262&rft_id=info:doi/10.1194%2Fjlr.M050682 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-15 N1 - Date created - 2014-10-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Semin Cancer Biol. 2000 Jun;10(3):173-84 [10936067] Biochimie. 2013 Mar;95(3):556-67 [23063693] Am J Pathol. 2003 Sep;163(3):1101-7 [12937151] Cell Signal. 2004 Sep;16(9):975-81 [15212758] Bioessays. 2004 Aug;26(8):870-81 [15273989] J Biol Chem. 1993 Jan 25;268(3):1960-4 [8380583] Mol Cell Biochem. 1999 Feb;192(1-2):17-31 [10331655] Biochem J. 2005 Apr 1;387(Pt 1):239-46 [15540987] Cell. 2005 Jul 1;121(7):977-90 [15989949] J Neurosci Res. 2005 Aug 15;81(4):541-50 [15968641] Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G194-8 [16407588] Oncogene. 2006 Feb 2;25(5):713-21 [16186798] Nat Rev Cancer. 2007 Apr;7(4):281-94 [17384583] World J Gastroenterol. 2008 Mar 21;14(11):1720-33 [18350603] World J Gastroenterol. 2008 Mar 21;14(11):1741-8 [18350605] Oncogene. 2008 Oct 9;27(46):6002-11 [18574468] Cancer Lett. 2009 Mar 18;275(2):277-84 [19081673] Ann N Y Acad Sci. 2009 Feb;1155:293-9 [19250220] J Lipid Res. 2009 Apr;50 Suppl:S225-30 [19066402] J Chromatogr B Analyt Technol Biomed Life Sci. 2013 May 15;927:209-13 [23588243] Adv Exp Med Biol. 2013;991:1-14 [23775687] Biol Cell. 2013 Aug;105(8):317-33 [23611148] J Biol Chem. 2013 Aug 30;288(35):25244-53 [23880760] J Hepatol. 2013 Oct;59(4):842-58 [23714158] Gastroenterology. 2013 Dec;145(6):1424-35.e1-25 [24012984] J Immunol. 2014 Feb 1;192(3):851-7 [24443508] Histol Histopathol. 2014 Mar;29(3):313-21 [24194373] Nutr Metab Cardiovasc Dis. 2014 Feb;24(2):124-31 [24113394] Prog Lipid Res. 2014 Apr;54:53-67 [24513486] J Biol Chem. 2009 Nov 27;284(48):33549-60 [19801672] IUBMB Life. 2010 May;62(5):347-56 [20222015] Mol Cancer. 2010;9:71 [20356387] Behav Brain Res. 2011 Jul 7;220(2):305-11 [21316396] Adv Enzyme Regul. 2011;51(1):219-28 [21035490] J Biol Chem. 2011 Aug 12;286(32):27855-62 [21693702] Cancer Metastasis Rev. 2011 Dec;30(3-4):557-65 [22002750] Am J Physiol Gastrointest Liver Physiol. 2012 Jan 1;302(1):G77-84 [21995961] Biochem J. 2012 Feb 1;441(3):789-802 [22248339] J Proteome Res. 2012 Feb 3;11(2):850-60 [22070544] Oncogene. 2012 Feb 16;31(7):842-57 [21743491] Anticancer Agents Med Chem. 2012 May;12(4):364-75 [22043999] Hepatology. 2012 Jul;56(1):186-97 [22318941] Biochim Biophys Acta. 2013 Jan;1831(1):42-60 [22867755] J Surg Res. 2012 Dec;178(2):879-87 [22947700] Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7824-9 [12810953] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1194/jlr.M050682 ER - TY - JOUR T1 - Inhaled nitric oxide usage in preterm infants in the NICHD neonatal research network: inter-site variation and propensity evaluation AN - 1618822747; 24901452 AB - The use of inhaled nitric oxide (iNO) in preterm infants remains controversial. In October 2010, a National Institutes of Health consensus development conference cautioned against use of iNO in preterm infants. This study aims (1) to determine the prevalence and variability in use of iNO in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network (NICHD NRN) before and after the consensus conference and (2) separately, to examine associations between iNO use and severe bronchopulmonary dysplasia (BPD) or death. The NICHD NRN Generic Database collects data including iNO use on very preterm infants. A total of 13 centers contributed data across the time period 2008 to 2011. Infants exposed or not to iNO were compared using logistic regression, which included factors related to risk as well as their likelihood of being exposed to iNO. A total of 4885 infants were assessed between 2008 and 2011; 128 (2.6%) received iNO before day 7, 140 (2.9%) between day 7 and 28, and 47 (1.0%) at >28 days. Center-specific iNO use during 2008 to 2010 ranged from 21.9 to 0.4%; 12 of 13 sites reduced usage and overall NRN iNO usage decreased from 4.6 to 1.6% (P<0.001) in 2011. The use of iNO started between day 7 and day 14 was more prevalent among younger infants with more severe courses in week 1 and associated with increased risk of severe BPD or death (odds ratio 2.24; 95% confidence interval 1.23 to 4.07). The variability and total use of iNO decreased in 2011 compared with 2008 to 2010. iNO administration started at day 7 was associated with more severe outcomes compared with infants without iNO exposure. JF - Journal of Perinatology AU - Truog, W E AU - Nelin, L D AU - Das, A AU - Kendrick, D E AU - Bell, E F AU - Carlo, W A AU - Higgins, R D AU - Laptook, A R AU - Sanchez, P J AU - Shankaran, S AU - Stoll, B J AU - Van Meurs, K P AU - Walsh, M C Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 842 EP - 6 CY - New York PB - Nature Publishing Group VL - 34 IS - 11 SN - 07438346 KW - Medical Sciences--Pediatrics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618822747?accountid=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=Journal+of+Perinatology&rft.atitle=Inhaled+nitric+oxide+usage+in+preterm+infants+in+the+NICHD+neonatal+research+network%3A+inter-site+variation+and+propensity+evaluation&rft.au=Truog%2C+W+E%3BNelin%2C+L+D%3BDas%2C+A%3BKendrick%2C+D+E%3BBell%2C+E+F%3BCarlo%2C+W+A%3BHiggins%2C+R+D%3BLaptook%2C+A+R%3BSanchez%2C+P+J%3BShankaran%2C+S%3BStoll%2C+B+J%3BVan+Meurs%2C+K+P%3BWalsh%2C+M+C&rft.aulast=Truog&rft.aufirst=W&rft.date=2014-11-01&rft.volume=34&rft.issue=11&rft.spage=842&rft.isbn=&rft.btitle=&rft.title=Journal+of+Perinatology&rft.issn=07438346&rft_id=info:doi/10.1038%2Fjp.2014.105 LA - English DB - ProQuest Central N1 - Copyright - Copyright Nature Publishing Group Nov 2014 N1 - Last updated - 2014-12-16 DO - http://dx.doi.org/10.1038/jp.2014.105 ER - TY - JOUR T1 - A phase I and pharmacokinetic study of oral perifosine with different loading schedules in patients with refractory neoplasms. AN - 1618156931; 25183650 AB - To determine the maximum tolerated dose (MTD) of perifosine (NSC 639966), an alkylphospholipid modulator of signal transduction, using different oral loading and maintenance regimens in an effort to avoid gastrointestinal toxicity while seeking maximal sustained plasma concentrations. Thirty-one patients with advanced neoplasms were treated with monthly cycles of perifosine loading doses of 300, 600, 900, 1,200 and 1,500 mg (dose levels 1 through 5, respectively) on days 1-2 depending on the actual dose of the initial cycle. For subsequent cycles, perifosine loading doses were reduced to 100, 200, 300, 400 and 1,000 mg at the respective corresponding dose levels. Daily perifosine "maintenance" doses of 50, 100, 150, 200 and 250 mg for levels 1 through 5, respectively, commenced on days 2 or 3 and continued for a total of 21 days. No treatment was given for days 22-27. The pharmacokinetics of perifosine with these schedules was characterized. Dose-limiting diarrhea developed at or above dose level 4. The MTD and recommended phase II dose was dose level 3B, with a loading dose of 900 mg on day 1 divided into two doses of 450 mg administered 6 h apart and a maintenance dose of 150 mg on day 2 through 21. On subsequent cycles, the loading dose was reduced to 300 mg. Non-gastrointestinal toxicities included three episodes of gout or gout-like syndromes observed at doses above the MTD. The median peak plasma concentration of perifosine achieved at the MTD was approximately 8.3 µg/mL. Four patients had stable disease ranging from 167 to 735 days. Perifosine given according to a loading and maintenance schedule can safely sustain concentrations of drug, approaching concentrations achieved in preclinical models with evidence of anti-tumor effect. JF - Cancer chemotherapy and pharmacology AU - Figg, William D AU - Monga, Manish AU - Headlee, Donna AU - Shah, Avni AU - Chau, Cindy H AU - Peer, Cody AU - Messman, Richard AU - Elsayed, Yusri A AU - Murgo, Anthony J AU - Melillo, Giovanni AU - Ryan, Qin C AU - Kalnitskiy, Mikhail AU - Senderowicz, Adrian M AU - Hollingshead, Melinda AU - Arbuck, Susan G AU - Sausville, Edward A AD - Medical Oncology Branch, National Cancer Institute, Bldg 10/Room 5A01, 9000 Rockville Pike, Bethesda, MD, 20892, USA, figgw@helix.nih.gov. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 955 EP - 967 VL - 74 IS - 5 KW - Phosphorylcholine KW - 107-73-3 KW - perifosine KW - 2GWV496552 KW - Index Medicus KW - Administration, Oral KW - Young Adult KW - Drug Administration Schedule KW - Area Under Curve KW - Dose-Response Relationship, Drug KW - Humans KW - Fatigue -- chemically induced KW - Disease Progression KW - Metabolic Clearance Rate KW - Aged KW - Diarrhea -- chemically induced KW - Aged, 80 and over KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Anorexia -- chemically induced KW - Male KW - Female KW - Neoplasms -- drug therapy KW - Neoplasms -- pathology KW - Phosphorylcholine -- pharmacokinetics KW - Phosphorylcholine -- analogs & derivatives KW - Phosphorylcholine -- adverse effects KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618156931?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+phase+I+and+pharmacokinetic+study+of+oral+perifosine+with+different+loading+schedules+in+patients+with+refractory+neoplasms.&rft.au=Figg%2C+William+D%3BMonga%2C+Manish%3BHeadlee%2C+Donna%3BShah%2C+Avni%3BChau%2C+Cindy+H%3BPeer%2C+Cody%3BMessman%2C+Richard%3BElsayed%2C+Yusri+A%3BMurgo%2C+Anthony+J%3BMelillo%2C+Giovanni%3BRyan%2C+Qin+C%3BKalnitskiy%2C+Mikhail%3BSenderowicz%2C+Adrian+M%3BHollingshead%2C+Melinda%3BArbuck%2C+Susan+G%3BSausville%2C+Edward+A&rft.aulast=Figg&rft.aufirst=William&rft.date=2014-11-01&rft.volume=74&rft.issue=5&rft.spage=955&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+pharmacology&rft.issn=1432-0843&rft_id=info:doi/10.1007%2Fs00280-014-2569-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-29 N1 - Date created - 2014-10-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00280-014-2569-7 ER - TY - JOUR T1 - Thymic stromal lymphopoietin and interleukin-4 mediate the pathogenesis of halothane-induced liver injury in mice. AN - 1618153390; 24723460 AB - Liver eosinophilia has been associated with incidences of drug-induced liver injury (DILI) for more than 50 years, although its role in this disease has remained largely unknown. In this regard, it was recently shown that eosinophils played a pathogenic role in a mouse model of halothane-induced liver injury (HILI). However, the signaling events that drove hepatic expression of eosinophil-associated chemokines, eotaxins, eosinophil infiltration, and subsequent HILI were unclear. We now provide evidence implicating hepatic epithelial-derived cytokine thymic stromal lymphopoietin (TSLP) and type 2 immunity, in particular, interleukin-4 (IL-4) production, in mediating hepatic eosinophilia and injury during HILI. TSLP was constitutively expressed by mouse hepatocytes and increased during HILI. Moreover, the severity of HILI was reduced in mice deficient in either the TSLP receptor (TSLPR) or IL-4 and was accompanied by decreases in serum levels of eotaxins and hepatic eosinophilia. Similarly, concanavalin A-induced liver injury, where type 2 cytokines and eosinophils play a significant role in its pathogenesis, was also reduced in TSLPR-deficient mice. Studies in vitro revealed that mouse and human hepatocytes produce TSLP and eotaxins in response to treatment with combinations of IL-4 and proinflammatory cytokines IL-1β and tumor necrosis factor alpha. This report provides the first evidence implicating roles for hepatic TSLP signaling, type 2 immunity, and eosinophilia in mediating liver injury caused by a drug. © 2014 by the American Association for the Study of Liver Diseases. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA. JF - Hepatology (Baltimore, Md.) AU - Proctor, William R AU - Chakraborty, Mala AU - Fullerton, Aaron M AU - Korrapati, Midhun C AU - Ryan, Pauline M AU - Semple, Kenrick AU - Morrison, Jeffrey C AU - Berkson, Julia D AU - Chea, Lynette S AU - Yang, Qian AU - Li, Albert P AU - Spolski, Rosanne AU - West, Erin E AU - Rochman, Yrina AU - Leonard, Warren J AU - Bourdi, Mohammed AU - Pohl, Lance R AD - Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 1741 EP - 1752 VL - 60 IS - 5 KW - Anesthetics, Inhalation KW - 0 KW - Cytokines KW - thymic stromal lymphopoietin KW - Concanavalin A KW - 11028-71-0 KW - Interleukin-4 KW - 207137-56-2 KW - Halothane KW - UQT9G45D1P KW - Index Medicus KW - Hepatitis, Animal -- metabolism KW - Animals KW - Hepatocytes -- secretion KW - Humans KW - Mice, Inbred BALB C KW - Female KW - Anesthetics, Inhalation -- adverse effects KW - Interleukin-4 -- metabolism KW - Chemical and Drug Induced Liver Injury -- etiology KW - Cytokines -- secretion KW - Halothane -- adverse effects KW - Cytokines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618153390?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Thymic+stromal+lymphopoietin+and+interleukin-4+mediate+the+pathogenesis+of+halothane-induced+liver+injury+in+mice.&rft.au=Proctor%2C+William+R%3BChakraborty%2C+Mala%3BFullerton%2C+Aaron+M%3BKorrapati%2C+Midhun+C%3BRyan%2C+Pauline+M%3BSemple%2C+Kenrick%3BMorrison%2C+Jeffrey+C%3BBerkson%2C+Julia+D%3BChea%2C+Lynette+S%3BYang%2C+Qian%3BLi%2C+Albert+P%3BSpolski%2C+Rosanne%3BWest%2C+Erin+E%3BRochman%2C+Yrina%3BLeonard%2C+Warren+J%3BBourdi%2C+Mohammed%3BPohl%2C+Lance+R&rft.aulast=Proctor&rft.aufirst=William&rft.date=2014-11-01&rft.volume=60&rft.issue=5&rft.spage=1741&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.27169 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-30 N1 - Date created - 2014-10-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Rhinol Allergy. 2010 Jan-Feb;24(1):e14-8 [20109311] Am J Respir Cell Mol Biol. 2009 Mar;40(3):368-74 [18787178] J Allergy Clin Immunol. 2010 Jul;126(1):160-5.e3 [20620568] Toxicol Lett. 2011 Feb 5;200(3):139-45 [21094227] Toxicol Sci. 2011 Apr;120(2):507-18 [21245496] Am J Respir Cell Mol Biol. 2011 Jun;44(6):787-93 [20656951] Chem Res Toxicol. 2012 Jan 13;25(1):83-93 [22107450] Science. 2012 Jul 27;337(6093):431-5 [22837519] J Appl Toxicol. 2012 Oct;32(10):815-22 [21735453] J Appl Toxicol. 2012 Oct;32(10):823-33 [22407903] J Allergy Clin Immunol. 2012 Oct;130(4):845-52 [22939755] Hepatology. 2013 Apr;57(4):1314-24 [23150092] Hepatology. 2013 May;57(5):2026-36 [23238640] Biochem Pharmacol. 2010 Jul 15;80(2):255-61 [20359463] Chem Res Toxicol. 2001 Apr;14(4):362-70 [11304124] J Hepatol. 2001 Apr;34(4):537-47 [11394653] Gastroenterology. 2002 Jun;122(7):2001-10 [12055605] J Immunol. 2003 Sep 15;171(6):3233-44 [12960353] Hepatology. 2004 May;39(5):1430-40 [15122773] J Exp Med. 2004 Jul 19;200(2):159-68 [15263024] Hepatology. 1993 Feb;17(2):206-12 [8428717] Hepatology. 1994 Sep;20(3):654-62 [7521317] J Gastroenterol. 1995 Aug;30(4):524-8 [7550866] J Immunol. 1997 Aug 1;159(3):1537-42 [9233653] J Exp Med. 2005 Sep 19;202(6):829-39 [16172260] Nat Immunol. 2005 Oct;6(10):1047-53 [16142237] Hepatology. 2006 Dec;44(6):1421-31 [17133481] J Immunol. 2007 Jan 1;178(1):219-27 [17182558] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):914-9 [17213320] J Immunol. 2007 Feb 1;178(3):1396-404 [17237387] J Immunol. 2007 Mar 15;178(6):3373-7 [17339431] Aliment Pharmacol Ther. 2007 Jun 15;25(12):1411-21 [17539980] J Viral Hepat. 2008 Jul;15(7):523-30 [18266647] Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):11875-80 [18711124] Gastroenterology. 2008 Dec;135(6):1924-34, 1934.e1-4 [18955056] Comment In: Hepatology. 2014 Nov;60(5):1473-5 [24913773] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/hep.27169 ER - TY - JOUR T1 - Parallel evolution of tetrodotoxin resistance in three voltage-gated sodium channel genes in the garter snake Thamnophis sirtalis. AN - 1618153170; 25135948 AB - Members of a gene family expressed in a single species often experience common selection pressures. Consequently, the molecular basis of complex adaptations may be expected to involve parallel evolutionary changes in multiple paralogs. Here, we use bacterial artificial chromosome library scans to investigate the evolution of the voltage-gated sodium channel (Nav) family in the garter snake Thamnophis sirtalis, a predator of highly toxic Taricha newts. Newts possess tetrodotoxin (TTX), which blocks Nav's, arresting action potentials in nerves and muscle. Some Thamnophis populations have evolved resistance to extremely high levels of TTX. Previous work has identified amino acid sites in the skeletal muscle sodium channel Nav1.4 that confer resistance to TTX and vary across populations. We identify parallel evolution of TTX resistance in two additional Nav paralogs, Nav1.6 and 1.7, which are known to be expressed in the peripheral nervous system and should thus be exposed to ingested TTX. Each paralog contains at least one TTX-resistant substitution identical to a substitution previously identified in Nav1.4. These sites are fixed across populations, suggesting that the resistant peripheral nerves antedate resistant muscle. In contrast, three sodium channels expressed solely in the central nervous system (Nav1.1-1.3) showed no evidence of TTX resistance, consistent with protection from toxins by the blood-brain barrier. We also report the exon-intron structure of six Nav paralogs, the first such analysis for snake genes. Our results demonstrate that the molecular basis of adaptation may be both repeatable across members of a gene family and predictable based on functional considerations. © The Author 2014. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution. JF - Molecular biology and evolution AU - McGlothlin, Joel W AU - Chuckalovcak, John P AU - Janes, Daniel E AU - Edwards, Scott V AU - Feldman, Chris R AU - Brodie, Edmund D AU - Pfrender, Michael E AD - Department of Biological Sciences, Virginia Tech, Blacksburg, VA Department of Biology, University of Virginia joelmcg@vt.edu. ; Department of Biology, University of Virginia Bio-Rad Laboratories, Hercules, CA. ; Department of Organismic and Evolutionary Biology, Harvard University Division of Genetics and Developmental Biology, National Institutes of Health, Bethesda, MD. ; Department of Organismic and Evolutionary Biology, Harvard University. ; Department of Biology, University of Nevada, Reno. ; Department of Biology, Utah State University. ; Department of Biological Sciences and Environmental Change Initiative, University of Notre Dame. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 2836 EP - 2846 VL - 31 IS - 11 KW - DNA Transposable Elements KW - 0 KW - Protein Isoforms KW - Sodium Channel Blockers KW - Voltage-Gated Sodium Channels KW - Tetrodotoxin KW - 4368-28-9 KW - Index Medicus KW - molecular evolution KW - coevolution KW - toxins KW - predator–prey interactions KW - gene families KW - adaptation KW - Animals KW - Salamandridae -- physiology KW - Exons KW - Protein Isoforms -- metabolism KW - Amino Acid Sequence KW - Chromosomes, Artificial, Bacterial KW - Microsatellite Repeats KW - Predatory Behavior KW - Sequence Alignment KW - Protein Isoforms -- chemistry KW - Introns KW - Molecular Sequence Data KW - Adaptation, Physiological KW - Protein Isoforms -- genetics KW - Gene Library KW - Voltage-Gated Sodium Channels -- genetics KW - Sodium Channel Blockers -- metabolism KW - Tetrodotoxin -- toxicity KW - Sodium Channel Blockers -- toxicity KW - Drug Resistance -- genetics KW - Tetrodotoxin -- biosynthesis KW - Biological Evolution KW - Voltage-Gated Sodium Channels -- chemistry KW - Voltage-Gated Sodium Channels -- metabolism KW - Colubridae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618153170?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+evolution&rft.atitle=Parallel+evolution+of+tetrodotoxin+resistance+in+three+voltage-gated+sodium+channel+genes+in+the+garter+snake+Thamnophis+sirtalis.&rft.au=McGlothlin%2C+Joel+W%3BChuckalovcak%2C+John+P%3BJanes%2C+Daniel+E%3BEdwards%2C+Scott+V%3BFeldman%2C+Chris+R%3BBrodie%2C+Edmund+D%3BPfrender%2C+Michael+E&rft.aulast=McGlothlin&rft.aufirst=Joel&rft.date=2014-11-01&rft.volume=31&rft.issue=11&rft.spage=2836&rft.isbn=&rft.btitle=&rft.title=Molecular+biology+and+evolution&rft.issn=1537-1719&rft_id=info:doi/10.1093%2Fmolbev%2Fmsu237 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-22 N1 - Date created - 2014-10-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: BMC Bioinformatics. 2006;7:474 [17064419] Syst Biol. 2006 Dec;55(6):902-11 [17345672] Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2767-72 [17307883] Evolution. 2007 May;61(5):995-1016 [17492956] Bioinformatics. 2007 May 15;23(10):1289-91 [17379693] Nature. 2007 Jun 14;447(7146):855-8 [17568746] PLoS Biol. 2007 Sep;5(9):e219 [17696646] PLoS Biol. 2008 Mar 11;6(3):e60 [18336073] Mol Biol Evol. 2008 Jun;25(6):1016-24 [18258611] J Cell Physiol. 2008 Sep;216(3):716-26 [18393272] Evolution. 2008 Sep;62(9):2155-77 [18616572] Eur J Pharm Biopharm. 2008 Oct;70(2):462-6 [18632257] Science. 2009 Feb 6;323(5915):746-51 [19197055] Proc Natl Acad Sci U S A. 2009 Aug 11;106(32):13415-20 [19666534] Annu Rev Genomics Hum Genet. 2009;10:483-511 [19640225] Mar Drugs. 2010;8(3):577-93 [20411116] Mar Drugs. 2010;8(3):741-62 [20411124] Proc Biol Sci. 2010 Nov 7;277(1698):3317-25 [20522513] Proc Natl Acad Sci U S A. 2000 May 9;97(10):5616-20 [10779552] Biochimie. 2000 Sep-Oct;82(9-10):883-92 [11086218] Annu Rev Physiol. 2001;63:871-94 [11181979] Toxicon. 2001 Aug;39(8):1261-3 [11306140] Annu Rev Genomics Hum Genet. 2000;1:41-73 [11701624] J Exp Biol. 2002 Mar;205(Pt 5):575-84 [11907047] Genome Res. 2002 Apr;12(4):656-64 [11932250] Trends Neurosci. 2002 May;25(5):253-9 [11972962] Science. 2002 Aug 23;297(5585):1336-9 [12193784] J Neurosci. 2002 Sep 1;22(17):7425-33 [12196564] Evolution. 2002 Oct;56(10):2067-82 [12449493] Biophys J. 2003 Jan;84(1):287-94 [12524282] Genome Biol. 2003;4(3):207 [12620097] J Physiol. 2003 Sep 15;551(Pt 3):741-50 [12843211] Syst Biol. 2003 Oct;52(5):696-704 [14530136] Annu Rev Physiol. 2004;66:477-519 [14977411] Nucleic Acids Res. 2004;32(5):1792-7 [15034147] Trends Genet. 2004 Apr;20(4):171-6 [15101391] Evolution. 2004 Aug;58(8):1794-808 [15446431] Pharmacol Rev. 1966 Jun;18(2):997-1049 [5328391] Q J Exp Physiol Cogn Med Sci. 1968 Apr;53(2):119-28 [5185564] Circ Res. 1968 Oct;23(4):553-65 [5677946] J Morphol. 1973 Jun;140(2):171-84 [4711262] Tissue Cell. 1974;6(2):319-33 [4416108] Am J Physiol. 1984 Mar;246(3 Pt 2):R277-88 [6367490] J Exp Biol. 1989 May;143:435-57 [2732666] Mol Biol Evol. 1989 Sep;6(5):526-38 [2677599] FEBS Lett. 1991 Nov 18;293(1-2):93-6 [1660007] Proc Natl Acad Sci U S A. 1995 Jan 3;92(1):9-13 [7816854] Cell Mol Neurobiol. 1994 Jun;14(3):227-44 [7712513] Biophys J. 1998 Dec;75(6):2647-57 [9826589] Philos Trans R Soc Lond B Biol Sci. 1998 Oct 29;353(1376):1685-93 [10021768] J Pharmacol Exp Ther. 1963 Apr;140:31-40 [13962288] Genome Res. 2005 Jan;15(1):166-73 [15590945] Ann Neurol. 2005 Mar;57(3):339-48 [15732107] Lancet Neurol. 2005 Apr;4(4):219-28 [15778101] Nature. 2005 Apr 7;434(7034):759-63 [15815629] PLoS Biol. 2005 Oct;3(10):e314 [16128622] J Biomed Biotechnol. 2011;2011:132975 [20981143] Mol Biol Evol. 2011 Jan;28(1):859-71 [20924084] J Comp Physiol A Neuroethol Sens Neural Behav Physiol. 2011 Jan;197(1):33-43 [20820785] BMC Genomics. 2010;11:694 [21138572] Mol Biol Evol. 2011 Apr;28(4):1415-24 [21148285] Genes Dev. 2011 May 15;25(10):1010-22 [21576262] Proc Natl Acad Sci U S A. 2011 May 31;108(22):9154-9 [21576472] Nature. 2011 Sep 29;477(7366):587-91 [21881562] Mar Drugs. 2011;9(11):2409-22 [22163193] Evolution. 2012 Jan;66(1):1-17 [22220860] Proc Natl Acad Sci U S A. 2012 Mar 20;109(12):4556-61 [22392995] Proc Natl Acad Sci U S A. 2012 Jun 26;109 Suppl 1:10619-25 [22723361] PLoS One. 2012;7(7):e41750 [22911851] Nucleic Acids Res. 2012 Aug;40(15):e115 [22730293] Nat Rev Neurosci. 2013 Jan;14(1):49-62 [23232607] Evolution. 2013 Feb;67(2):305-14 [23356605] Toxicon. 2013 Mar 1;63:165-83 [23261990] J Comp Physiol A Neuroethol Sens Neural Behav Physiol. 2013 Oct;199(10):829-42 [23979192] Science. 2013 Oct 25;342(6157):441-6 [24159039] Proc Natl Acad Sci U S A. 2013 Dec 17;110(51):20651-6 [24297900] Proc Natl Acad Sci U S A. 2013 Dec 17;110(51):20645-50 [24297902] Pharmacol Rev. 2005 Dec;57(4):387-95 [16382097] Pharmacol Rev. 2005 Dec;57(4):397-409 [16382098] Genome Biol. 2006;7(5):R43 [16723033] Science. 2006 Jul 7;313(5783):101-4 [16825572] Mol Biol Evol. 2006 Dec;23(12):2392-404 [16980575] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/molbev/msu237 ER - TY - JOUR T1 - Gynecologic Cancer InterGroup (GCIG) consensus review for squamous cell carcinoma of the ovary. AN - 1618151666; 25126954 AB - Squamous cell carcinoma of the ovary is a rare complication of mature cystic teratoma. The epidemiology, pathology, diagnosis, and management of this rare tumor are reviewed. Clinical characteristics, preoperative imaging, and tumor markers may help to predict malignancy preoperatively. Complete cytoreduction should be the aim of surgery. The prognosis for stage 1A disease is good, but for women with advanced or recurrent disease, it is very poor and has not improved in recent years. At present, there are insufficient data to provide clear guidance on the optimal management strategy for advanced disease, and there is a need to gain an understanding of the biology and to develop novel effective therapies. This will require coordinated international collaboration. JF - International journal of gynecological cancer : official journal of the International Gynecological Cancer Society AU - Glasspool, Rosalind M AU - González Martín, Antonio AU - Millan, David AU - Lorusso, Domenica AU - Åvall-Lundqvist, Elisabeth AU - Hurteau, Jean A AU - Davis, Alison AU - Hilpert, Felix AU - Kim, Jae-Weon AU - Alexandre, Jérôme AU - Ledermann, Jonathan A AD - *Beatson West of Scotland Cancer Centre, Glasgow, UK (SGCTG); †Medical Oncology Department, MD Anderson Cancer Centre, Madrid, Spain (GEICO); ‡Southern General Hospital, Glasgow, UK (SGCTG); §Gynecologic Oncology Unit, Fondazione IRCCS National Cancer institute of Milan (MITO), Milan, Italy; ‖Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden (NSGO); ¶Division of Gynecologic Oncology, NorthShore University Health System, University of Chicago Pritzker School of Medicine, Evanston, IL (GOG); #The Canberra Hospital, Canberra, Australia (ANZGOG); **University Hospital of Schleswig-Holstein Campus, Kiel, Germany (AGO); ††Department of Obstectrics and Gynecology, Seoul National University College of Medicine, Seoul, Republic of Korea (KGOG); ‡‡Medical Oncology, Cochin-Hôtel Dieu, Paris Descartes University, Paris, France (GINECO); and §§UCL Cancer Institute, London, UK (NCRI/MRC). Y1 - 2014/11// PY - 2014 DA - November 2014 SP - S26 EP - S29 VL - 24 IS - 9 Suppl 3 KW - Index Medicus KW - Combined Modality Therapy KW - Humans KW - Consensus KW - Societies, Medical KW - Female KW - Carcinoma, Squamous Cell -- pathology KW - Ovarian Neoplasms -- pathology KW - Practice Guidelines as Topic KW - Medical Oncology KW - Ovarian Neoplasms -- therapy KW - Carcinoma, Squamous Cell -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618151666?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+gynecological+cancer+%3A+official+journal+of+the+International+Gynecological+Cancer+Society&rft.atitle=Gynecologic+Cancer+InterGroup+%28GCIG%29+consensus+review+for+squamous+cell+carcinoma+of+the+ovary.&rft.au=Glasspool%2C+Rosalind+M%3BGonz%C3%A1lez+Mart%C3%ADn%2C+Antonio%3BMillan%2C+David%3BLorusso%2C+Domenica%3B%C3%85vall-Lundqvist%2C+Elisabeth%3BHurteau%2C+Jean+A%3BDavis%2C+Alison%3BHilpert%2C+Felix%3BKim%2C+Jae-Weon%3BAlexandre%2C+J%C3%A9r%C3%B4me%3BLedermann%2C+Jonathan+A&rft.aulast=Glasspool&rft.aufirst=Rosalind&rft.date=2014-11-01&rft.volume=24&rft.issue=9+Suppl+3&rft.spage=S26&rft.isbn=&rft.btitle=&rft.title=International+journal+of+gynecological+cancer+%3A+official+journal+of+the+International+Gynecological+Cancer+Society&rft.issn=1525-1438&rft_id=info:doi/10.1097%2FIGC.0000000000000209 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-07 N1 - Date created - 2014-10-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/IGC.0000000000000209 ER - TY - JOUR T1 - Association between treatment toxicity and outcomes in oncology clinical trials. AN - 1616481934; 25193993 AB - Whether or not toxicity predicts clinical outcomes has long been a question regarding cancer treatments. While prior studies have focused on specific cancers, therapies, and toxicities, no comprehensive evidence exists on whether treatment toxicity predicts favorable outcomes. We abstracted treatment toxicity and clinical outcome data from a sample of phase III oncology randomized clinical trials (n = 99 trials). We investigated whether treatments with relatively greater toxicity compared with their controls had relatively higher, lower, or equivocal rates of clinical efficacy, measured by progression-free survival (PFS) and overall survival (OS). Several toxicities were assessed (all grades, grades III/IV, cutaneous rash, gastrointestinal toxicity, and myelosuppression). Toxicity and efficacy were greater among treatments than controls (e.g. 3.5 instances of all-grade toxicity per patient in treatment arms versus 2.8 instances in controls, P < 0.001; mean PFS of 9.1 months across treatment arms versus 7.1 months across controls, P < 0.001; mean OS of 18.6 months across treatment arms versus 16.9 months across controls, P < 0.001). Across trials, greater relative treatment toxicity was strongly associated with greater PFS in treatments versus controls (P < 0.001), but not OS (P = 0.44). Although higher relative rates of myelosuppression and cutaneous rash among treatments were not associated with greater treatment efficacy, greater relative gastrointestinal toxicity among treatments was associated with greater relative PFS compared with controls (P = 0.007). Across trials, treatments with relatively greater all-grade toxicity compared with controls are associated with relatively greater PFS but not OS. © The Author 2014. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com. JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Abola, M V AU - Prasad, V AU - Jena, A B AD - Department of Family Medicine, Case Western Reserve University School of Medicine, Cleveland. ; Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda. ; Department of Health Care Policy, Harvard Medical School, Boston Department of Medicine, Massachusetts General Hospital, Boston, USA jena@hcp.med.harvard.edu. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 2284 EP - 2289 VL - 25 IS - 11 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - treatment toxicity KW - clinical trials KW - Randomized Controlled Trials as Topic KW - Clinical Trials, Phase III as Topic KW - Humans KW - Treatment Outcome KW - Neoplasms -- drug therapy KW - Disease-Free Survival KW - Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1616481934?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Association+between+treatment+toxicity+and+outcomes+in+oncology+clinical+trials.&rft.au=Abola%2C+M+V%3BPrasad%2C+V%3BJena%2C+A+B&rft.aulast=Abola&rft.aufirst=M&rft.date=2014-11-01&rft.volume=25&rft.issue=11&rft.spage=2284&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%2Fmdu444 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-03 N1 - Date created - 2014-10-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Genitourin Cancer. 2013 Jun;11(2):107-14 [23391371] N Engl J Med. 2013 Apr 11;368(15):1408-16 [23574119] Lancet Oncol. 2013 Sep;14(10):1020-6 [23948349] N Engl J Med. 2013 Nov 14;369(20):1915-25 [24224624] Breast Cancer Res Treat. 2014 Jan;143(1):159-69 [24305979] Br J Cancer. 1997;75(2):301-5 [9010042] Br J Cancer. 1999 Aug;80(11):1763-6 [10468293] Lancet Oncol. 2005 Sep;6(9):669-77 [16129367] Br J Cancer. 2005 Oct 3;93(7):744-8 [16160693] N Engl J Med. 2007 Jan 11;356(2):115-24 [17215529] Br J Cancer. 2007 Jul 2;97(1):37-42 [17551497] Oncologist. 2008 Mar;13(3):277-83 [18378537] Anticancer Res. 2008 Sep-Oct;28(5B):2913-20 [19031934] Lung Cancer. 2008 Dec;62(3):356-63 [18501466] J Clin Oncol. 2009 Jul 1;27(19):3073-6 [19451415] Lancet. 2009 Oct 17;374(9698):1331-8 [19767092] Acta Oncol. 2009;48(8):1204-6 [19863230] Lancet Oncol. 2011 Jan;12(1):30-7 [21169060] Br J Cancer. 2011 Jul 26;105(3):360-5 [21750553] J Clin Oncol. 2012 Sep 1;30(25):3051-7 [22851566] J Clin Oncol. 2013 Jun 20;31(18):2257-64 [23610112] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/annonc/mdu444 ER - TY - JOUR T1 - Moving beyond rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone for diffuse large B-cell lymphoma. AN - 1615745030; 24438195 AB - Diffuse large B-cell lymphoma (DLBCL) is the most common B-cell non-Hodgkin lymphoma (NHL). While the de facto treatment standard R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) is curative in most cases, it is ineffective for a significant proportion of patients, particularly those with intermediate and high-risk disease. Efforts to improve upon the results of R-CHOP have principally explored dose intensification of chemotherapy and resulted in considerable additive toxicity without clear benefit. DLBCL is not a uniform disease, however, and can be dissected into distinct molecular subtypes by gene expression profiling. These subtypes are characterized by distinct oncogenic mechanisms of activation and addictions to aberrant intracellular signaling pathways. Novel therapeutic agents that target these pathway addictions are emerging, and may have specific activity within molecular subtypes of DLBCL. To move beyond R-CHOP for all patients with DLBCL, targeted therapies added to the most effective chemotherapy platforms must be studied within the context of molecularly defined subsets. JF - Leukemia & lymphoma AU - Roschewski, Mark AU - Dunleavy, Kieron AU - Wilson, Wyndham H AD - Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Bethesda, MD , USA. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 2428 EP - 2437 VL - 55 IS - 11 KW - Antibodies, Monoclonal, Murine-Derived KW - 0 KW - Rituximab KW - 4F4X42SYQ6 KW - Vincristine KW - 5J49Q6B70F KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - chemotherapeutic approaches KW - Lymphoma and Hodgkin disease KW - molecular genetics KW - Cyclophosphamide -- administration & dosage KW - Humans KW - Antibodies, Monoclonal, Murine-Derived -- administration & dosage KW - Vincristine -- administration & dosage KW - Treatment Outcome KW - Doxorubicin -- administration & dosage KW - Prednisone -- administration & dosage KW - Lymphoma, Large B-Cell, Diffuse -- drug therapy KW - Molecular Targeted Therapy -- methods KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Molecular Targeted Therapy -- trends UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1615745030?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia+%26+lymphoma&rft.atitle=Moving+beyond+rituximab%2C+cyclophosphamide%2C+doxorubicin%2C+vincristine+and+prednisone+for+diffuse+large+B-cell+lymphoma.&rft.au=Roschewski%2C+Mark%3BDunleavy%2C+Kieron%3BWilson%2C+Wyndham+H&rft.aulast=Roschewski&rft.aufirst=Mark&rft.date=2014-11-01&rft.volume=55&rft.issue=11&rft.spage=2428&rft.isbn=&rft.btitle=&rft.title=Leukemia+%26+lymphoma&rft.issn=1029-2403&rft_id=info:doi/10.3109%2F10428194.2014.883075 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-20 N1 - Date created - 2014-10-22 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/10428194.2014.883075 ER - TY - JOUR T1 - Incidence of hospitalization in patients receiving short course palliative cranial radiotherapy on outpatient basis in a limited resource setting - Experience from a regional cancer center in India. AN - 1615739090; 25337417 AB - To investigate incidence of toxicity and related hospitalization among patients treated at our institute by a short course of palliative cranial radiotherapy against a longer, widely established schedule. Shorter schedule palliative cranial radiotherapy is more convenient for patients and reduce waiting times. Although many studies have established safety of short schedules, the need for hospitalization due to acute treatment toxicity remains under-explored. Hospital admissions are an economic burden both for the patient and healthcare system in a limited resource setting. Delivery of treatment on an outpatient basis and within shorter times is preferred by patients, caregivers and healthcare staff. This was a prospective study on 68 patients treated with palliative whole brain radiotherapy between November 2010 and October 2012. One group received 20 Gy in 5 fractions over 1 week and the other group, 30 Gy in 10 fractions over 2 weeks. Treatment toxicity due to cranial radiotherapy was assessed as per RTOG acute and late toxicity criteria. Need for hospitalization owing to acute toxicity was also noted. Significant differences in the study parameters between the two groups were calculated by Fisher's t-test. Requirement for hospital stay due to acute toxicity was not significantly different between the two groups. Patients in both groups experienced similar toxicity both during and after treatment. The shorter course entailed no significant increase in toxicity related admissions, suitable for limited resource settings where patient transport is difficult, there are financial constraints, and the healthcare system is overburdened. JF - Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology AU - Gangopadhyay, Aparna AU - Das, Joydeep AU - Nath, Partha AU - Maji, Tapas AU - Biswas, Jaydip AD - Dept. of Radiation Oncology, Chittaranjan National Cancer Institute, Kolkata, India. ; Dept. of Medical Oncology, Chittaranjan National Cancer Institute, Kolkata, India. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 428 EP - 432 VL - 19 IS - 6 SN - 1507-1367, 1507-1367 KW - Palliative cranial radiation KW - Radiation toxicity and patient care KW - In-hospital care for brain metastases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1615739090?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reports+of+practical+oncology+and+radiotherapy+%3A+journal+of+Greatpoland+Cancer+Center+in+Poznan+and+Polish+Society+of+Radiation+Oncology&rft.atitle=Incidence+of+hospitalization+in+patients+receiving+short+course+palliative+cranial+radiotherapy+on+outpatient+basis+in+a+limited+resource+setting+-+Experience+from+a+regional+cancer+center+in+India.&rft.au=Gangopadhyay%2C+Aparna%3BDas%2C+Joydeep%3BNath%2C+Partha%3BMaji%2C+Tapas%3BBiswas%2C+Jaydip&rft.aulast=Gangopadhyay&rft.aufirst=Aparna&rft.date=2014-11-01&rft.volume=19&rft.issue=6&rft.spage=428&rft.isbn=&rft.btitle=&rft.title=Reports+of+practical+oncology+and+radiotherapy+%3A+journal+of+Greatpoland+Cancer+Center+in+Poznan+and+Polish+Society+of+Radiation+Oncology&rft.issn=15071367&rft_id=info:doi/10.1016%2Fj.rpor.2014.04.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-22 N1 - Date created - 2014-10-22 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.rpor.2014.04.006 ER - TY - JOUR T1 - Phase 1 study of the antimesothelin immunotoxin SS1P in combination with pemetrexed and cisplatin for front-line therapy of pleural mesothelioma and correlation of tumor response with serum mesothelin, megakaryocyte potentiating factor, and cancer antigen 125. AN - 1615262375; 24989332 AB - The primary objective of this study was to determine the safety and maximum tolerated dose (MTD) of the antimesothelin immunotoxin SS1(dsFv)PE38 (SS1P) (a recombinant antimesothelin immunotoxin consisting of a murine antimesothelin variable antibody fragment [Fv] linked to PE38, a truncated portion of Pseudomonas exotoxin A) in combination with pemetrexed and cisplatin in chemotherapy-naive patients with advanced malignant pleural mesothelioma (MPM). Secondary objectives included tumor response, SS1P pharmacokinetics, and serum biomarkers of response. Chemotherapy-naive patients with stage III or IV, unresectable, epithelial or biphasic MPM and normal organ functions were eligible. Pemetrexed (500 mg/m(2) on day 1) and cisplatin (75 mg/m(2) on day 1) were administered every 3 weeks for up to 6 cycles with escalating doses of SS1P administered intravenously on days 1, 3, and 5 during cycles 1 and 2. Tumor response was evaluated every 6 weeks. Twenty-four patients received SS1P at 4 dose levels from 25 to 55 mcg/kg. Grade 3 fatigue was dose-limiting in 1 patient at 55 mcg/kg. The MTD of SS1P was established as 45 mcg/kg. Other grade 3 toxicities associated with SS1P included hypoalbuminemia (21%), back pain (13%), and hypotension (8%). Of 20 evaluable patients, 12 (60%) had a partial response, 3 had stable disease, and 5 had progressive disease. Of 13 patients who received the MTD, 10 (77%) had a partial response, 1 had stable disease, and 2 had progressive disease. Objective radiologic responses were associated with significant decreases in serum mesothelin (P=.0030), megakaryocyte potentiating factor (P=.0005), and cancer antigen 125 (P < .0001). SS1P given with pemetrexed and cisplatin is safe and well tolerated and exhibits significant antitumor activity in patients with unresectable, advanced pleural mesothelioma. Serum mesothelin, megakaryocyte potentiating factor, and cancer antigen 125 levels correlated with objective tumor responses. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - Cancer AU - Hassan, Raffit AU - Sharon, Elad AU - Thomas, Anish AU - Zhang, Jingli AU - Ling, Alexander AU - Miettinen, Markku AU - Kreitman, Robert J AU - Steinberg, Seth M AU - Hollevoet, Kevin AU - Pastan, Ira AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/11/01/ PY - 2014 DA - 2014 Nov 01 SP - 3311 EP - 3319 VL - 120 IS - 21 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - CA-125 Antigen KW - Exotoxins KW - GPI-Linked Proteins KW - Glutamates KW - SS1(dsFv)PE38 KW - Virulence Factors KW - mesothelin KW - Pemetrexed KW - 04Q9AIZ7NO KW - Guanine KW - 5Z93L87A1R KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Cisplatin KW - Q20Q21Q62J KW - Abridged Index Medicus KW - Index Medicus KW - pleural mesothelioma KW - SS1P KW - immunotoxin KW - Neoplasm Staging KW - Humans KW - Aged KW - GPI-Linked Proteins -- administration & dosage KW - Cisplatin -- administration & dosage KW - CA-125 Antigen -- blood KW - GPI-Linked Proteins -- blood KW - Middle Aged KW - Maximum Tolerated Dose KW - Female KW - Male KW - Antibodies, Monoclonal -- blood KW - Pleural Neoplasms -- blood KW - Lung Neoplasms -- blood KW - Lung Neoplasms -- drug therapy KW - Pleural Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Antibodies, Monoclonal -- administration & dosage KW - Guanine -- administration & dosage KW - Mesothelioma -- drug therapy KW - Mesothelioma -- blood KW - Glutamates -- administration & dosage KW - Pleural Neoplasms -- drug therapy KW - Mesothelioma -- pathology KW - Guanine -- analogs & derivatives KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1615262375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+1+study+of+the+antimesothelin+immunotoxin+SS1P+in+combination+with+pemetrexed+and+cisplatin+for+front-line+therapy+of+pleural+mesothelioma+and+correlation+of+tumor+response+with+serum+mesothelin%2C+megakaryocyte+potentiating+factor%2C+and+cancer+antigen+125.&rft.au=Hassan%2C+Raffit%3BSharon%2C+Elad%3BThomas%2C+Anish%3BZhang%2C+Jingli%3BLing%2C+Alexander%3BMiettinen%2C+Markku%3BKreitman%2C+Robert+J%3BSteinberg%2C+Seth+M%3BHollevoet%2C+Kevin%3BPastan%2C+Ira&rft.aulast=Hassan&rft.aufirst=Raffit&rft.date=2014-11-01&rft.volume=120&rft.issue=21&rft.spage=3311&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=1097-0142&rft_id=info:doi/10.1002%2Fcncr.28875 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-13 N1 - Date created - 2014-10-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: Cancer. 2014 Nov 1;120(21):3268-71 [24989696] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/cncr.28875 ER - TY - JOUR T1 - Correlation between CYP1A1 transcript, protein level, enzyme activity and DNA adduct formation in normal human mammary epithelial cell strains exposed to benzo[a]pyrene. AN - 1614694870; 25245543 AB - The polycyclic aromatic hydrocarbon (PAH) benzo(a)pyrene (BP) is thought to bind covalently to DNA, through metabolism by cytochrome P450 1A1 (CYP1A1) and CYP1B1, and other enzymes, to form r7, t8, t9-trihydroxy-c-10-(N(2)-deoxyguanosyl)-7,8,9,10-tetrahydro-benzo[a]-pyrene (BPdG). Evaluation of RNA expression data, to understand the contribution of different metabolic enzymes to BPdG formation, is typically presented as fold-change observed upon BP exposure, leaving the actual number of RNA transcripts unknown. Here, we have quantified RNA copies/ng cDNA (RNA cpn) for CYP1A1 and CYP1B1, as well as quinone oxidoreductase 1 (NQO1), which may reduce formation of BPdG adducts, using primary normal human mammary epithelial cell (NHMEC) strains, and the MCF-7 breast cancer cell line. In unexposed NHMECs, basal RNA cpn values were 58-836 for CYP1A1, 336-5587 for CYP1B1 and 5943-40112 for NQO1. In cells exposed to 4.0 µM BP for 12h, RNA cpn values were 251-13234 for CYP1A1, 4133-57078 for CYP1B1 and 4456-55887 for NQO1. There were 3.5 (mean, range 0.2-15.8) BPdG adducts/10(8) nucleotides in the NHMECs (n = 16), and 790 in the MCF-7s. In the NHMECs, BP-induced CYP1A1 RNA cpn was highly associated with BPdG (P = 0.002), but CYP1B1 and NQO1 were not. Western blots of four NHMEC strains, chosen for different levels of BPdG adducts, showed a linear correlation between BPdG and CYP1A1, but not CYP1B1 or NQO1. Ethoxyresorufin-O-deethylase (EROD) activity, which measures CYP1A1 and CYP1B1 together, correlated with BPdG, but NQO1 activity did not. Despite more numerous levels of CYP1B1 and NQO1 RNA cpn in unexposed and BP-exposed NHMECs and MCF-7cells, BPdG formation was only correlated with induction of CYP1A1 RNA cpn. The higher level of BPdG in MCF-7 cells, compared to NHMECs, may have been due to a much increased induction of CYP1A1 and EROD. Overall, BPdG correlation was observed with CYP1A1 protein and CYP1A1/1B1 enzyme activity, but not with CYP1B1 or NQO1 protein, or NQO1 enzyme activity. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society 2014. JF - Mutagenesis AU - Divi, Rao L AU - Lindeman, Tracey L Einem AU - Shockley, Marie E AU - Keshava, Channa AU - Weston, Ainsley AU - Poirier, Miriam C AD - Carcinogen-DNA Interactions Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20817, USA, National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA and Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV 26505, USA. ; National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA and. ; Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV 26505, USA. ; Carcinogen-DNA Interactions Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20817, USA, National Center for Environmental Assessment, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA and Division of Respiratory Disease Studies, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV 26505, USA. poirierm@exchange.nih.gov. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 409 EP - 417 VL - 29 IS - 6 KW - DNA Adducts KW - 0 KW - RNA, Messenger KW - Benzo(a)pyrene KW - 3417WMA06D KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP1B1 KW - NAD(P)H Dehydrogenase (Quinone) KW - EC 1.6.5.2 KW - NQO1 protein, human KW - Index Medicus KW - Blotting, Western KW - RNA, Messenger -- metabolism KW - Cytochrome P-450 CYP1B1 -- metabolism KW - Humans KW - MCF-7 Cells KW - NAD(P)H Dehydrogenase (Quinone) -- metabolism KW - RNA, Messenger -- genetics KW - Epithelial Cells -- metabolism KW - Mammary Glands, Human -- cytology KW - Cytochrome P-450 CYP1A1 -- genetics KW - Epithelial Cells -- drug effects KW - Benzo(a)pyrene -- toxicity KW - Cytochrome P-450 CYP1A1 -- metabolism KW - DNA Adducts -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1614694870?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutagenesis&rft.atitle=Correlation+between+CYP1A1+transcript%2C+protein+level%2C+enzyme+activity+and+DNA+adduct+formation+in+normal+human+mammary+epithelial+cell+strains+exposed+to+benzo%5Ba%5Dpyrene.&rft.au=Divi%2C+Rao+L%3BLindeman%2C+Tracey+L+Einem%3BShockley%2C+Marie+E%3BKeshava%2C+Channa%3BWeston%2C+Ainsley%3BPoirier%2C+Miriam+C&rft.aulast=Divi&rft.aufirst=Rao&rft.date=2014-11-01&rft.volume=29&rft.issue=6&rft.spage=409&rft.isbn=&rft.btitle=&rft.title=Mutagenesis&rft.issn=1464-3804&rft_id=info:doi/10.1093%2Fmutage%2Fgeu049 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-18 N1 - Date created - 2014-10-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Carcinogenesis. 2000 Jul;21(7):1281-9 [10874004] Discov Med. 2012 Oct;14(77):283-8 [23114584] Cancer Res. 2001 Dec 1;61(23):8465-9 [11731429] Environ Mol Mutagen. 2002;39(2-3):201-7 [11921190] Carcinogenesis. 2002 Dec;23(12):2043-9 [12507927] Methods Enzymol. 2004;382:115-44 [15047100] Nature. 1974 Nov 22;252(5481):326-8 [4473724] In Vitro. 1980 May;16(5):415-25 [6993343] Br J Cancer. 1981 Jul;44(1):24-34 [6789855] Nature. 1983 Jun 9-15;303(5917):468-72 [6304528] Prog Clin Biol Res. 1989;298:3-15 [2501799] Nucleic Acids Res. 1991 Aug 11;19(15):4293 [1870982] Carcinogenesis. 1991 Oct;12(10):1939-44 [1934274] Carcinogenesis. 1994 Feb;15(2):247-52 [8313515] Proc Natl Acad Sci U S A. 1994 Aug 30;91(18):8413-7 [8078896] Br J Cancer. 1998 Mar;77(5):709-19 [9514048] Carcinogenesis. 1998 Nov;19(11):1949-53 [9855008] Chem Res Toxicol. 1999 Jul;12(7):623-9 [10409402] Mol Pharmacol. 1999 Oct;56(4):760-7 [10496959] Mar Biotechnol (NY). 2004 Jul-Aug;6(4):307-11 [15546046] Cancer Lett. 2005 Apr 28;221(2):213-24 [15808407] Toxicol Lett. 2006 Mar 15;162(1):3-15 [16321483] Mol Pharmacol. 2006 Apr;69(4):1103-14 [16377763] Arch Environ Health. 2004 Dec;59(12):640-9 [16789472] Toxicol Lett. 2006 Dec 15;167(3):173-82 [17049425] Chem Res Toxicol. 2007 Mar;20(3):424-31 [17295519] Carcinogenesis. 2007 Mar;28(3):611-24 [16973675] Epidemiology. 2007 May;18(3):373-82 [17435448] Cancer. 2007 Jun 15;109(12 Suppl):2667-711 [17503436] Drug Metab Dispos. 2007 Jul;35(7):1009-16 [17431034] Carcinogenesis. 2007 Jul;28(7):1426-9 [17277232] Chem Res Toxicol. 2008 Jan;21(1):70-83 [18052394] Environ Mol Mutagen. 2009 Mar;50(2):134-44 [19152381] Int J Cancer. 2010 Nov 15;127(10):2334-50 [20127859] IARC Monogr Eval Carcinog Risks Hum. 2010;92:1-853 [21141735] Breast Cancer Res Treat. 2011 Sep;129(2):477-84 [21452020] Int J Environ Res Public Health. 2011 Jul;8(7):2675-91 [21845152] Toxicol Lett. 2012 Sep 3;213(2):160-6 [22759596] Carcinogenesis. 2000 Jul;21(7):1433-40 [10874023] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/mutage/geu049 ER - TY - JOUR T1 - Adolescent alcohol use: a reflection of national drinking patterns and policy? AN - 1613949946; 4610454 AB - To analyse how adolescent drunkenness and frequency of drinking were associated with adult drinking patterns and alcohol control policies. Cross-sectional survey data on 13- and 15-year-olds in 37 countries who participated in the Health Behaviour in School-Aged Children (HBSC) Study in 2010 (n=144788) were linked to national-level indicators on alcohol control policies and adult drinking patterns. Outcome measures were self-reported weekly drinking and life-time drunkenness (drunk once or more). Data were analysed using multi-level logistic regression models. In the mutually adjusted models, adolescent drunkenness was associated significantly with high adult alcohol consumption [odds ratio (OR)=3.15 among boys, 95% confidence interval (CI)=2.13-4.64, OR girls=2.44, CI=1.57-3.80] and risky drinking patterns in the adult population (OR boys=2.02, CI=1.33-3.05, OR girls=1.61, CI=1.18-2.18). The level of abstainers in the adult population was also associated significantly with girls' drunkenness; a 10% increase in the number of abstainers in a country reduced the odds of drunkenness with 21% (OR=0.79, CI= 0.68-0.90). Weekly drinking was associated significantly with weak restrictions on availability (OR boys=2.82, CI=1.74-4.54, OR girls=2.00, CI=1.15-3.46) and advertising (OR boys=1.56, CI=1.02-2.40, OR girls=1.79, CI=1.10-2.94). Comparing data cross-nationally, high levels of adult alcohol consumption and limited alcohol control policies are associated with high levels of alcohol use among adolescents. Reprinted by permission of Blackwell Publishing JF - Addiction AU - Ter Bogt, Tom AU - Holstein, Bjørn E AU - Bendtsen, Pernille AU - Damsgaard, Mogens Trab AU - Huckle, Taisia AU - Casswell, Sally AU - Kuntsche, Emmanuel AU - Arnold, Petra AU - De Looze, Margreet E AU - Hofmann, Felix AU - Hublet, Anne AU - Simons-Morton, Bruce AD - University of Southern Denmark ; Massey University ; Swiss Institute for the Prevention of Alcohol and Drug Problems ; Radboud University Nijmegen ; Utrecht University ; Ludwig Boltzmann Institut ; Ghent University ; Eunice Kennedy Shriver National Institute of Child Health and Human Development Y1 - 2014/11// PY - 2014 DA - Nov 2014 SP - 1857 EP - 1868 VL - 109 IS - 11 SN - 0965-2140, 0965-2140 KW - Sociology KW - Alcohol KW - Adolescence KW - Alcoholism KW - Regression analysis KW - Consumption KW - Advertising KW - Youth KW - Adolescents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1613949946?accountid=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=Adolescent+alcohol+use%3A+a+reflection+of+national+drinking+patterns+and+policy%3F&rft.au=Ter+Bogt%2C+Tom%3BHolstein%2C+Bj%C3%B8rn+E%3BBendtsen%2C+Pernille%3BDamsgaard%2C+Mogens+Trab%3BHuckle%2C+Taisia%3BCasswell%2C+Sally%3BKuntsche%2C+Emmanuel%3BArnold%2C+Petra%3BDe+Looze%2C+Margreet+E%3BHofmann%2C+Felix%3BHublet%2C+Anne%3BSimons-Morton%2C+Bruce&rft.aulast=Ter+Bogt&rft.aufirst=Tom&rft.date=2014-11-01&rft.volume=109&rft.issue=11&rft.spage=1857&rft.isbn=&rft.btitle=&rft.title=Addiction&rft.issn=09652140&rft_id=info:doi/10.1111%2Fadd.12681 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-10-20 N1 - Last updated - 2014-10-20 N1 - SubjectsTermNotLitGenreText - 590 652 5676 646 6091; 593; 13779 652 5676 646 6091; 909; 913 561 6220; 608 7738 11245 11239; 2805 3872 554 971; 10739 12228 10919 DO - http://dx.doi.org/10.1111/add.12681 ER - TY - JOUR T1 - DNA methyltransferases 3a and 3b are differentially expressed in the early stages of a rat liver carcinogenesis model. AN - 1613942424; 25190601 AB - Carcinogenesis is driven by the accumulation of mutations and abnormal DNA methylation patterns, particularly the hypermethylation of tumor‑suppressor genes. Changes in genomic DNA methylation patterns are established by the DNA methyltransferases (DNMTs) family: DNMT1, DNMT3a and DNMT3b. The DNMTs are known to be overexpressed in tumors. However, when the DNMTs expression profile is altered in earlier stages of carcinogenesis remains to be elucidated. The resistant hepatocyte model (RHM) allows the analysis of the hepatocellular carcinoma (HCC) from the formation of altered cell foci to the appearance of tumors in rats. To investigate the DNMTs expression in this model, we first observed that timp3, rassf1a and p16 genes became methylated during cancer development by methylation‑specific PCR (MSP) and the bisulphate sequencing PCR (BSP) of timp3. The differential expression at the RNA and protein level of the three DNMTs was also assessed. dnmt1 expression was higher in tumors than in normal and early cancer stages. However, no evident overexpression of the enzyme was identified by immunohistochemistry. By contrast, DNMT3a and DNMT3b were consistently subexpressed in tumors. In the present study, we report a carcinogenesis model that does not feature the overexpression of DNMT1 but exhibits a transient expression of DNMT3a and DNMT3b. JF - Oncology reports AU - Valencia Antúnez, Carlos Alberto AU - Taja Chayeb, Lucía AU - Rodríguez-Segura, Miguel Ángel AU - López Álvarez, Guadalupe Soledad AU - García-Cuéllar, Claudia M AU - Villa Treviño, Saúl AD - Department of Cell Biology Center for Research and Advanced Studies (CINVESTAV) IPN, Basic Research Branch, Mexico, D.F., Mexico. ; National Cancer Institute, Basic Research Branch, Mexico, D.F., Mexico. ; Department of Physics, Center for Research and Advanced Studies (CINVESTAV) IPN, Basic Research Branch, Mexico, D.F., Mexico. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 2093 EP - 2103 VL - 32 IS - 5 KW - Cyclin-Dependent Kinase Inhibitor p16 KW - 0 KW - RASSF1 protein, rat KW - Tissue Inhibitor of Metalloproteinase-3 KW - Tumor Suppressor Proteins KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - DNA (Cytosine-5-)-Methyltransferase KW - EC 2.1.1.37 KW - DNA methyltransferase 3A KW - DNA methyltransferase 3B KW - Index Medicus KW - Rats KW - Gene Expression Regulation, Neoplastic KW - Animals KW - DNA Methylation KW - Tumor Suppressor Proteins -- genetics KW - Tissue Inhibitor of Metalloproteinase-3 -- genetics KW - Cyclin-Dependent Kinase Inhibitor p16 -- genetics KW - Male KW - DNA (Cytosine-5-)-Methyltransferase -- genetics KW - Liver Neoplasms, Experimental -- pathology KW - Liver Neoplasms, Experimental -- enzymology KW - Liver Neoplasms, Experimental -- chemically induced KW - DNA (Cytosine-5-)-Methyltransferase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1613942424?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+methyltransferases+3a+and+3b+are+differentially+expressed+in+the+early+stages+of+a+rat+liver+carcinogenesis+model.&rft.au=Valencia+Ant%C3%BAnez%2C+Carlos+Alberto%3BTaja+Chayeb%2C+Luc%C3%ADa%3BRodr%C3%ADguez-Segura%2C+Miguel+%C3%81ngel%3BL%C3%B3pez+%C3%81lvarez%2C+Guadalupe+Soledad%3BGarc%C3%ADa-Cu%C3%A9llar%2C+Claudia+M%3BVilla+Trevi%C3%B1o%2C+Sa%C3%BAl&rft.aulast=Valencia+Ant%C3%BAnez&rft.aufirst=Carlos&rft.date=2014-11-01&rft.volume=32&rft.issue=5&rft.spage=2093&rft.isbn=&rft.btitle=&rft.title=Oncology+reports&rft.issn=1791-2431&rft_id=info:doi/10.3892%2For.2014.3462 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-26 N1 - Date created - 2014-10-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3892/or.2014.3462 ER - TY - JOUR T1 - Raltegravir pharmacokinetics in neonates following maternal dosing. AN - 1612290493; 25162819 AB - : International Maternal Pediatric Adolescent AIDS Clinical Trials P1097 was a multicenter trial to determine washout pharmacokinetics and safety of in utero/intrapartum exposure to raltegravir in infants born to HIV-infected pregnant women receiving raltegravir-based antiretroviral therapy. Twenty-two mother-infant pairs were enrolled; evaluable pharmacokinetic data were available from 19 mother-infant pairs. Raltegravir readily crossed the placenta, with a median cord blood/maternal delivery plasma raltegravir concentration ratio of 1.48 (range, 0.32-4.33). Raltegravir elimination was highly variable and extremely prolonged in some infants; [median t1/2 26.6 (range, 9.3-184) hours]. Prolonged raltegravir elimination likely reflects low neonatal UGT1A1 enzyme activity and enterohepatic recirculation. Excessive raltegravir concentrations must be avoided in the neonate because raltegravir at high plasma concentrations may increase the risk of bilirubin neurotoxicity. Subtherapeutic concentrations, which could lead to inadequate viral suppression and development of raltegravir resistance, must also be avoided. Two ongoing International Maternal Pediatric Adolescent AIDS Clinical Trials studies are further investigating the pharmacology of raltegravir in neonates. JF - Journal of acquired immune deficiency syndromes (1999) AU - Clarke, Diana F AU - Acosta, Edward P AU - Rizk, Matthew L AU - Bryson, Yvonne J AU - Spector, Stephen A AU - Mofenson, Lynne M AU - Handelsman, Edward AU - Teppler, Hedy AU - Welebob, Carolee AU - Persaud, Deborah AU - Cababasay, Mae P AU - Wang, JiaJia AU - Mirochnick, Mark AU - International Maternal Pediatric Adolescent AIDS Clinical Trials (IMPAACT) P1097 Study Team AD - *Section of Pediatric Infectious Diseases, Boston Medical Center, Boston, MA; †Division of Clinical Pharmacology, University of Alabama at Birmingham, Birmingham, AL; ‡Merck & Co., Inc., Whitehouse Station, NJ; §Department of Pediatric Infectious Diseases, David Geffen School of Medicine at University of California at Los Angeles, Los Angeles, CA; ‖Department of Pediatrics, University of California, San Diego and Rady Children's Hospital San Diego, La Jolla, CA; ¶Eunice Kennedy Shriver National Institute of Child Health and Human Development, #Division of AIDS, National Institute of Health, Bethesda, MD; **Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD; ††Statistical and Data Analysis Center, Harvard School of Public Health, Boston, MA; and ‡‡Department of Pediatrics, Boston University School of Medicine, Boston, MA. ; International Maternal Pediatric Adolescent AIDS Clinical Trials (IMPAACT) P1097 Study Team Y1 - 2014/11/01/ PY - 2014 DA - 2014 Nov 01 SP - 310 EP - 315 VL - 67 IS - 3 KW - Anti-HIV Agents KW - 0 KW - Pyrrolidinones KW - Raltegravir Potassium KW - 43Y000U234 KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Adult KW - Infant, Newborn KW - Male KW - Female KW - Pregnancy KW - Anti-HIV Agents -- pharmacokinetics KW - HIV Infections -- drug therapy KW - Pregnancy Complications, Infectious -- metabolism KW - HIV Infections -- metabolism KW - Anti-HIV Agents -- administration & dosage KW - Pyrrolidinones -- pharmacokinetics KW - Pregnancy Complications, Infectious -- drug therapy KW - Pyrrolidinones -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1612290493?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+acquired+immune+deficiency+syndromes+%281999%29&rft.atitle=Raltegravir+pharmacokinetics+in+neonates+following+maternal+dosing.&rft.au=Clarke%2C+Diana+F%3BAcosta%2C+Edward+P%3BRizk%2C+Matthew+L%3BBryson%2C+Yvonne+J%3BSpector%2C+Stephen+A%3BMofenson%2C+Lynne+M%3BHandelsman%2C+Edward%3BTeppler%2C+Hedy%3BWelebob%2C+Carolee%3BPersaud%2C+Deborah%3BCababasay%2C+Mae+P%3BWang%2C+JiaJia%3BMirochnick%2C+Mark%3BInternational+Maternal+Pediatric+Adolescent+AIDS+Clinical+Trials+%28IMPAACT%29+P1097+Study+Team&rft.aulast=Clarke&rft.aufirst=Diana&rft.date=2014-11-01&rft.volume=67&rft.issue=3&rft.spage=310&rft.isbn=&rft.btitle=&rft.title=Journal+of+acquired+immune+deficiency+syndromes+%281999%29&rft.issn=1944-7884&rft_id=info:doi/10.1097%2FQAI.0000000000000316 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-15 N1 - Date created - 2014-10-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Perinatol. 2001 Dec;21 Suppl 1:S40-2; discussion S59-62 [11803415] Toxicology. 2002 Dec 27;181-182:453-6 [12505351] Pediatrics. 2004 Jul;114(1):297-316 [15231951] Biochem J. 1979 Dec 15;184(3):705-7 [120201] Pediatrics. 1956 Oct;18(4):614-25 [13370229] Clin Pharmacol Ther. 2008 Feb;83(2):293-9 [17713476] Antimicrob Agents Chemother. 2013 Dec;57(12):6393-4 [24080650] Expert Opin Drug Metab Toxicol. 2010 Sep;6(9):1151-60 [20701552] AIDS. 2010 Sep 24;24(15):2416-8 [20827058] N Engl J Med. 2012 Jun 21;366(25):2368-79 [22716975] AIDS. 2012 Nov 28;26(18):2421-3 [23151500] Pediatr Infect Dis J. 2013 Sep;32(9):978-80 [23470680] N Engl J Med. 2013 Nov 7;369(19):1828-35 [24152233] J Chromatogr B Analyt Technol Biomed Life Sci. 2008 May 15;867(2):165-71 [18430616] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/QAI.0000000000000316 ER - TY - JOUR T1 - Activity of the EGFR-HER2 dual inhibitor afatinib in EGFR-mutant lung cancer patients with acquired resistance to reversible EGFR tyrosine kinase inhibitors. AN - 1611618184; 25242668 AB - The purpose of this study was to evaluate the efficacy of afatinib in EGFR-mutant metastatic NSCLC patients with acquired resistance to erlotinib or gefitinib. We retrospectively analyzed the outcome of patients with EGFR-mutant advanced NSCLC treated with afatinib after failure of chemotherapy and EGFR TKIs. A total of 96 individuals were included in the study. According to EGFR status, most patients (n = 63; 65.6%) harbored a deletion in exon 19, and de novo T790M mutation was detected in 2 cases (T790M and exon 19). Twenty-four (25%) patients underwent repeated biopsy immediately before starting afatinib and secondary T790M was detected in 8 (33%) samples. Among the 86 patients evaluable for efficacy, response rate was 11.6%, with a median progression free-survival (PFS) and overall survival (OS) of 3.9 and 7.3 months, respectively. No significant difference in PFS and OS was observed according to type of last therapy received before afatinib, type of EGFR mutation or adherence to Jackman criteria, and patients benefiting from afatinib therapy had longer PFS and OS (P < .001). Outcome results for repeated biopsy patients were similar to the whole population, with no evidence of response in T790M-positive patients. All patients were evaluable for toxicity, and 81% experienced an AE of any grade, with grade 3 to 4 AEs, mainly diarrhea and skin toxicity, occurring in 19 (20%) patients. Our results showed that afatinib has only modest efficacy in a real life population of EGFR mutant NSCLC patients with acquired resistance to erlotinib or gefitinib. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Clinical lung cancer AU - Landi, Lorenza AU - Tiseo, Marcello AU - Chiari, Rita AU - Ricciardi, Serena AU - Rossi, Elisa AU - Galetta, Domenico AU - Novello, Silvia AU - Milella, Michele AU - D'Incecco, Armida AU - Minuti, Gabriele AU - Tibaldi, Carmelo AU - Salvini, Jessica AU - Facchinetti, Francesco AU - Haspinger, Eva Regina AU - Cortinovis, Diego AU - Santo, Antonio AU - Banna, Giuseppe AU - Catino, Annamaria AU - GiajLevra, Matteo AU - Crinò, Lucio AU - de Marinis, Filippo AU - Cappuzzo, Federico AD - Department of MedicalOncology, Istituto Toscano Tumori, Livorno, Italy. ; Medical Oncology Unit, University Hospital of Parma, Parma, Italy. ; Division of Medical Oncology, Ospedale Santa Maria della Misericordia, Perugia, Italy. ; High Specialization Hospitals, Oncological Pulmonary First Unit, Rome, Italy. ; Fondazione Ricerca Traslazionale, FoRT, Rome, Italy. ; Division Of Medical Oncology, Istituto Tumori "Giovanni Paolo II", IRCCS, Bari, Italy. ; Department of Oncology, University of Turin, Azienda Ospedaliero-Universitaria, San Luigi Gonzaga, Turin, Italy. ; Division of Medical Oncology A, Regina Elena National Cancer Institute, Rome, Italy. ; Division of Medical Oncology, Fondazione IRCSS Istituto Nazionale dei Tumori, Milan, Italy. ; Division of Medical Oncology, Ospedale San Gerardo, Monza, Italy. ; Division of Medical Oncology, Azienda Ospedaliera Universitaria Integrate, Verona, Italy. ; Medical Oncology Service, Cannizzaro Hospital, Catania, Italy. ; Division of Thoracic Oncology, Istituto Europeo di Oncologia, Milano, Italy. ; Department of MedicalOncology, Istituto Toscano Tumori, Livorno, Italy. Electronic address: f.cappuzzo@gmail.com. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 411 EP - 417.e4 VL - 15 IS - 6 KW - Antineoplastic Agents KW - 0 KW - Protein Kinase Inhibitors KW - Quinazolines KW - afatinib KW - 41UD74L59M KW - EGFR protein, human KW - EC 2.7.10.1 KW - ERBB2 protein, human KW - Receptor, Epidermal Growth Factor KW - Receptor, ErbB-2 KW - Index Medicus KW - Erlotinib KW - Afatinib KW - NSCLC KW - Gefitinib KW - Acquired resistance KW - Receptor, Epidermal Growth Factor -- antagonists & inhibitors KW - Disease-Free Survival KW - Neoplasm Staging KW - Receptor, ErbB-2 -- antagonists & inhibitors KW - Humans KW - Retrospective Studies KW - Aged KW - Receptor, Epidermal Growth Factor -- genetics KW - Aged, 80 and over KW - Adult KW - Treatment Outcome KW - Neoplasm Metastasis KW - Mutation -- genetics KW - Middle Aged KW - Diarrhea -- etiology KW - Female KW - Male KW - Quinazolines -- administration & dosage KW - Protein Kinase Inhibitors -- therapeutic use KW - Protein Kinase Inhibitors -- pharmacology KW - Carcinoma, Non-Small-Cell Lung -- mortality KW - Antineoplastic Agents -- administration & dosage KW - Lung Neoplasms -- drug therapy KW - Lung Neoplasms -- mortality KW - Drug Resistance, Neoplasm KW - Quinazolines -- adverse effects KW - Carcinoma, Non-Small-Cell Lung -- drug therapy KW - Lung Neoplasms -- pathology KW - Carcinoma, Non-Small-Cell Lung -- pathology KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611618184?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+lung+cancer&rft.atitle=Activity+of+the+EGFR-HER2+dual+inhibitor+afatinib+in+EGFR-mutant+lung+cancer+patients+with+acquired+resistance+to+reversible+EGFR+tyrosine+kinase+inhibitors.&rft.au=Landi%2C+Lorenza%3BTiseo%2C+Marcello%3BChiari%2C+Rita%3BRicciardi%2C+Serena%3BRossi%2C+Elisa%3BGaletta%2C+Domenico%3BNovello%2C+Silvia%3BMilella%2C+Michele%3BD%27Incecco%2C+Armida%3BMinuti%2C+Gabriele%3BTibaldi%2C+Carmelo%3BSalvini%2C+Jessica%3BFacchinetti%2C+Francesco%3BHaspinger%2C+Eva+Regina%3BCortinovis%2C+Diego%3BSanto%2C+Antonio%3BBanna%2C+Giuseppe%3BCatino%2C+Annamaria%3BGiajLevra%2C+Matteo%3BCrin%C3%B2%2C+Lucio%3Bde+Marinis%2C+Filippo%3BCappuzzo%2C+Federico&rft.aulast=Landi&rft.aufirst=Lorenza&rft.date=2014-11-01&rft.volume=15&rft.issue=6&rft.spage=411&rft.isbn=&rft.btitle=&rft.title=Clinical+lung+cancer&rft.issn=1938-0690&rft_id=info:doi/10.1016%2Fj.cllc.2014.07.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-19 N1 - Date created - 2014-10-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.cllc.2014.07.002 ER - TY - JOUR T1 - Oesophageal squamous cell carcinoma in high-risk Chinese populations: Possible role for vascular epithelial growth factor A. AN - 1610760353; 25172294 AB - Mechanisms involved in wound healing play some role in carcinogenesis in multiple organs, likely by creating a chronic inflammatory milieu. This study sought to assess the role of genetic markers in selected inflammation-related genes involved in wound healing (interleukin (IL)-1a, IL-1b, IL-1 Receptor type I (IL-1Ra), IL-1 Receptor type II (IL-1Rb), tumour necrosis factor (TNF)-α, tumour necrosis factor receptor superfamily member (TNFRSF)1A, nuclear factor kappa beta (NF-kB)1, NF-kB2, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, hypoxia induced factor (HIF)-1α, vascular endothelial growth factor (VEGF)A and P-53) in risk to oesophageal squamous cell carcinoma (OSCC). We genotyped 125 tag single nucleotide polymorphism (SNP)s in 410 cases and 377 age and sex matched disease-free individuals from Nutritional Intervention Trial (NIT) cohort, and 546 cases and 556 controls individually matched for age, sex and neighbourhood from Shanxi case-control study, both conducted in high-risk areas of north-central China (1985-2007). Cox proportional-hazard models and conditional logistic regression models were used for SNPs analyses for NIT and Shanxi, respectively. Fisher's inverse test statistics were used to obtain gene-level significance. Multiple SNPs were significantly associated with OSCC in both studies, however, none retained their significance after a conservative Bonferroni adjustment. Empiric p-values for tag SNPs in VEGFA in NIT were highly concentrated in the lower tail of the distribution, suggesting this gene may be influencing risk. Permutation tests confirmed the significance of this pattern. At the gene level, VEGFA yielded an empiric significance (P=0.027) in NIT. We also observed some evidence for interaction between environmental factors and some VEGFA tag SNPs. Our finding adds further evidence for a potential role for markers in the VEGFA gene in the development and progression of early precancerous lesions of oesophagus. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - European journal of cancer (Oxford, England : 1990) AU - Golozar, Asieh AU - Beaty, Terri H AU - Gravitt, Patti E AU - Ruczinski, Ingo AU - Qiao, You-Lin AU - Fan, Jin-Hu AU - Ding, Ti AU - Tang, Ze-Zhong AU - Etemadi, Arash AU - Hu, Nan AU - Hyland, Paula L AU - Wang, Lemin AU - Wang, Chaoyu AU - Dawsey, Sanford M AU - Freedman, Neal D AU - Abnet, Christian C AU - Goldstein, Alisa M AU - Taylor, Philip R AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. Electronic address: agolozar@jhu.edu. ; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. ; Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. ; Department of Epidemiology, Cancer Institute (Hospital), Chinese Academy of Medical Sciences, Beijing, People's Republic of China. ; Shanxi Cancer Hospital, Taiyuan, Shanxi, People's Republic of China. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 2855 EP - 2865 VL - 50 IS - 16 KW - VEGFA protein, human KW - 0 KW - Vascular Endothelial Growth Factor A KW - Index Medicus KW - Genetics KW - Genetic marker KW - Wound-healing KW - Vascular endothelial growth factor A KW - VEGFA KW - Inflammation-related events KW - Oesophageal squamous cell carcinoma KW - Inflammation KW - Esophagus -- metabolism KW - Reproducibility of Results KW - Humans KW - Aged KW - Gene Expression Regulation, Neoplastic KW - Genotype KW - Cohort Studies KW - Case-Control Studies KW - Middle Aged KW - Quality Control KW - China KW - Female KW - Male KW - Proportional Hazards Models KW - Polymorphism, Single Nucleotide KW - Carcinoma, Squamous Cell -- epidemiology KW - Esophageal Neoplasms -- metabolism KW - Carcinoma, Squamous Cell -- metabolism KW - Vascular Endothelial Growth Factor A -- metabolism KW - Esophageal Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1610760353?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.atitle=Oesophageal+squamous+cell+carcinoma+in+high-risk+Chinese+populations%3A+Possible+role+for+vascular+epithelial+growth+factor+A.&rft.au=Golozar%2C+Asieh%3BBeaty%2C+Terri+H%3BGravitt%2C+Patti+E%3BRuczinski%2C+Ingo%3BQiao%2C+You-Lin%3BFan%2C+Jin-Hu%3BDing%2C+Ti%3BTang%2C+Ze-Zhong%3BEtemadi%2C+Arash%3BHu%2C+Nan%3BHyland%2C+Paula+L%3BWang%2C+Lemin%3BWang%2C+Chaoyu%3BDawsey%2C+Sanford+M%3BFreedman%2C+Neal+D%3BAbnet%2C+Christian+C%3BGoldstein%2C+Alisa+M%3BTaylor%2C+Philip+R&rft.aulast=Golozar&rft.aufirst=Asieh&rft.date=2014-11-01&rft.volume=50&rft.issue=16&rft.spage=2855&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.issn=1879-0852&rft_id=info:doi/10.1016%2Fj.ejca.2014.07.022 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-08 N1 - Date created - 2014-10-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 1993 Sep 15;85(18):1492-8 [8360932] J Natl Cancer Inst. 1993 Sep 15;85(18):1483-92 [8360931] Circulation. 1996 Apr 15;93(8):1493-5 [8608615] Cancer. 1997 Jan 15;79(2):206-13 [9010092] Cancer Res. 1999 Jan 1;59(1):198-204 [9892207] J Biol Chem. 1999 Apr 16;274(16):10911-5 [10196169] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078] Oncology. 2005;69 Suppl 3:4-10 [16301830] Arch Surg. 2006 May;141(5):476-81; discussion 481-2 [16702519] Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1148-52 [16775174] Nat Rev Genet. 2006 Oct;7(10):812-20 [16983377] Br J Cancer. 2006 Dec 4;95(11):1568-75 [17088911] J Invest Dermatol. 2007 Mar;127(3):514-25 [17299434] Anticancer Res. 2007 Jul-Aug;27(4B):2535-9 [17695550] Yale J Biol Med. 2006 Dec;79(3-4):123-30 [17940622] Drug Discov Today. 2007 Dec;12(23-24):1054-60 [18061885] Best Pract Res Clin Gastroenterol. 2007;21(6):921-45 [18070696] Anticancer Res. 2008 Mar-Apr;28(2B):1271-6 [18505065] Carcinogenesis. 2008 Dec;29(12):2330-4 [18780893] Front Biosci (Landmark Ed). 2009;14:3872-8 [19273317] Gastroenterol Clin North Am. 2009 Mar;38(1):27-57, vii [19327566] J Natl Cancer Inst. 2009 Apr 1;101(7):507-18 [19318634] Mol Cancer Ther. 2009 Sep;8(9):2635-44 [19723887] BMC Gastroenterol. 2009;9:77 [19835575] Eur J Cancer. 2009 Dec;45(18):3156-65 [19800783] J Gastroenterol Hepatol. 2010 Apr;25(4):795-9 [20492336] Eur J Hum Genet. 2010 Sep;18(9):1045-53 [20442747] Cancer Lett. 2008 Apr 8;262(1):71-6 [18171601] Am J Hum Genet. 2007 Dec;81(6):1278-83 [17966091] PLoS One. 2011;6(7):e22152 [21811567] Cytokine. 2000 Aug;12(8):1232-5 [10930302] J Vasc Res. 2000 Nov-Dec;37(6):443-8 [11146397] Oncogene. 2001 Nov 1;20(50):7368-74 [11704866] J Am Soc Nephrol. 2002 Jan;13(1):260-4 [11752046] BMC Cancer. 2002 Apr 29;2:8 [11978184] Nat Rev Cancer. 2003 Jun;3(6):401-10 [12778130] Int J Cancer. 2003 Sep 10;106(4):468-71 [12845639] Eur J Surg Oncol. 2003 Dec;29(10):890-4 [14624783] N Engl J Med. 2003 Dec 4;349(23):2241-52 [14657432] Oncol Rep. 2004 Feb;11(2):315-9 [14719061] Semin Oncol. 2004 Aug;31(4):498-512 [15297942] Science. 2004 Sep 17;305(5691):1736-9 [15375259] Cancer Res. 1994 Aug 15;54(16):4342-6 [8044781] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ejca.2014.07.022 ER - TY - JOUR T1 - DAP1, a negative regulator of autophagy, controls SubAB-mediated apoptosis and autophagy. AN - 1609505449; 25183729 AB - Autophagy and apoptosis play critical roles in cellular homeostasis and survival. Subtilase cytotoxin (SubAB), produced by non-O157 type Shiga-toxigenic Escherichia coli (STEC), is an important virulence factor in disease. SubAB, a protease, cleaves a specific site on the endoplasmic reticulum (ER) chaperone protein BiP/GRP78, leading to ER stress, and induces apoptosis. Here we report that in HeLa cells, activation of a PERK (RNA-dependent protein kinase [PKR]-like ER kinase)-eIF2α (α subunit of eukaryotic initiation factor 2)-dependent pathway by SubAB-mediated BiP cleavage negatively regulates autophagy and induces apoptosis through death-associated protein 1 (DAP1). We found that SubAB treatment decreased the amounts of autophagy markers LC3-II and p62 as well as those of mTOR (mammalian target of rapamycin) signaling proteins ULK1 and S6K. These proteins showed increased expression levels in PERK knockdown or DAP1 knockdown cells. In addition, depletion of DAP1 in HeLa cells dramatically inhibited the SubAB-stimulated apoptotic pathway: SubAB-induced Bax/Bak conformational changes, Bax/Bak oligomerization, cytochrome c release, activation of caspases, and poly(ADP-ribose) polymerase (PARP) cleavage. These results show that DAP1 is a key regulator, through PERK-eIF2α-dependent pathways, of the induction of apoptosis and reduction of autophagy by SubAB. Copyright © 2014, American Society for Microbiology. All Rights Reserved. JF - Infection and immunity AU - Yahiro, Kinnosuke AU - Tsutsuki, Hiroyasu AU - Ogura, Kohei AU - Nagasawa, Sayaka AU - Moss, Joel AU - Noda, Masatoshi AD - Department of Molecular Infectiology, Graduate School of Medicine, Chiba University, Chiba, Japan yahirok@faculty.chiba-u.jp. ; Department of Molecular Infectiology, Graduate School of Medicine, Chiba University, Chiba, Japan. ; Department of Molecular Infectiology, Graduate School of Medicine, Chiba University, Chiba, Japan Department of Legal Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan. ; Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 4899 EP - 4908 VL - 82 IS - 11 KW - Apoptosis Regulatory Proteins KW - 0 KW - BAK1 protein, human KW - BAX protein, human KW - DAP protein, human KW - Escherichia coli Proteins KW - bcl-2 Homologous Antagonist-Killer Protein KW - bcl-2-Associated X Protein KW - Subtilisins KW - EC 3.4.21.- KW - subtilase cytotoxin, E coli KW - Index Medicus KW - bcl-2-Associated X Protein -- genetics KW - bcl-2 Homologous Antagonist-Killer Protein -- genetics KW - HeLa Cells KW - Humans KW - Escherichia coli KW - bcl-2-Associated X Protein -- metabolism KW - bcl-2 Homologous Antagonist-Killer Protein -- metabolism KW - Escherichia coli Proteins -- metabolism KW - Apoptosis Regulatory Proteins -- genetics KW - Subtilisins -- genetics KW - Gene Expression Regulation -- immunology KW - Apoptosis -- physiology KW - Apoptosis Regulatory Proteins -- metabolism KW - Autophagy -- physiology KW - Subtilisins -- metabolism KW - Escherichia coli Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1609505449?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+immunity&rft.atitle=DAP1%2C+a+negative+regulator+of+autophagy%2C+controls+SubAB-mediated+apoptosis+and+autophagy.&rft.au=Yahiro%2C+Kinnosuke%3BTsutsuki%2C+Hiroyasu%3BOgura%2C+Kohei%3BNagasawa%2C+Sayaka%3BMoss%2C+Joel%3BNoda%2C+Masatoshi&rft.aulast=Yahiro&rft.aufirst=Kinnosuke&rft.date=2014-11-01&rft.volume=82&rft.issue=11&rft.spage=4899&rft.isbn=&rft.btitle=&rft.title=Infection+and+immunity&rft.issn=1098-5522&rft_id=info:doi/10.1128%2FIAI.02213-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-15 N1 - Date created - 2014-10-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2003 Feb 14;278(7):5367-76 [12454021] Infect Immun. 2010 Nov;78(11):4691-6 [20713620] J Exp Med. 2004 Jul 5;200(1):35-46 [15226357] N Engl J Med. 1983 Mar 24;308(12):681-5 [6338386] J Biol Chem. 1995 Jan 13;270(2):815-22 [7822316] Genes Dev. 1995 Jan 1;9(1):15-30 [7828849] Nihon Rinsho. 1997 Mar;55(3):686-92 [9086782] Oncogene. 1998 Dec 24;17(25):3331-40 [9916995] J Biol Chem. 1999 Apr 9;274(15):10145-53 [10187798] J Clin Microbiol. 2005 Jun;43(6):2944-7 [15956427] Hum Mol Genet. 2006 Apr 1;15(7):1209-16 [16497721] Nature. 2006 Oct 5;443(7111):548-52 [17024087] Infect Immun. 2007 Jan;75(1):488-96 [17101670] Proc Natl Acad Sci U S A. 2007 Feb 6;104(6):1829-34 [17267617] J Biol Chem. 2007 Aug 17;282(33):24131-45 [17580304] FEMS Microbiol Lett. 2007 Sep;274(2):329-34 [17651390] Autophagy. 2007 Nov-Dec;3(6):542-5 [17611390] Enferm Infecc Microbiol Clin. 2007 Nov;25(9):603-4 [17953903] Eur J Clin Microbiol Infect Dis. 2010 Nov;29(11):1395-9 [20680367] J Biol Chem. 2010 Nov 5;285(45):34447-59 [20805228] Cell Death Differ. 2010 Dec;17(12):1807-15 [20865012] Autophagy. 2010 Nov;6(8):1179-80 [20818178] Infect Immun. 2011 Feb;79(2):617-27 [21098100] Cell Death Dis. 2010;1:e18 [21364619] Cell Death Differ. 2011 Apr;18(4):571-80 [21311563] Cell Microbiol. 2011 Jul;13(7):992-1013 [21501364] Autophagy. 2011 Sep;7(9):957-65 [21606683] Cell Microbiol. 2011 Oct;13(10):1479-96 [21722286] Annu Rev Cell Dev Biol. 2011;27:107-32 [21801009] Exp Mol Med. 2012 Feb 29;44(2):99-108 [22257885] Infect Immun. 2012 May;80(5):1803-14 [22354021] Cancer Genomics Proteomics. 2012 Jul-Aug;9(4):199-201 [22798505] Infect Immun. 2012 Nov;80(11):3939-51 [22949549] Pharmacol Res. 2012 Dec;66(6):513-25 [22982482] J Clin Invest. 2012 Dec;122(12):4621-34 [23143306] Annu Rev Physiol. 2013;75:241-62 [23216414] Oncogene. 2013 Oct 10;32(41):4932-40 [23160380] Oncol Rep. 2014 Jan;31(1):175-82 [24270644] Infect Immun. 2014 Sep;82(9):3542-54 [24914224] Cell Microbiol. 2008 Mar;10(3):795-806 [18042253] Cell Microbiol. 2008 Apr;10(4):921-9 [18005237] Autophagy. 2008 Oct;4(7):849-50 [18758232] Autophagy. 2008 Oct;4(7):887-95 [18769149] Nature. 2008 Dec 4;456(7222):648-52 [18971931] Oncogene. 2009 Jan 22;28(3):334-44 [18931699] Autophagy. 2009 Apr;5(3):370-9 [19164948] Mol Biol Cell. 2009 Apr;20(7):1992-2003 [19225151] J Cell Sci. 2009 Jun 1;122(Pt 11):1707-11 [19461070] Infect Immun. 2009 Jul;77(7):2919-24 [19380466] J Immunol. 2009 Jul 15;183(2):1480-7 [19561103] J Cell Biochem. 2009 Aug 1;107(5):973-83 [19492336] J Clin Microbiol. 2009 Sep;47(9):3058-9 [19571032] Traffic. 2009 Oct;10(10):1502-17 [19678899] J Clin Microbiol. 2010 Jan;48(1):178-83 [19940059] Nat Med. 2010 Jan;16(1):90-7 [19966812] J Vet Med Sci. 2010 May;72(5):589-97 [20103992] Curr Biol. 2010 Jun 22;20(12):1093-8 [20537536] Microb Pathog. 2010 Oct;49(4):153-63 [20561923] J Am Soc Nephrol. 2010 Oct;21(10):1702-12 [20705711] J Infect Dis. 2004 Feb 1;189(3):355-9 [14745691] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/IAI.02213-14 ER - TY - JOUR T1 - Role of white adipose lipolysis in the development of NASH induced by methionine- and choline-deficient diet. AN - 1609101863; 25178843 AB - Methionine- and choline-deficient diet (MCD) is a model for nonalcoholic steatohepatitis (NASH) in rodents. However, the mechanism of NASH development by dietary methionine/choline deficiency remains undetermined. To elucidate the early metabolic changes associated with MCD-NASH, serum metabolomic analysis was performed using mice treated with MCD and control diet for 3 days and 1 week, revealing significant increases in oleic and linoleic acids after MCD treatment. These increases were correlated with reduced body weight and white adipose tissue (WAT) mass, increased phosphorylation of hormone-sensitive lipase, and up-regulation of genes encoding carboxylesterase 3 and β2-adrenergic receptor in WAT, indicating accelerated lipolysis in adipocytes. The changes in serum fatty acids and WAT by MCD treatment were reversed by methionine supplementation, and similar alterations were detected in mice fed a methionine-deficient diet (MD), thus demonstrating that dietary methionine deficiency enhances lipolysis in WAT. MD treatment decreased glucose and increased fibroblast growth factor 21 in serum, thus exhibiting a similar metabolic phenotype as the fasting response. Comparison between MCD and choline-deficient diet (CD) treatments suggested that the addition of MD-induced metabolic alterations, such as WAT lipolysis, to CD-induced hepatic steatosis promotes liver injury. Collectively, these results demonstrate an important role for dietary methionine deficiency and WAT lipolysis in the development of MCD-NASH. Published by Elsevier B.V. JF - Biochimica et biophysica acta AU - Tanaka, Naoki AU - Takahashi, Shogo AU - Fang, Zhong-Ze AU - Matsubara, Tsutomu AU - Krausz, Kristopher W AU - Qu, Aijuan AU - Gonzalez, Frank J AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA; Department of Toxicology, School of Public Health, Tianjin Medical University, Tianjin, China. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA; Department of Anatomy and Regenerative Biology, Osaka City University, Osaka, Japan. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: gonzalef@mail.nih.gov. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 1596 EP - 1607 VL - 1841 IS - 11 SN - 0006-3002, 0006-3002 KW - Index Medicus KW - Fasting response KW - Choline deficiency KW - Lipolysis KW - Oleic acid KW - Metabolomics KW - Linoleic acid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1609101863?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Role+of+white+adipose+lipolysis+in+the+development+of+NASH+induced+by+methionine-+and+choline-deficient+diet.&rft.au=Tanaka%2C+Naoki%3BTakahashi%2C+Shogo%3BFang%2C+Zhong-Ze%3BMatsubara%2C+Tsutomu%3BKrausz%2C+Kristopher+W%3BQu%2C+Aijuan%3BGonzalez%2C+Frank+J&rft.aulast=Tanaka&rft.aufirst=Naoki&rft.date=2014-11-01&rft.volume=1841&rft.issue=11&rft.spage=1596&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbalip.2014.08.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2014-10-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hepatology. 2010 Aug;52(2):774-88 [20683968] Biochim Biophys Acta. 2014 Jul;1842(7):959-70 [24594481] Hepatology. 2010 Nov;52(5):1836-46 [21038418] Hepatology. 2011 Jan;53(1):116-26 [20967758] J Gastroenterol. 2011 Jun;46(6):758-68 [21267748] Science. 2011 Jun 24;332(6037):1519-23 [21700865] Aliment Pharmacol Ther. 2011 Aug;34(3):274-85 [21623852] J Biol Chem. 2011 Nov 11;286(45):39336-48 [21941003] Cell Metab. 2011 Dec 7;14(6):804-10 [22152305] Mech Ageing Dev. 2001 May 31;122(7):617-57 [11322990] J Lipid Res. 2001 Oct;42(10):1521-42 [11590208] J Biol Chem. 2004 Sep 24;279(39):40683-9 [15220344] Hepatology. 2004 Oct;40(4):972-80 [15382117] J Biol Chem. 1988 Feb 25;263(6):2998-3004 [3343237] Am J Gastroenterol. 1992 Jun;87(6):775-9 [1590319] Gastroenterology. 1998 Apr;114(4):842-5 [9547102] J Clin Invest. 2005 May;115(5):1343-51 [15864352] J Clin Invest. 2005 Jun;115(6):1627-35 [15902306] Diabetes. 2006 Jul;55(7):2091-7 [16804080] Endocrinology. 2007 Feb;148(2):774-81 [17068132] Cell Metab. 2007 Jun;5(6):415-25 [17550777] Cell Metab. 2007 Nov;6(5):348-51 [17983580] J Clin Invest. 2008 Feb;118(2):683-94 [18188449] Biochim Biophys Acta. 2009 Jun;1791(6):494-500 [19010445] Hepatology. 2010 Feb;51(2):595-602 [20014114] Cell Metab. 2010 Mar 3;11(3):183-93 [20197051] J Biol Chem. 2010 Jun 11;285(24):18528-36 [20395294] Hepatology. 2012 Jul;56(1):118-29 [22290395] Clin Gastroenterol Hepatol. 2012 Aug;10(8):837-58 [22446927] J Hepatol. 2012 Oct;57(4):852-9 [22687340] Cell Metab. 2012 Nov 7;16(5):634-44 [23140643] PLoS One. 2012;7(12):e51357 [23236485] J Hepatol. 2013 Mar;58(3):557-63 [23142063] Hepatology. 2014 Mar;59(3):858-69 [24002947] J Hepatol. 2010 Nov;53(5):934-40 [20675007] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbalip.2014.08.015 ER - TY - JOUR T1 - Salvinorin A regulates dopamine transporter function via a kappa opioid receptor and ERK1/2-dependent mechanism. AN - 1609099054; 25107591 AB - Salvinorin A (SalA), a selective κ-opioid receptor (KOR) agonist, produces dysphoria and pro-depressant like effects. These actions have been attributed to inhibition of striatal dopamine release. The dopamine transporter (DAT) regulates dopamine transmission via uptake of released neurotransmitter. KORs are apposed to DAT in dopamine nerve terminals suggesting an additional target by which SalA modulates dopamine transmission. SalA produced a concentration-dependent, nor-binaltorphimine (BNI)- and pertussis toxin-sensitive increase of ASP(+) accumulation in EM4 cells coexpressing myc-KOR and YFP-DAT, using live cell imaging and the fluorescent monoamine transporter substrate, trans 4-(4-(dimethylamino)-styryl)-N-methylpyridinium) (ASP(+)). Other KOR agonists also increased DAT activity that was abolished by BNI pretreatment. While SalA increased DAT activity, SalA treatment decreased serotonin transporter (SERT) activity and had no effect on norepinephrine transporter (NET) activity. In striatum, SalA increased the Vmax for DAT mediated DA transport and DAT surface expression. SalA up-regulation of DAT function is mediated by KOR activation and the KOR-linked extracellular signal regulated kinase-½ (ERK1/2) pathway. Co-immunoprecipitation and BRET studies revealed that DAT and KOR exist in a complex. In live cells, DAT and KOR exhibited robust FRET signals under basal conditions. SalA exposure caused a rapid and significant increase of the FRET signal. This suggests that the formation of KOR and DAT complexes is promoted in response to KOR activation. Together, these data suggest that enhanced DA transport and decreased DA release resulting in decreased dopamine signalling may contribute to the dysphoric and pro-depressant like effects of SalA and other KOR agonists. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - Neuropharmacology AU - Kivell, Bronwyn AU - Uzelac, Zeljko AU - Sundaramurthy, Santhanalakshmi AU - Rajamanickam, Jeyaganesh AU - Ewald, Amy AU - Chefer, Vladimir AU - Jaligam, Vanaja AU - Bolan, Elizabeth AU - Simonson, Bridget AU - Annamalai, Balasubramaniam AU - Mannangatti, Padmanabhan AU - Prisinzano, Thomas E AU - Gomes, Ivone AU - Devi, Lakshmi A AU - Jayanthi, Lankupalle D AU - Sitte, Harald H AU - Ramamoorthy, Sammanda AU - Shippenberg, Toni S AD - School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand; Integrative Neuroscience Section, National Institutes of Health, National Institute on Drug Abuse Intramural Research Program, Baltimore, MD 21224, USA. ; Medical University Vienna, Center for Physiology and Pharmacology, Institute of Pharmacology, Waehringerstrasse 13a, A-1090 Vienna, Austria. ; Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA. ; School of Biological Sciences, Victoria University of Wellington, Wellington, New Zealand. ; Integrative Neuroscience Section, National Institutes of Health, National Institute on Drug Abuse Intramural Research Program, Baltimore, MD 21224, USA. ; Department of Neurosciences, Medical University of South Carolina, Charleston, SC 29425, USA. ; Department of Medicinal Chemistry, University of Kansas, Lawrence, KS 66045, USA. ; Department of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, NY 10029, USA. ; Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA 23298, USA. Electronic address: sramamoorthy@vcu.edu. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 228 EP - 240 VL - 86 KW - Diterpenes, Clerodane KW - 0 KW - Dopamine Agents KW - Dopamine Plasma Membrane Transport Proteins KW - Norepinephrine Plasma Membrane Transport Proteins KW - Receptors, Opioid, kappa KW - SLC6A2 protein, human KW - SLC6A4 protein, human KW - Serotonin Plasma Membrane Transport Proteins KW - p38 Mitogen-Activated Protein Kinases KW - EC 2.7.11.24 KW - salvinorin A KW - T56W91NG6J KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Dopamine transporter KW - Serotonin transporter KW - Kappa opioid receptor KW - Dysphoric KW - Pro-depressant KW - Trafficking KW - Salvinorin A KW - Serotonin Plasma Membrane Transport Proteins -- metabolism KW - Cell Membrane -- drug effects KW - Humans KW - HEK293 Cells KW - Corpus Striatum -- metabolism KW - Norepinephrine Plasma Membrane Transport Proteins -- metabolism KW - Dopamine -- metabolism KW - Corpus Striatum -- drug effects KW - Cell Membrane -- metabolism KW - p38 Mitogen-Activated Protein Kinases -- metabolism KW - MAP Kinase Signaling System -- drug effects KW - MAP Kinase Signaling System -- physiology KW - Receptors, Opioid, kappa -- agonists KW - Dopamine Agents -- pharmacology KW - Receptors, Opioid, kappa -- metabolism KW - Dopamine Plasma Membrane Transport Proteins -- metabolism KW - Diterpenes, Clerodane -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1609099054?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropharmacology&rft.atitle=Salvinorin+A+regulates+dopamine+transporter+function+via+a+kappa+opioid+receptor+and+ERK1%2F2-dependent+mechanism.&rft.au=Kivell%2C+Bronwyn%3BUzelac%2C+Zeljko%3BSundaramurthy%2C+Santhanalakshmi%3BRajamanickam%2C+Jeyaganesh%3BEwald%2C+Amy%3BChefer%2C+Vladimir%3BJaligam%2C+Vanaja%3BBolan%2C+Elizabeth%3BSimonson%2C+Bridget%3BAnnamalai%2C+Balasubramaniam%3BMannangatti%2C+Padmanabhan%3BPrisinzano%2C+Thomas+E%3BGomes%2C+Ivone%3BDevi%2C+Lakshmi+A%3BJayanthi%2C+Lankupalle+D%3BSitte%2C+Harald+H%3BRamamoorthy%2C+Sammanda%3BShippenberg%2C+Toni+S&rft.aulast=Kivell&rft.aufirst=Bronwyn&rft.date=2014-11-01&rft.volume=86&rft.issue=&rft.spage=228&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=1873-7064&rft_id=info:doi/10.1016%2Fj.neuropharm.2014.07.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-14 N1 - Date created - 2014-10-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Neuron. 2006 Aug 17;51(4):417-29 [16908408] Mol Interv. 2006 Oct;6(5):257-65 [17035666] Nat Methods. 2006 Dec;3(12):1001-6 [17086179] J Pharmacol Exp Ther. 2007 Jan;320(1):300-6 [17060493] Am J Psychiatry. 2007 Apr;164(4):630-7 [17403977] EMBO J. 2007 Apr 18;26(8):2127-36 [17380124] Mol Pharmacol. 2007 May;71(5):1222-32 [17267664] Biochemistry. 2007 Sep 18;46(37):10484-97 [17711354] Pharmacol Ther. 2007 Nov;116(2):306-21 [17868902] J Biol Chem. 2007 Dec 7;282(49):35842-54 [17923483] J Pharmacol Exp Ther. 2008 Apr;325(1):293-301 [18198344] Psychopharmacology (Berl). 2008 Apr;197(3):509-17 [18246329] J Biol Chem. 2008 Apr 18;283(16):10978-91 [18252709] Neuroimage. 2008 Jul 1;41(3):1044-50 [18434204] J Psychoactive Drugs. 2008 Jun;40(2):183-91 [18720668] Neuroreport. 2008 Sep 17;19(14):1417-22 [18766023] Neurosci Lett. 2008 Dec 3;446(2-3):101-4 [18824069] Biochemistry. 2009 Feb 10;48(5):1067-76 [19146407] Synapse. 2009 Aug;63(8):698-704 [19391150] Neuropharmacology. 2009 Oct-Nov;57(5-6):523-30 [19628000] Mol Pharmacol. 2009 Oct;76(4):812-23 [19628755] Pharmacol Biochem Behav. 2009 Dec;94(2):244-9 [19747933] J Biol Chem. 2010 Apr 2;285(14):10924-38 [20118234] J Neurochem. 2010 Apr;113(1):27-41 [20085610] J Neurosci. 2010 Apr 28;30(17):6048-57 [20427663] Psychopharmacology (Berl). 2010 Jun;210(2):241-52 [20372879] Psychopharmacology (Berl). 2010 Jun;210(2):137-47 [20401607] Proc Natl Acad Sci U S A. 2010 Nov 16;107(46):20115-9 [21041644] Pharmacol Ther. 2011 Feb;129(2):220-38 [20951731] J Biol Chem. 2011 Feb 18;286(7):5175-86 [21118819] Neuron. 2011 Aug 11;71(3):498-511 [21835346] Mol Pharmacol. 2011 Sep;80(3):458-65 [21705486] Biol Psychiatry. 2011 Oct 15;70(8):744-53 [21757186] J Biol Chem. 2012 Aug 24;287(35):29702-12 [22722938] J Neurosci. 2012 Sep 5;32(36):12325-36 [22956823] Mol Aspects Med. 2013 Apr-Jun;34(2-3):197-219 [23506866] Neuropsychopharmacology. 2013 Jul;38(8):1585-97 [23446450] Neuropsychopharmacology. 2013 Aug;38(9):1770-9 [23542927] Trends Pharmacol Sci. 2013 Sep;34(9):489-96 [23968642] J Biol Chem. 2013 Oct 4;288(40):28599-610 [23979140] Neuropsychopharmacology. 2013 Dec;38(13):2623-31 [23921954] J Neurochem. 2007 Jun;101(5):1258-71 [17419806] J Neurochem. 2000 Feb;74(2):564-73 [10646507] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3684-9 [10725388] Mol Pharmacol. 2001 Jan;59(1):113-21 [11125031] J Neurosci. 2000 Dec 15;20(24):9333-40 [11125013] J Pharmacol Exp Ther. 2001 Mar;296(3):931-8 [11181926] J Neurochem. 2001 Mar;76(5):1282-90 [11238713] J Biol Chem. 2001 Feb 9;276(6):3805-10 [11071889] Biophys J. 2001 Oct;81(4):2395-402 [11566809] Synapse. 2001 Dec 1;42(3):185-92 [11746715] J Neurochem. 2002 May;81(4):859-69 [12065645] Curr Opin Oncol. 2003 Jan;15(1):55-64 [12490762] J Biol Chem. 2003 Feb 14;278(7):4990-5000 [12464618] J Biol Chem. 2003 Mar 14;278(11):9768-77 [12499385] Methods Mol Med. 2003;84:157-83 [12703323] J Biol Chem. 2003 Jun 13;278(24):22168-74 [12682063] J Neurosci. 2003 Sep 17;23(24):8480-8 [13679416] J Biol Chem. 2004 Feb 20;279(8):6650-7 [14660642] PLoS Biol. 2004 Mar;2(3):E78 [15024426] Psychopharmacology (Berl). 2004 Apr;172(4):463-70 [14727002] J Biol Chem. 2004 May 14;279(20):21012-20 [15024013] Mol Pharmacol. 2004 Jun;65(6):1462-74 [15155839] Bioorg Med Chem Lett. 2004 Oct 18;14(20):5099-102 [15380207] Pharmacol Ther. 2004 Oct;104(1):17-27 [15500906] Eur J Pharmacol. 1990 Jun 8;181(3):267-78 [2166675] J Neurochem. 1990 Nov;55(5):1734-40 [1976759] Proc Natl Acad Sci U S A. 1992 Mar 15;89(6):2046-50 [1347943] Annu Rev Neurosci. 1993;16:73-93 [8096377] J Biol Chem. 1995 Nov 17;270(46):27489-94 [7499206] Br J Pharmacol. 1996 Dec;119(7):1491-7 [8968560] Biochem Pharmacol. 1997 Mar 7;53(5):677-88 [9113087] Nature. 1999 Jun 17;399(6737):697-700 [10385123] J Neurosci. 1999 Jul 15;19(14):5750-7 [10407016] Psychopharmacology (Berl). 1999 Jun;144(4):339-46 [10435406] J Neurosci. 2005 May 18;25(20):5029-37 [15901784] Mol Pharmacol. 2005 Jul;68(1):102-9 [15795321] J Biol Chem. 2005 Jul 29;280(30):27662-9 [15944153] Synapse. 2005 Dec 1;58(3):208-10 [16138318] Microsc Res Tech. 2005 Sep;68(1):51-8 [16208719] J Biol Chem. 2005 Oct 21;280(42):35617-24 [16109712] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.neuropharm.2014.07.016 ER - TY - JOUR T1 - Quantitative determination of mithramycin in human plasma by a novel, sensitive ultra-HPLC-MS/MS method for clinical pharmacokinetic application. AN - 1609098943; 25247492 AB - Mithramycin is a neoplastic antibiotic synthesized by various Streptomyces bacteria. It is under investigation as a chemotherapeutic treatment for a wide variety of cancers. Ongoing and forthcoming clinical trials will require pharmacokinetic analysis of mithramycin in humans, both to see if target concentrations are achieved and to optimize dosing and correlate outcomes (response/toxicity) with pharmacokinetics. Two published methods for mithramycin quantitation exist, but both are immunoassays that lack current bioanalytical standards of selectivity and sensitivity. To provide an upgraded and more widely applicable assay, a UPLC-MS/MS method for quantitation of mithramycin in human plasma was developed. Solid-phase extraction allowed for excellent recoveries (>90%) necessary for high throughput analyses on sensitive instrumentation. However, a ∼55% reduction in analyte signal was observed as a result of plasma matrix effects. Mithramycin and the internal standard chromomycin were separated on a Waters Acquity BEH C18 column (2.1×50 mm, 1.7 μm) and detected using electrospray ionization operated in the negative mode at mass transitions m/z 1083.5→268.9 and 1181.5→269.0, respectively, on an AB Sciex QTrap 5500. The assay range was 0.5-500 ng/mL and proved to be linear (r(2)>0.996), accurate (≤10% deviation), and precise (CV<15%). Mithramycin was stable in plasma at room temperature for 24 h, as well as through three freeze-thaw cycles. This method was subsequently used to quantitate mithramycin plasma concentrations from patients enrolled on two clinical trials at the NCI. Published by Elsevier B.V. JF - Journal of chromatography. B, Analytical technologies in the biomedical and life sciences AU - Roth, Jeffrey AU - Peer, Cody J AU - Widemann, Brigitte AU - Cole, Diane E AU - Ershler, Rachel AU - Helman, Lee AU - Schrump, David AU - Figg, William D AD - Clinical Pharmacology Program, National Cancer Institute, Bethesda, MD, United States. ; Pediatric Oncology Branch, National Cancer Institute, Bethesda, MD, United States. ; Thoracic Oncology Branch, National Cancer Institute, Bethesda, MD, United States. ; Clinical Pharmacology Program, National Cancer Institute, Bethesda, MD, United States. Electronic address: figgw@helix.nih.gov. Y1 - 2014/11/01/ PY - 2014 DA - 2014 Nov 01 SP - 95 EP - 101 VL - 970 KW - Blood Proteins KW - 0 KW - Plicamycin KW - NIJ123W41V KW - Index Medicus KW - Mithramycin KW - Tandem mass spectrometry KW - Ultra-HPLC KW - Sensitivity and Specificity KW - Reproducibility of Results KW - Humans KW - Linear Models KW - Solid Phase Extraction KW - Blood Proteins -- metabolism KW - Plicamycin -- chemistry KW - Plicamycin -- pharmacokinetics KW - Tandem Mass Spectrometry -- methods KW - Chromatography, High Pressure Liquid -- methods KW - Plicamycin -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1609098943?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chromatography.+B%2C+Analytical+technologies+in+the+biomedical+and+life+sciences&rft.atitle=Quantitative+determination+of+mithramycin+in+human+plasma+by+a+novel%2C+sensitive+ultra-HPLC-MS%2FMS+method+for+clinical+pharmacokinetic+application.&rft.au=Roth%2C+Jeffrey%3BPeer%2C+Cody+J%3BWidemann%2C+Brigitte%3BCole%2C+Diane+E%3BErshler%2C+Rachel%3BHelman%2C+Lee%3BSchrump%2C+David%3BFigg%2C+William+D&rft.aulast=Roth&rft.aufirst=Jeffrey&rft.date=2014-11-01&rft.volume=970&rft.issue=&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography.+B%2C+Analytical+technologies+in+the+biomedical+and+life+sciences&rft.issn=1873-376X&rft_id=info:doi/10.1016%2Fj.jchromb.2014.08.021 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-27 N1 - Date created - 2014-10-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Am Chem Soc. 2003 May 14;125(19):5745-53 [12733914] PLoS One. 2013;8(5):e62818 [23667526] Cancer Treat Rep. 1984 Nov;68(11):1379-81 [6238672] Cancer Res. 1986 Mar;46(3):1084-8 [2935248] Biochemistry. 1991 Apr 30;30(17):4290-7 [1827033] Mol Pharmacol. 2013 Jan;83(1):33-41 [23019217] Cancer Res. 2012 Aug 15;72(16):4178-92 [22751465] J Med Chem. 2012 Jun 28;55(12):5813-25 [22578073] BMC Cancer. 2011;11:470 [22044796] J Natl Cancer Inst. 2011 Jun 22;103(12):962-78 [21653923] J Neurooncol. 2011 Feb;101(3):365-77 [20556479] Biochemistry. 2010 Dec 14;49(49):10543-52 [21067184] Cancer. 2007 Dec 15;110(12):2682-90 [17973266] Mol Cancer Ther. 2006 Nov;5(11):2737-46 [17121920] J Neurosci. 2004 Nov 17;24(46):10335-42 [15548647] Leuk Res. 1997 May;21(5):375-80 [9225062] Ther Drug Monit. 1992 Jun;14(3):255-60 [1412612] JAMA. 1968 Jun 17;204(12):1030-6 [5694748] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jchromb.2014.08.021 ER - TY - JOUR T1 - Necrotizing myopathies: beyond statins. AN - 1566109435; 25203117 AB - This review discusses the spectrum of diseases associated with a necrotizing muscle biopsy. Although patients with toxic myopathies, endocrine dysfunction, and heritable myopathies may have prominent necrosis on muscle biopsy, immune-mediated myopathies are emphasized here. A decade ago, immune-mediated necrotizing myopathy was recognized as a distinct form of myositis. Recent evidence now suggests that immune-mediated necrotizing myopathy is not one disease, but can be divided on the basis of the presence of distinct autoantibodies recognizing either the signal recognition particle or 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. Anti-HMG-CoA reductase-positive patients can be further subdivided into those with and without statin exposure, the latter of which may be particularly refractory to immunosuppressive therapy. A significant number of patients with autoimmune myopathy have a predominantly necrotizing muscle biopsy with minimal lymphocytic infiltration. This biopsy finding occurs in various forms myositis, including the antisynthetase syndrome, scleroderma-associated myopathy, antisignal recognition particle-associated myopathy, statin-associated anti-HMG-CoA reductase-positive autoimmune myopathy, and statin-naïve anti-HMG-CoA reductase-positive myopathy. Future progress in elucidating pathogenic mechanisms and defining optimal treatment strategies may depend upon recognizing these distinct forms of myositis and analyzing them as separate entities. JF - Current opinion in rheumatology AU - Mammen, Andrew L AD - Muscle Disease Unit, Laboratory of Muscle Stem Cells and Gene Expression, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 679 EP - 683 VL - 26 IS - 6 KW - Index Medicus KW - Humans KW - Muscular Diseases -- pathology KW - Muscle, Skeletal -- pathology KW - Muscular Diseases -- immunology KW - Autoimmune Diseases -- pathology KW - Muscle, Skeletal -- immunology KW - Autoimmune Diseases -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566109435?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+rheumatology&rft.atitle=Necrotizing+myopathies%3A+beyond+statins.&rft.au=Mammen%2C+Andrew+L&rft.aulast=Mammen&rft.aufirst=Andrew&rft.date=2014-11-01&rft.volume=26&rft.issue=6&rft.spage=679&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+rheumatology&rft.issn=1531-6963&rft_id=info:doi/10.1097%2FBOR.0000000000000106 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-10 N1 - Date created - 2014-09-25 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/BOR.0000000000000106 ER - TY - JOUR T1 - Induced pluripotency enables differentiation of human nullipotent embryonal carcinoma cells N2102Ep. AN - 1561032450; 25086345 AB - Embryonal carcinoma (EC) cells, which are considered to be malignant counterparts of embryonic stem cells, comprise the pluripotent stem cell component of teratocarcinomas, a form of testicular germ cell tumors (GCTs). Nevertheless, many established human EC cell lines are nullipotent with limited or no capacity to differentiate under normal circumstances. In this study, we tested whether an over-expression of Yamanaka's reprogramming factors OCT4, SOX2, c-MYC and KLF4 might enable differentiation of the human nullipotent EC cells N2102Ep. Using OCT4 knockdown differentiated N2102Ep cells, we are able to derive reprogrammed N2102Ep cell lines. The induced pluripotency of N2102Ep allows the cells to differentiate toward neural lineage by retinoic acid; the expression of SSEA3 and SSEA4 is down-regulated, whereas that of neural surface markers is up-regulated. Consistent with the up-regulation of neural surface markers, the expression of the master neuroectodermal transcription factor PAX6 is also induced in reprogrammed N2102Ep. We next investigated whether PAX6 might induce spontaneous differentiation of nullipotent stem cells N2102Ep. However, while an ectopic expression of PAX6 promotes differentiation of NTERA2, it induces cell death in N2102Ep. We nevertheless find that upon induction of retinoic acid, the reprogrammed N2102Ep cells form mature neuronal morphology similar to differentiated pluripotent stem cells NTERA2 as determined by TUJ1 expression, which is absent in N2102Ep parental cells. Altogether, we conclude that the nullipotent state of human EC cells can be reprogrammed to acquire a more relaxed state of differentiation potential by Yamanaka's factors. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biochimica et biophysica acta AU - Sutiwisesak, Rujapope AU - Kitiyanant, Narisorn AU - Kotchabhakdi, Naiphinich AU - Felsenfeld, Gary AU - Andrews, Peter W AU - Wongtrakoongate, Patompon AD - Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakhonpathom 73170, Thailand; Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. ; Stem Cell Research Group, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakhonpathom, 73170, Thailand. ; Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol University, Salaya, Nakhonpathom 73170, Thailand. ; Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. ; Centre for Stem Cell Biology, University of Sheffield, S10 2TN, UK. ; Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA; Centre for Stem Cell Biology, University of Sheffield, S10 2TN, UK. Electronic address: p.wongtrakoongate@gmail.com. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 2611 EP - 2619 VL - 1843 IS - 11 SN - 0006-3002, 0006-3002 KW - Index Medicus KW - Embryonal carcinoma cell KW - Nullipotency KW - Induced pluripotency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561032450?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Induced+pluripotency+enables+differentiation+of+human+nullipotent+embryonal+carcinoma+cells+N2102Ep.&rft.au=Sutiwisesak%2C+Rujapope%3BKitiyanant%2C+Narisorn%3BKotchabhakdi%2C+Naiphinich%3BFelsenfeld%2C+Gary%3BAndrews%2C+Peter+W%3BWongtrakoongate%2C+Patompon&rft.aulast=Sutiwisesak&rft.aufirst=Rujapope&rft.date=2014-11-01&rft.volume=1843&rft.issue=11&rft.spage=2611&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbamcr.2014.07.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2014-09-08 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbamcr.2014.07.013 ER - TY - JOUR T1 - Adjusting serum concentrations of organochlorine compounds by lipids and symptoms: a causal framework for the association with K-ras mutations in pancreatic cancer. AN - 1553106665; 25113205 AB - In clinically aggressive diseases, patients experience pathophysiological changes that often alter concentrations of lipids and environmental lipophilic factors; such changes are related to disease signs and symptoms. The aim of the study was to compare the effects of correcting for total serum lipids (TSL) and other clinical factors on the odds of mutations in the K-ras oncogene by organochlorine compounds (OCs), in logistic models, in 103 patients with exocrine pancreatic cancer (EPC) using a causal directed acyclic graph (DAG) framework. Results and likelihood of bias were discussed in the light of possible causal scenarios. The odds of K-ras mutated EPC was associated with some TSL-corrected OCs, including p,p'-DDT (p-value: 0.008) and polychlorinated biphenyl 138 (p-trend: 0.024). When OCs were not corrected by TSL, the OR of a K-ras mutation was significant for p,p'-DDT (p-trend: 0.035). Additionally adjusting for cholestatic syndrome increased the ORs of TSL-corrected OCs. When models were adjusted by the interval from first symptom to blood extraction (ISE), the ORs increased for both TSL-corrected and uncorrected OCs. Models with TSL-corrected OCs and adjusted for cholestatic syndrome or ISE yielded the highest ORs. We show that DAGs clarify the covariates necessary to minimize bias, and demonstrate scenarios under which adjustment for TSL-corrected OCs and failure to adjust for symptoms or ISE may induce bias. Models with TSL-uncorrected OCs may be biased too, and adjusting by symptoms or ISE may not control such biases. Our findings may have implications as well for studying environmental causes of other clinically aggressive diseases. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - Chemosphere AU - López, Tomàs AU - Pumarega, José A AU - Pollack, Anna Z AU - Lee, Duk-Hee AU - Richiardi, Lorenzo AU - Jacobs, David R AU - Schisterman, Enrique F AU - Porta, Miquel AD - Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain; Facultat de Medicina, Universitat Autònoma de Barcelona, Catalonia, Spain. ; Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain; CIBER en Epidemiología y Salud Pública (CIBERESP), Spain. ; Epidemiology Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Rockville, MD, USA. ; Department of Preventive Medicine and Health Promotion Research Center, School of Medicine, Kyungpook National University, Daegu, Republic of Korea. ; Cancer Epidemiology Unit, Department of Medical Sciences, University of Turin and CPO-Piemonte, Torino, Italy. ; Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN, USA. ; Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain; Facultat de Medicina, Universitat Autònoma de Barcelona, Catalonia, Spain; CIBER en Epidemiología y Salud Pública (CIBERESP), Spain. Electronic address: mporta@imim.es. Y1 - 2014/11// PY - 2014 DA - November 2014 SP - 219 EP - 225 VL - 114 KW - Environmental Pollutants KW - 0 KW - Hydrocarbons, Chlorinated KW - Lipids KW - ras Proteins KW - EC 3.6.5.2 KW - Index Medicus KW - Organochlorine compounds KW - Pancreatic neoplasm KW - Disease progression KW - Causal directed acyclic graph (DAG) KW - K-ras gene KW - Pancreas -- pathology KW - ras Proteins -- genetics KW - Logistic Models KW - Pancreas -- metabolism KW - Humans KW - Lipids -- blood KW - Pancreatic Neoplasms -- pathology KW - Hydrocarbons, Chlorinated -- toxicity KW - Environmental Pollutants -- toxicity KW - Pancreatic Neoplasms -- blood KW - Hydrocarbons, Chlorinated -- blood KW - Genes, ras -- drug effects KW - Pancreatic Neoplasms -- chemically induced KW - Pancreatic Neoplasms -- genetics KW - Mutation KW - Environmental Pollutants -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1553106665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adjusting+serum+concentrations+of+organochlorine+compounds+by+lipids+and+symptoms%3A+a+causal+framework+for+the+association+with+K-ras+mutations+in+pancreatic+cancer.&rft.au=L%C3%B3pez%2C+Tom%C3%A0s%3BPumarega%2C+Jos%C3%A9+A%3BPollack%2C+Anna+Z%3BLee%2C+Duk-Hee%3BRichiardi%2C+Lorenzo%3BJacobs%2C+David+R%3BSchisterman%2C+Enrique+F%3BPorta%2C+Miquel&rft.aulast=L%C3%B3pez&rft.aufirst=Tom%C3%A0s&rft.date=2014-11-01&rft.volume=114&rft.issue=&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=Chemosphere&rft.issn=1879-1298&rft_id=info:doi/10.1016%2Fj.chemosphere.2014.04.066 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-28 N1 - Date created - 2014-08-12 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.chemosphere.2014.04.066 ER - TY - JOUR T1 - Enhanced neonatal Fc receptor function improves protection against primate SHIV infection. AN - 1619316990; 25119033 AB - To protect against human immunodeficiency virus (HIV-1) infection, broadly neutralizing antibodies (bnAbs) must be active at the portals of viral entry in the gastrointestinal or cervicovaginal tracts. The localization and persistence of antibodies at these sites is influenced by the neonatal Fc receptor (FcRn), whose role in protecting against infection in vivo has not been defined. Here, we show that a bnAb with enhanced FcRn binding has increased gut mucosal tissue localization, which improves protection against lentiviral infection in non-human primates. A bnAb directed to the CD4-binding site of the HIV-1 envelope (Env) protein (denoted VRC01) was modified by site-directed mutagenesis to increase its binding affinity for FcRn. This enhanced FcRn-binding mutant bnAb, denoted VRC01-LS, displayed increased transcytosis across human FcRn-expressing cellular monolayers in vitro while retaining FcγRIIIa binding and function, including antibody-dependent cell-mediated cytotoxicity (ADCC) activity, at levels similar to VRC01 (the wild type). VRC01-LS had a threefold longer serum half-life than VRC01 in non-human primates and persisted in the rectal mucosa even when it was no longer detectable in the serum. Notably, VRC01-LS mediated protection superior to that afforded by VRC01 against intrarectal infection with simian-human immunodeficiency virus (SHIV). These findings suggest that modification of FcRn binding provides a mechanism not only to increase serum half-life but also to enhance mucosal localization that confers immune protection. Mutations that enhance FcRn function could therefore increase the potency and durability of passive immunization strategies to prevent HIV-1 infection. JF - Nature AU - Ko, Sung-Youl AU - Pegu, Amarendra AU - Rudicell, Rebecca S AU - Yang, Zhi-yong AU - Joyce, M Gordon AU - Chen, Xuejun AU - Wang, Keyun AU - Bao, Saran AU - Kraemer, Thomas D AU - Rath, Timo AU - Zeng, Ming AU - Schmidt, Stephen D AU - Todd, John-Paul AU - Penzak, Scott R AU - Saunders, Kevin O AU - Nason, Martha C AU - Haase, Ashley T AU - Rao, Srinivas S AU - Blumberg, Richard S AU - Mascola, John R AU - Nabel, Gary J AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 40, Room 4502, MSC-3005, 40 Convent Drive, Bethesda, Maryland 20892-3005, USA. ; 1] Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 40, Room 4502, MSC-3005, 40 Convent Drive, Bethesda, Maryland 20892-3005, USA [2] Sanofi, 640 Memorial Drive, Cambridge, Massachusetts 02139, USA (R.S.R., Z.-Y.Y. and G.J.N.); Center for Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235-8505, USA (M.Z.); University of North Texas System College of Pharmacy, 3500 Camp Bowie Boulevard, RES-340J, Fort Worth, Texas 76107, USA (S.R.P.). ; Division of Gastroenterology, Department of Medicine, Brigham &Women's Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA. ; 1] Department of Microbiology, Medical School, University of Minnesota, 420 Delaware Street South East, Minneapolis, Minnesota 55455, USA [2] Sanofi, 640 Memorial Drive, Cambridge, Massachusetts 02139, USA (R.S.R., Z.-Y.Y. and G.J.N.); Center for Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235-8505, USA (M.Z.); University of North Texas System College of Pharmacy, 3500 Camp Bowie Boulevard, RES-340J, Fort Worth, Texas 76107, USA (S.R.P.). ; 1] Clinical Pharmacokinetics Laboratory, Pharmacy Department, Clinical Center, National Institutes of Health, Building 10, 10 Center Drive, Bethesda, Maryland 20814, USA [2] Sanofi, 640 Memorial Drive, Cambridge, Massachusetts 02139, USA (R.S.R., Z.-Y.Y. and G.J.N.); Center for Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235-8505, USA (M.Z.); University of North Texas System College of Pharmacy, 3500 Camp Bowie Boulevard, RES-340J, Fort Worth, Texas 76107, USA (S.R.P.). ; Biostatistics Research Branch, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 6700A Rockledge Drive, Room 5235, Bethesda, Maryland 20892, USA. ; Department of Microbiology, Medical School, University of Minnesota, 420 Delaware Street South East, Minneapolis, Minnesota 55455, USA. Y1 - 2014/10/30/ PY - 2014 DA - 2014 Oct 30 SP - 642 EP - 645 VL - 514 IS - 7524 KW - Antibodies, Neutralizing KW - 0 KW - Antibodies, Viral KW - Antigens, CD4 KW - FCGR3A protein, human KW - Fc receptor, neonatal KW - HIV Antibodies KW - HIV Envelope Protein gp160 KW - Histocompatibility Antigens Class I KW - Receptors, Fc KW - Receptors, IgG KW - Index Medicus KW - Animals KW - Receptors, IgG -- immunology KW - Transcytosis KW - Receptors, IgG -- metabolism KW - Administration, Rectal KW - Antigens, CD4 -- metabolism KW - Mutagenesis, Site-Directed KW - HIV Antibodies -- blood KW - Half-Life KW - Immunity, Mucosal -- immunology KW - Macaca mulatta KW - Binding Sites -- genetics KW - Male KW - Simian Immunodeficiency Virus -- immunology KW - HIV Envelope Protein gp160 -- immunology KW - HIV -- immunology KW - Intestinal Mucosa -- immunology KW - HIV Antibodies -- genetics KW - Rectum -- immunology KW - Mice KW - Antibody Affinity -- immunology KW - Antibody Affinity -- genetics KW - HIV Antibodies -- immunology KW - HIV Envelope Protein gp160 -- chemistry KW - Immunization, Passive KW - HIV Antibodies -- analysis KW - Antibody-Dependent Cell Cytotoxicity -- immunology KW - Female KW - HIV -- chemistry KW - Simian Acquired Immunodeficiency Syndrome -- immunology KW - Antibodies, Neutralizing -- analysis KW - Histocompatibility Antigens Class I -- immunology KW - Simian Acquired Immunodeficiency Syndrome -- prevention & control KW - Antibodies, Viral -- immunology KW - Antibodies, Viral -- analysis KW - Antibodies, Viral -- blood KW - Receptors, Fc -- immunology KW - Antibodies, Viral -- genetics KW - Antibodies, Neutralizing -- genetics KW - HIV Infections -- immunology KW - HIV Infections -- prevention & control KW - Antibodies, Neutralizing -- blood KW - Antibodies, Neutralizing -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1619316990?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Enhanced+neonatal+Fc+receptor+function+improves+protection+against+primate+SHIV+infection.&rft.au=Ko%2C+Sung-Youl%3BPegu%2C+Amarendra%3BRudicell%2C+Rebecca+S%3BYang%2C+Zhi-yong%3BJoyce%2C+M+Gordon%3BChen%2C+Xuejun%3BWang%2C+Keyun%3BBao%2C+Saran%3BKraemer%2C+Thomas+D%3BRath%2C+Timo%3BZeng%2C+Ming%3BSchmidt%2C+Stephen+D%3BTodd%2C+John-Paul%3BPenzak%2C+Scott+R%3BSaunders%2C+Kevin+O%3BNason%2C+Martha+C%3BHaase%2C+Ashley+T%3BRao%2C+Srinivas+S%3BBlumberg%2C+Richard+S%3BMascola%2C+John+R%3BNabel%2C+Gary+J&rft.aulast=Ko&rft.aufirst=Sung-Youl&rft.date=2014-10-30&rft.volume=514&rft.issue=7524&rft.spage=642&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=1476-4687&rft_id=info:doi/10.1038%2Fnature13612 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-04 N1 - Date created - 2014-10-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Immunol. 2006 Jan 1;176(1):346-56 [16365427] J Virol. 2005 Aug;79(16):10108-25 [16051804] J Biol Chem. 2006 Aug 18;281(33):23514-24 [16793771] Int Immunol. 2006 Dec;18(12):1759-69 [17077181] Vaccine. 2007 Feb 9;25(8):1398-408 [17113201] Nat Rev Immunol. 2007 Sep;7(9):715-25 [17703228] Nature. 2007 Sep 6;449(7158):101-4 [17805298] Nat Rev Immunol. 2008 Jan;8(1):34-47 [18064051] Proc Natl Acad Sci U S A. 2008 May 27;105(21):7552-7 [18490657] PLoS Pathog. 2009 May;5(5):e1000433 [19436712] Adv Immunol. 2009;103:77-115 [19755184] Science. 2009 Oct 9;326(5950):285-9 [19729618] J Virol. 2010 Feb;84(3):1302-13 [19906907] J Virol. 2010 Feb;84(3):1439-52 [19939925] Nat Biotechnol. 2010 Feb;28(2):157-9 [20081867] Science. 2010 Aug 13;329(5993):856-61 [20616233] Proc Natl Acad Sci U S A. 2011 Mar 15;108(11):4388-93 [21368166] J Clin Invest. 2011 Mar;121(3):998-1008 [21393864] Nature. 2011 Sep 22;477(7365):466-70 [21849977] J Virol. 2012 Aug;86(16):8672-80 [22674985] Proc Natl Acad Sci U S A. 2012 Nov 13;109(46):18921-5 [23100539] Nature. 2012 Nov 15;491(7424):406-12 [23151583] Nat Rev Immunol. 2013 Sep;13(9):693-701 [23969737] J Virol. 2013 Nov;87(21):11604-16 [23966410] Antimicrob Agents Chemother. 2013 Dec;57(12):6147-53 [24080653] Immunity. 2013 Dec 12;39(6):1095-107 [24290911] Sci Transl Med. 2014 Jul 2;6(243):243ra88 [24990883] J Biol Chem. 2002 Aug 2;277(31):28038-50 [12023961] J Immunol. 2002 Nov 1;169(9):5171-80 [12391234] J Immunol. 2003 Apr 1;170(7):3528-33 [12646614] Immunity. 2004 Jun;20(6):769-83 [15189741] Proc Natl Acad Sci U S A. 2004 Jun 29;101(26):9763-8 [15210944] Proc Natl Acad Sci U S A. 1969 May;63(1):78-85 [5257969] Gastroenterology. 1990 Jan;98(1):56-8 [2152776] J Infect Dis. 1991 Jan;163(1):1-6 [1845806] Proc Natl Acad Sci U S A. 1992 Jan 15;89(2):638-42 [1530991] J Immunol Methods. 2006 Jan 20;308(1-2):53-67 [16343526] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nature13612 ER - TY - JOUR T1 - Epigenetic silencing of microRNA-373 to epithelial-mesenchymal transition in non-small cell lung cancer through IRAK2 and LAMP1 axes. AN - 1561972937; 25063738 AB - The role of microRNAs (miRNAs) in carcinogenesis as tumor suppressors or oncogenes has been widely reported. Epigenetic change is one of the mechanisms of transcriptional silencing of miRNAs in cancer. To identify lung cancer-related miRNAs that are mediated by histone modification, we conducted microarray analysis in the Calu-6 non-small cell lung cancer (NSCLC) cell line after treatment with suberoylanilide hydroxamic acid (SAHA), a histone deacetylase (HDAC) inhibitor. The expression level of miR-373 was enhanced by SAHA treatment in this cell line by microarray and the following quantitative RT-PCR analyses. Treatment with another HDAC inhibitor, Trichostatin A, restored the levels of miR-373 expression in A549 and Calu-6 cells, while demethylation drug treatment did not. Importantly, miR-373 was found to be down-regulated in NSCLC tissues and cell lines. Transfection of miR-373 into A549 and Calu-6 cells attenuated cell proliferation, migration, and invasion and reduced the expression of mesenchymal markers. Additional microarray analysis of miR-373-transfected cells and computational predictions identified IRAK2 and LAMP1 as targets of miR-373. Knockdown of these two genes showed similar biological effects to those of miR-373 overexpression. In clinical samples, overexpression of IRAK2 correlated with decreased disease-free survival of patients with non-adenocarcinoma. In conclusion, we found that miR-373 is silenced by histone modification in lung cancer cells and identified its function as a tumor suppressor and negative regulator of the mesenchymal phenotype through downstream IRAK2 and LAMP1 target genes. Published by Elsevier Ireland Ltd. JF - Cancer letters AU - Seol, Hyang Sook AU - Akiyama, Yoshimitsu AU - Shimada, Shu AU - Lee, Hee Jin AU - Kim, Tae Im AU - Chun, Sung Min AU - Singh, Shree Ram AU - Jang, Se Jin AD - Department of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea; Asan Center for Cancer Genome Discovery, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea. ; Department of Molecular Oncology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8519, Japan. ; Department of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea. ; Asan Center for Cancer Genome Discovery, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea. ; Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. Electronic address: singhshr@mail.nih.gov. ; Department of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea; Asan Center for Cancer Genome Discovery, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea. Electronic address: jangsejin@amc.seoul.kr. Y1 - 2014/10/28/ PY - 2014 DA - 2014 Oct 28 SP - 232 EP - 241 VL - 353 IS - 2 KW - Histones KW - 0 KW - LAMP1 protein, human KW - Lysosome-Associated Membrane Glycoproteins KW - MIRN373 microRNA, human KW - MicroRNAs KW - Interleukin-1 Receptor-Associated Kinases KW - EC 2.7.11.1 KW - Index Medicus KW - IRAK2 KW - LAMP1 KW - Histone deacetylase KW - Non-small cell lung cancer KW - microRNA-373 KW - Tumor suppressor KW - Kaplan-Meier Estimate KW - Gene Expression Regulation, Neoplastic KW - Disease-Free Survival KW - Humans KW - Histones -- metabolism KW - Protein Processing, Post-Translational KW - Cell Line, Tumor KW - Male KW - Female KW - Proportional Hazards Models KW - Multivariate Analysis KW - Epithelial-Mesenchymal Transition KW - Carcinoma, Non-Small-Cell Lung -- metabolism KW - MicroRNAs -- metabolism KW - Carcinoma, Non-Small-Cell Lung -- mortality KW - Lung Neoplasms -- mortality KW - Lysosome-Associated Membrane Glycoproteins -- metabolism KW - Epigenesis, Genetic KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism KW - Interleukin-1 Receptor-Associated Kinases -- metabolism KW - Carcinoma, Non-Small-Cell Lung -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561972937?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Epigenetic+silencing+of+microRNA-373+to+epithelial-mesenchymal+transition+in+non-small+cell+lung+cancer+through+IRAK2+and+LAMP1+axes.&rft.au=Seol%2C+Hyang+Sook%3BAkiyama%2C+Yoshimitsu%3BShimada%2C+Shu%3BLee%2C+Hee+Jin%3BKim%2C+Tae+Im%3BChun%2C+Sung+Min%3BSingh%2C+Shree+Ram%3BJang%2C+Se+Jin&rft.aulast=Seol&rft.aufirst=Hyang&rft.date=2014-10-28&rft.volume=353&rft.issue=2&rft.spage=232&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=1872-7980&rft_id=info:doi/10.1016%2Fj.canlet.2014.07.019 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-11 N1 - Date created - 2014-09-11 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.canlet.2014.07.019 ER - TY - JOUR T1 - Systemic DNA damage accumulation under in vivo tumor growth can be inhibited by the antioxidant Tempol. AN - 1561969754; 25069035 AB - Recently we found that mice bearing subcutaneous non-metastatic tumors exhibited elevated levels of two types of complex DNA damage, i.e., double-strand breaks and oxidatively-induced clustered DNA lesions in various tissues throughout the body, both adjacent to and distant from the tumor site. This DNA damage was dependent on CCL2, a cytokine involved in the recruitment and activation of macrophages, suggesting that this systemic DNA damage was mediated via tumor-induced chronic inflammatory responses involving cytokines, activation of macrophages, and consequent free radical production. If free radicals are involved, then a diet containing an antioxidant may decrease the distant DNA damage. Here we repeated our standard protocol in cohorts of two syngeneic tumor-bearing C57BL/6NCr mice that were on a Tempol-supplemented diet. We show that double-strand break and oxidatively-induced clustered DNA lesion levels were considerably decreased, about two- to three fold, in the majority of tissues studied from the tumor-bearing mice fed the antioxidant Tempol compared to the control tumor-bearing mice. Similar results were also observed in nude mice suggesting that the Tempol effects are independent of functioning adaptive immunity. This is the first in vivo study demonstrating the effect of a dietary antioxidant on abscopal DNA damage in tissues distant from a localized source of genotoxic stress. These findings may be important for understanding the mechanisms of genomic instability and carcinogenesis caused by chronic stress-induced systemic DNA damage and for developing preventative strategies. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Cancer letters AU - Georgakilas, Alexandros G AU - Redon, Christophe E AU - Ferguson, Nicholas F AU - Kryston, Thomas B AU - Parekh, Palak AU - Dickey, Jennifer S AU - Nakamura, Asako J AU - Mitchell, James B AU - Bonner, William M AU - Martin, Olga A AD - Department of Biology, Thomas Harriot College of Arts and Sciences, East Carolina University, Greenville, NC 27858, USA; Department of Physics, National Technical University of Athens, Zografou Campus, Athens GR-15773, Greece. ; Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. ; Department of Biology, Thomas Harriot College of Arts and Sciences, East Carolina University, Greenville, NC 27858, USA. ; Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA; Office of In Vitro Diagnostics, Center for Devices and Radiological Health, Food and Drug Administration, Silver Spring, MD 20993, USA. ; Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA; Department of Biological Sciences, Faculty of Science, Ibaraki University, Ibaraki 310-8512, Japan. ; Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. ; Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA; Division of Radiation Oncology and Cancer Imaging, Peter MacCallum Cancer Centre, Vic. 3002, Australia; Laboratory of Molecular Radiation Biology, Peter MacCallum Cancer Centre, Vic. 3002, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Melbourne, Vic. 3002, Australia. Electronic address: olga.martin@petermac.org. Y1 - 2014/10/28/ PY - 2014 DA - 2014 Oct 28 SP - 248 EP - 257 VL - 353 IS - 2 KW - Antioxidants KW - 0 KW - Cyclic N-Oxides KW - Reactive Oxygen Species KW - Spin Labels KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - DNA damage KW - Tumor-bearing mice KW - Non-targeted effects KW - Tempol KW - Neoplasm Transplantation KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Gastrointestinal Tract -- pathology KW - Gastrointestinal Tract -- drug effects KW - Mice, Inbred C57BL KW - Mice, Nude KW - Mice KW - Female KW - Antioxidants -- pharmacology KW - Cyclic N-Oxides -- pharmacology KW - DNA Breaks, Double-Stranded KW - Melanoma, Experimental -- genetics KW - Carcinoma, Lewis Lung -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561969754?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Systemic+DNA+damage+accumulation+under+in+vivo+tumor+growth+can+be+inhibited+by+the+antioxidant+Tempol.&rft.au=Georgakilas%2C+Alexandros+G%3BRedon%2C+Christophe+E%3BFerguson%2C+Nicholas+F%3BKryston%2C+Thomas+B%3BParekh%2C+Palak%3BDickey%2C+Jennifer+S%3BNakamura%2C+Asako+J%3BMitchell%2C+James+B%3BBonner%2C+William+M%3BMartin%2C+Olga+A&rft.aulast=Georgakilas&rft.aufirst=Alexandros&rft.date=2014-10-28&rft.volume=353&rft.issue=2&rft.spage=248&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=1872-7980&rft_id=info:doi/10.1016%2Fj.canlet.2014.07.030 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-11 N1 - Date created - 2014-09-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Free Radic Biol Med. 2003 Jan 1;34(1):93-102 [12498984] Neurosci Res. 2003 Jan;45(1):1-8 [12507718] Nat Rev Cancer. 2003 Apr;3(4):276-85 [12671666] Am J Physiol Cell Physiol. 2003 Aug;285(2):C353-69 [12686516] Cancer Biol Ther. 2003 May-Jun;2(3):233-5 [12878854] Mutat Res. 2003 Oct 29;531(1-2):93-107 [14637248] Br J Pharmacol. 2004 Jan;141(1):105-13 [14656807] Hypertension. 2004 Feb;43(2):329-34 [14707156] Nat Cell Biol. 2004 Feb;6(2):168-70 [14755273] Mutagenesis. 2004 May;19(3):169-85 [15123782] Hepatology. 2004 Jun;39(6):1663-72 [15185308] Clin Cancer Res. 2004 Oct 1;10(19):6411-7 [15475427] Cancer Res. 1991 Feb 1;51(3):794-8 [1846317] Int J Radiat Oncol Biol Phys. 1992;22(4):803-6 [1544853] FEBS Lett. 1995 Jan 16;358(1):1-3 [7821417] Free Radic Biol Med. 1997;23(6):879-84 [9378367] Radiat Res. 2005 Mar;163(3):316-23 [15733038] Hum Mol Genet. 2005 Jun 15;14(12):1699-708 [15888486] Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14641-6 [16203985] Oncogene. 2005 Nov 10;24(49):7257-65 [16170376] Mutat Res. 2006 May 11;597(1-2):113-8 [16413041] Mutat Res. 2010 Feb;696(1):16-20 [20018253] Free Radic Biol Med. 2010 Mar 1;48(5):704-12 [20035861] Nat Rev Mol Cell Biol. 2010 Mar;11(3):220-8 [20177397] Oncologist. 2010;15(4):360-71 [20413641] Cancer Metastasis Rev. 2010 Jun;29(2):351-78 [20386957] J Biomed Opt. 2010 Mar-Apr;15(2):027006 [20459280] Mutat Res. 2010 Apr-Jun;704(1-3):152-9 [20060490] Cell Cycle. 2010 Aug 15;9(16):3256-76 [20814239] Chem Biol Interact. 2010 Nov 5;188(2):350-8 [20371364] Proc Natl Acad Sci U S A. 2010 Oct 19;107(42):17992-7 [20855610] Free Radic Biol Med. 2011 Feb 1;50(3):459-68 [21130158] Acta Cytol. 2010 Nov-Dec;54(6):1127-9 [21428160] Cancer Res. 2011 May 15;71(10):3437-41 [21558390] Mutat Res. 2011 Jun 3;711(1-2):142-9 [21185842] Mutat Res. 2011 Jun 3;711(1-2):193-201 [21216256] Free Radic Biol Med. 2011 Aug 1;51(3):780-90 [21664459] Cancer Immunol Immunother. 2011 Aug;60(8):1161-71 [21626032] Cell Cycle. 2011 Aug 1;10(15):2504-20 [21778829] J Thorac Cardiovasc Surg. 2011 Nov;142(5):1254-62 [21843894] Mutagenesis. 2012 Jan;27(1):77-86 [21980144] Cancer Res. 2012 Jun 1;72(11):2768-79 [22472119] Int J Radiat Oncol Biol Phys. 2012 Jul 15;83(4):1284-90 [22197226] Curr Mol Med. 2012 Jul 1;12(6):672-80 [22292435] Cancer Res. 2012 Sep 15;72(18):4846-55 [22805306] Cancer Lett. 2012 Dec 31;327(1-2):123-33 [22198208] Nucleic Acids Res. 2012 Nov 1;40(20):10274-86 [22941641] Radiat Res. 2013 Jul;180(1):100-9 [23682596] PLoS One. 2013;8(8):e70575 [23940596] Cancer Lett. 2015 Jan 1;356(1):72-81 [24041866] Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):103-8 [10618378] J Neurosurg. 2000 Apr;92(4):646-51 [10761655] Cancer J Sci Am. 1996 Sep-Oct;2(5):273-8 [9166544] J Leukoc Biol. 2006 Oct;80(4):705-13 [16864600] Eur J Pharmacol. 2006 Nov 7;549(1-3):50-7 [16989807] J Nutr. 2007 Jan;137(1 Suppl):229S-232S [17182831] Radiat Res. 2007 Feb;167(2):207-16 [17390728] Free Radic Biol Med. 2007 Jun 1;42(11):1632-50 [17462532] Cancer Res. 2007 May 1;67(9):4295-302 [17483342] Cell Cycle. 2007 Sep 15;6(18):2210-2 [17881892] Radiat Res. 2007 Nov;168(5):527-34 [17973547] Am J Physiol Heart Circ Physiol. 2007 Nov;293(5):H2726-37 [17675574] Mol Biosyst. 2008 Jan;4(1):30-5 [18075671] Oncogene. 2008 Jan 17;27(4):434-40 [17621264] Int J Radiat Oncol Biol Phys. 2008 Feb 1;70(2):554-62 [18207032] Aging Cell. 2008 Jan;7(1):89-100 [18005250] Nat Rev Cancer. 2008 Mar;8(3):180-92 [18273037] Nat Genet. 2008 Mar;40(3):356-61 [18246068] Cancer Res. 2008 Mar 1;68(5):1601-8 [18316625] J Radiat Res. 2008 May;49(3):203-10 [18413977] Cell Cycle. 2008 May 1;7(9):1238-45 [18418050] Science. 2008 Jun 13;320(5882):1507-10 [18483401] Nature. 2008 Jul 24;454(7203):436-44 [18650914] Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12445-50 [18711141] Cancer Res. 2008 Sep 1;68(17):7059-65 [18757420] Nat Rev Cancer. 2008 Dec;8(12):957-67 [19005492] PLoS Biol. 2008 Dec 2;6(12):2853-68 [19053174] Mutat Res. 2009 Mar 31;674(1-2):131-6 [18948225] Blood. 2000 Jul 1;96(1):307-13 [10891466] Oncogene. 2006 Jul 20;25(31):4267-75 [16532033] Nat Rev Cancer. 2009 May;9(5):351-60 [19377507] NMR Biomed. 2009 Jun;22(5):532-7 [19156686] Carcinogenesis. 2009 Oct;30(10):1686-95 [19651821] Int J Radiat Oncol Biol Phys. 2009 Nov 15;75(4):1247-53 [19857788] Chromosoma. 2009 Dec;118(6):683-92 [19707781] Am J Physiol Renal Physiol. 2010 Jan;298(1):F86-94 [19906952] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.canlet.2014.07.030 ER - TY - CPAPER T1 - Neutrophils in the Pathogenesis of Systemic Autoimmune Diseases T2 - 2014 Joint Meeting of the Society for Leukocyte Biology and The International Endotoxin and Innate Immunity Society (SLB IEIIS 2014) AN - 1645158836; 6316123 JF - 2014 Joint Meeting of the Society for Leukocyte Biology and The International Endotoxin and Innate Immunity Society (SLB IEIIS 2014) AU - Kaplan, Mariana Y1 - 2014/10/23/ PY - 2014 DA - 2014 Oct 23 KW - Autoimmune diseases KW - Leukocytes (neutrophilic) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645158836?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Joint+Meeting+of+the+Society+for+Leukocyte+Biology+and+The+International+Endotoxin+and+Innate+Immunity+Society+%28SLB+IEIIS+2014%29&rft.atitle=Neutrophils+in+the+Pathogenesis+of+Systemic+Autoimmune+Diseases&rft.au=Kaplan%2C+Mariana&rft.aulast=Kaplan&rft.aufirst=Mariana&rft.date=2014-10-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Joint+Meeting+of+the+Society+for+Leukocyte+Biology+and+The+International+Endotoxin+and+Innate+Immunity+Society+%28SLB+IEIIS+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://slbieiis2014.org/2014/PDFs-Images/2014-09-23-SLB-IEIIS-2014-Program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Jakinibs: Bedside to Genomic Switches T2 - 2014 Joint Meeting of the Society for Leukocyte Biology and The International Endotoxin and Innate Immunity Society (SLB IEIIS 2014) AN - 1645158626; 6316138 JF - 2014 Joint Meeting of the Society for Leukocyte Biology and The International Endotoxin and Innate Immunity Society (SLB IEIIS 2014) AU - O'Shea, John Y1 - 2014/10/23/ PY - 2014 DA - 2014 Oct 23 KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645158626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Joint+Meeting+of+the+Society+for+Leukocyte+Biology+and+The+International+Endotoxin+and+Innate+Immunity+Society+%28SLB+IEIIS+2014%29&rft.atitle=Jakinibs%3A+Bedside+to+Genomic+Switches&rft.au=O%27Shea%2C+John&rft.aulast=O%27Shea&rft.aufirst=John&rft.date=2014-10-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Joint+Meeting+of+the+Society+for+Leukocyte+Biology+and+The+International+Endotoxin+and+Innate+Immunity+Society+%28SLB+IEIIS+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://slbieiis2014.org/2014/PDFs-Images/2014-09-23-SLB-IEIIS-2014-Program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - JOUR T1 - A CXCR1 haplotype hampers HIV-1 matrix protein p17 biological activity. AN - 1566824279; 25121556 AB - Monocyte inflammatory processes are fundamental events in AIDS pathogenesis. HIV-1 matrix protein p17, released from infected cells, was found to exert an interleukin (IL)-8 chemokine-like activity on human monocytes, promoting their trafficking and sustaining inflammatory processes, after binding to CXCR1. A haplotype of the CXCR1 gene (CXCR1_300_142) has been associated with slow HIV disease progression. Here, we determine how CXCR1 genetic variations impact on p17 biological activity. Our results show that Jurkat cells overexpressing CXCR1 or the receptor carrying single polymorphism CXCR1_300 or CXCR1_142 are able to adhere and migrate in response to both IL-8 and p17. On the contrary, Jurkat cells overexpressing CXCR1_300_142 and monocytes of individuals with such CXCR1 polymorphisms lose the capacity to adhere and migrate in response to p17, but not to their physiological ligand IL-8. Surface plasmon resonance (SPR) and multispectral imaging flow cytometry showed that p17 bound with similar affinity to CXCR1 and CXCR1_300_142. Moreover, whereas p17 was able to activate CXCR1, it was incapable of functionally interacting with CXCR1_300_142 by phosphorylating extracellular signal-regulated kinase 1/2, which regulates chemokine-induced cellular responses. Finally, mutagenesis studies showed that, unlike IL-8, p17 does not use Glu-Leu-Arg-like motifs to activate CXCR1. Our results, showing the inability of p17 to activate CXCR1_300_142, a receptor found to be expressed on immune cells of patients with a low progression of HIV disease, point to a crucial role of p17 in AIDS pathogenesis. Our findings herein call for an exploration of the therapeutic potential of blocking the p17/CXCR1 axis in HIV infection. 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins JF - AIDS (London, England) AU - Giagulli, Cinzia AU - Caccuri, Francesca AU - Cignarella, Francesca AU - Lougaris, Vassilios AU - Martorelli, Debora AU - Bugatti, Antonella AU - Rusnati, Marco AU - Dolcetti, Riccardo AU - Vitali, Massimiliano AU - Plebani, Alessandro AU - Fiorentini, Simona AU - Caruso, Arnaldo AD - aSection of Microbiology, Department of Molecular and Translational Medicine, School of Medicine, University of Brescia, Brescia bPediatrics Clinic and Institute for Molecular Medicine 'A. Nocivelli', Department of Clinical and Experimental Sciences, University of Brescia, Brescia cCancer Bio-Immunotherapy Unit, CRO-IRCCS, National Cancer Institute, Aviano (PN) dSection of Experimental Oncology and Immunology, Department of Molecular and Translational Medicine, School of Medicine, University of Brescia, Brescia, Italy. Y1 - 2014/10/23/ PY - 2014 DA - 2014 Oct 23 SP - 2355 EP - 2364 VL - 28 IS - 16 KW - HIV Antigens KW - 0 KW - Interleukin-8 KW - Receptors, Interleukin-8A KW - gag Gene Products, Human Immunodeficiency Virus KW - p17 protein, Human Immunodeficiency Virus Type 1 KW - Index Medicus KW - AIDS/HIV KW - Cell Movement KW - HIV Infections -- virology KW - Humans KW - HIV Infections -- immunology KW - Surface Plasmon Resonance KW - Jurkat Cells KW - Flow Cytometry KW - Interleukin-8 -- metabolism KW - Protein Binding KW - HIV Antigens -- physiology KW - Receptors, Interleukin-8A -- genetics KW - Receptors, Interleukin-8A -- metabolism KW - Haplotypes KW - gag Gene Products, Human Immunodeficiency Virus -- physiology KW - gag Gene Products, Human Immunodeficiency Virus -- metabolism KW - T-Lymphocytes -- virology KW - HIV Antigens -- metabolism KW - T-Lymphocytes -- immunology KW - Host-Pathogen Interactions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566824279?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+%28London%2C+England%29&rft.atitle=A+CXCR1+haplotype+hampers+HIV-1+matrix+protein+p17+biological+activity.&rft.au=Giagulli%2C+Cinzia%3BCaccuri%2C+Francesca%3BCignarella%2C+Francesca%3BLougaris%2C+Vassilios%3BMartorelli%2C+Debora%3BBugatti%2C+Antonella%3BRusnati%2C+Marco%3BDolcetti%2C+Riccardo%3BVitali%2C+Massimiliano%3BPlebani%2C+Alessandro%3BFiorentini%2C+Simona%3BCaruso%2C+Arnaldo&rft.aulast=Giagulli&rft.aufirst=Cinzia&rft.date=2014-10-23&rft.volume=28&rft.issue=16&rft.spage=2355&rft.isbn=&rft.btitle=&rft.title=AIDS+%28London%2C+England%29&rft.issn=1473-5571&rft_id=info:doi/10.1097%2FQAD.0000000000000423 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-01 N1 - Date created - 2014-09-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/QAD.0000000000000423 ER - TY - JOUR T1 - Characterization of Functional Reprogramming during Osteoclast Development Using Quantitative Proteomics and mRNA Profiling AN - 1808675670; PQ0003450021 AB - In addition to forming macrophages and dendritic cells, monocytes in adult peripheral blood retain the ability to develop into osteoclasts, mature bone-resorbing cells. The extensive morphological and functional transformations that occur during osteoclast differentiation require substantial reprogramming of gene and protein expression. Here we employ -omic-scale technologies to examine in detail the molecular changes at discrete developmental stages in this process (precursor cells, intermediate osteoclasts, and multinuclear osteoclasts), quantitatively comparing their transcriptomes and proteomes. The data have been deposited to the ProteomeXchange with identifier PXD000471.Our analysis identified mitochondrial changes, along with several alterations in signaling pathways, as central to the development of mature osteoclasts, while also confirming changes in pathways previously implicated in osteoclast biology. In particular, changes in the expression of proteins involved in metabolism and redirection of energy flow from basic cellular function toward bone resorption appeared to play a key role in the switch from monocytic immune system function to specialized bone-turnover function. These findings provide new insight into the differentiation program involved in the generation of functional osteoclasts. JF - Molecular and Cellular Proteomics AU - An, Eunkyung AU - Narayanan, Manikandan AU - Manes, Nathan P AU - Nita-Lazar, Aleksandra AD - From the Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, nitalazarau@niaid.nih.gov Y1 - 2014/10/20/ PY - 2014 DA - 2014 Oct 20 SP - 2687 EP - 2704 PB - American Society for Biochemistry and Molecular Biology, 9650 Rockville Pike Bethesda MD 20814-3996 United States VL - 13 IS - 10 SN - 1535-9476, 1535-9476 KW - Biotechnology and Bioengineering Abstracts KW - Macrophages KW - Transformation KW - Data processing KW - Osteoclasts KW - Immune system KW - Mitochondria KW - Developmental stages KW - Peripheral blood KW - Gene expression KW - Dendritic cells KW - Energy flow KW - Osteoprogenitor cells KW - Bone resorption KW - Monocytes KW - proteomics KW - Osteoclastogenesis KW - Metabolism KW - Signal transduction KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808675670?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Proteomics&rft.atitle=Characterization+of+Functional+Reprogramming+during+Osteoclast+Development+Using+Quantitative+Proteomics+and+mRNA+Profiling&rft.au=An%2C+Eunkyung%3BNarayanan%2C+Manikandan%3BManes%2C+Nathan+P%3BNita-Lazar%2C+Aleksandra&rft.aulast=An&rft.aufirst=Eunkyung&rft.date=2014-10-20&rft.volume=13&rft.issue=10&rft.spage=2687&rft.isbn=&rft.btitle=&rft.title=Molecular+and+Cellular+Proteomics&rft.issn=15359476&rft_id=info:doi/10.1074%2Fmcp.M113.034371 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Transformation; Macrophages; Data processing; Immune system; Osteoclasts; Developmental stages; Mitochondria; Peripheral blood; Gene expression; Dendritic cells; Energy flow; Osteoprogenitor cells; Bone resorption; proteomics; Monocytes; Osteoclastogenesis; Metabolism; Signal transduction DO - http://dx.doi.org/10.1074/mcp.M113.034371 ER - TY - JOUR T1 - Formation of epichlorohydrin, a known rodent carcinogen, following oral administration of 1,3-dichloro-2-propanol in rats. AN - 1614699869; 25254956 AB - The observed toxicity and carcinogenicity of 1,3-dichloro-2-propanol (DCP) in rodents is thought to be due to the formation of reactive metabolites, epichlorohydrin (ECH) and dichloroacetone (DCA). However, there is no direct evidence for the formation of these metabolites from exposure to DCP in rodents due to the challenges of measuring these reactive intermediates directly in vivo. The objective of this work was to investigate the metabolism of DCP to ECH and DCA in vivo by first developing a sensitive analytical method in a suitable biological matrix and analyzing samples from rats administered DCP. DCA reacted rapidly in vitro in rat blood, plasma, and liver homogenate, precluding its detection. Because ECH rapidly disappeared in liver homogenate, but was relatively long-lived in plasma and blood in vitro, blood was selected for analysis of this metabolite. Following a single oral dose of 50 mg/kg DCP in male or female Harlan Sprague-Dawley rats, ECH was detected in blood with a maximum concentration reached at ≤13.7 min. ECH was cleared rapidly with a half-life of ca. 33 and 48 min in males and females, respectively. Following a single oral dose of 25 mg/kg ECH in male and female rats, the elimination half-life of ECH was ca. 34 and 20 min, respectively; the oral bioavailability of ECH was low (males, 5.2%; females, 2.1%), suggesting extensive first pass metabolism of ECH following oral administration. The area under the concentration vs time curve for ECH following oral administration of DCP and intravenous administration of ECH was used to estimate the percent of the DCP dose converted to ECH in rats. On the basis of this analysis, we concluded that in male and female rats following oral administration of 50 mg/kg DCP, ≥1.26% or ≥1.78% of the administered dose was metabolized to ECH, respectively. JF - Chemical research in toxicology AU - Waidyanatha, Suramya AU - Gaudette, Norman F AU - Hong, Yan AU - Fennell, Timothy R AD - Division of National Toxicology Program, National Institute of Environmental Health Sciences , Research Triangle Park, North Carolina 27709, United States. Y1 - 2014/10/20/ PY - 2014 DA - 2014 Oct 20 SP - 1787 EP - 1795 VL - 27 IS - 10 KW - Epichlorohydrin KW - 08OOR508C0 KW - 1,3-dichloro-2-propanol KW - 0F4P2VQC07 KW - alpha-Chlorohydrin KW - 96-24-2 KW - Index Medicus KW - Administration, Oral KW - Animals KW - Serum -- metabolism KW - Area Under Curve KW - ROC Curve KW - Liver -- metabolism KW - Mice KW - Administration, Intravenous KW - Rats KW - Rats, Sprague-Dawley KW - Half-Life KW - Liver -- drug effects KW - Gas Chromatography-Mass Spectrometry KW - Female KW - Male KW - alpha-Chlorohydrin -- analogs & derivatives KW - Epichlorohydrin -- toxicity KW - Epichlorohydrin -- metabolism KW - alpha-Chlorohydrin -- metabolism KW - Epichlorohydrin -- chemistry KW - alpha-Chlorohydrin -- toxicity KW - alpha-Chlorohydrin -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1614699869?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Formation+of+epichlorohydrin%2C+a+known+rodent+carcinogen%2C+following+oral+administration+of+1%2C3-dichloro-2-propanol+in+rats.&rft.au=Waidyanatha%2C+Suramya%3BGaudette%2C+Norman+F%3BHong%2C+Yan%3BFennell%2C+Timothy+R&rft.aulast=Waidyanatha&rft.aufirst=Suramya&rft.date=2014-10-20&rft.volume=27&rft.issue=10&rft.spage=1787&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=1520-5010&rft_id=info:doi/10.1021%2Ftx500239q LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-23 N1 - Date created - 2014-10-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mutat Res. 1983 Aug;118(3):213-26 [6877269] Biochem Pharmacol. 1983 Jun 1;32(11):1783-8 [6870920] Toxicology. 1985 Sep;36(4):325-39 [4049437] Bull Environ Contam Toxicol. 1986 Jul;37(1):41-6 [3719141] Toxicol Appl Pharmacol. 1987 Oct;91(1):46-54 [3313810] Chem Biol Interact. 1991;80(1):73-88 [1913979] J UOEH. 1992 Mar 1;14(1):13-22 [1509208] Liver. 1993 Jun;13(3):123-9 [8336524] Pharm Res. 1993 Jul;10(7):1093-5 [8378254] FEBS Lett. 1994 Feb 7;338(3):251-6 [8307189] Hum Exp Toxicol. 1994 Apr;13(4):267-70 [8204313] Mutat Res. 1994 Nov;341(1):1-15 [7523939] Toxicology. 1997 Mar 28;118(2-3):171-9 [9129171] Hum Exp Toxicol. 1997 May;16(5):262-6 [9192205] Toxicol Appl Pharmacol. 1999 Mar 15;155(3):287-91 [10079215] Chem Biol Interact. 1999 Jan 1;117(1):49-64 [10190544] Xenobiotica. 1999 May;29(5):533-45 [10379989] Food Chem Toxicol. 1999 Apr;37(4):351-5 [10418953] IARC Monogr Eval Carcinog Risks Hum. 1999;71 Pt 2:603-28 [10476464] Chem Biol Interact. 1999 Sep 30;122(2):107-15 [10528996] Bioinformatics. 2004 Nov 1;20(16):2845-7 [15117755] J Chromatogr B Analyt Technol Biomed Life Sci. 2009 May 1;877(13):1402-15 [19059011] Environ Mol Mutagen. 1988;11 Suppl 12:1-157 [3277844] Toxicol In Vitro. 2002 Jun;16(3):259-65 [12020599] Mutat Res. 1979 Apr;66(4):373-80 [379633] Xenobiotica. 1979 Oct;9(10):595-9 [532212] Toxicol Appl Pharmacol. 1981 Mar 15;57(3):401-13 [7222047] Gan. 1980 Dec;71(6):922-3 [7274636] Drug Metab Dispos. 1981 Sep-Oct;9(5):434-41 [6117442] Environ Mutagen. 1980;2(1):59-66 [7035158] Mutat Res. 1982 Jan;103(1):77-81 [7035914] Drug Metab Dispos. 1985 May-Jun;13(3):333-41 [2861993] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/tx500239q ER - TY - CPAPER T1 - The Expansion of NIH's Genomic Data Sharing Policy T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167957; 6312499 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Luetkemeier, E AU - Langlais, K AU - Baker, R AU - Fomous, C AU - Paine, T AU - Paltoo, D Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Policies KW - Data processing KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167957?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=The+Expansion+of+NIH%27s+Genomic+Data+Sharing+Policy&rft.au=Luetkemeier%2C+E%3BLanglais%2C+K%3BBaker%2C+R%3BFomous%2C+C%3BPaine%2C+T%3BPaltoo%2C+D&rft.aulast=Luetkemeier&rft.aufirst=E&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - A mouse model of cblA class isolated methylmalonic acidemia (MMA) displays reduced survival, growth failure, renal disease and secondary mitochondrial dysfunction T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167849; 6312434 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Epping, M AU - Wang, C AU - Zerfas, P AU - Elliot, G AU - Li, L. AU - Manoli, I AU - Venditti, C Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Growth rate KW - Kidney diseases KW - Animal models KW - Renal failure KW - Mitochondria KW - Survival UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167849?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=A+mouse+model+of+cblA+class+isolated+methylmalonic+acidemia+%28MMA%29+displays+reduced+survival%2C+growth+failure%2C+renal+disease+and+secondary+mitochondrial+dysfunction&rft.au=Epping%2C+M%3BWang%2C+C%3BZerfas%2C+P%3BElliot%2C+G%3BLi%2C+L.%3BManoli%2C+I%3BVenditti%2C+C&rft.aulast=Epping&rft.aufirst=M&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Imputation and subset based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33 T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167822; 6312672 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Wang, Z AU - Zhang, M AU - Zhu, B AU - Parikh, H AU - Jia, J AU - Chung, C AU - Sampson, J AU - Hoskins, J AU - Hutchinson, A AU - Burdette, L AU - Kraft, P AU - Chanock, S AU - Landi, M Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Health risks KW - Association analysis KW - Chromosomes KW - chromosome 5 KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167822?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Imputation+and+subset+based+association+analysis+across+different+cancer+types+identifies+multiple+independent+risk+loci+in+the+TERT-CLPTM1L+region+on+chromosome+5p15.33&rft.au=Wang%2C+Z%3BZhang%2C+M%3BZhu%2C+B%3BParikh%2C+H%3BJia%2C+J%3BChung%2C+C%3BSampson%2C+J%3BHoskins%2C+J%3BHutchinson%2C+A%3BBurdette%2C+L%3BKraft%2C+P%3BChanock%2C+S%3BLandi%2C+M&rft.aulast=Wang&rft.aufirst=Z&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Alignment to an Ancestry Specific Reference Genome Discovers Additional Variants Among 1000 Genomes ASW Cohort T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167758; 6312321 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Neff, R AU - Vargas, J AU - Gibbons, G AU - Davis, A Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Genomes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167758?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Alignment+to+an+Ancestry+Specific+Reference+Genome+Discovers+Additional+Variants+Among+1000+Genomes+ASW+Cohort&rft.au=Neff%2C+R%3BVargas%2C+J%3BGibbons%2C+G%3BDavis%2C+A&rft.aulast=Neff&rft.aufirst=R&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - DbGaP Genotype Fingerprint Collection T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167715; 6312373 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Jin, Y AU - Stefanov, S AU - Dracheva, S AU - Wang, Z AU - Sharopova, N AU - Sturcke, A AU - Sherry, S AU - Feolo, M Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Genotypes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=DbGaP+Genotype+Fingerprint+Collection&rft.au=Jin%2C+Y%3BStefanov%2C+S%3BDracheva%2C+S%3BWang%2C+Z%3BSharopova%2C+N%3BSturcke%2C+A%3BSherry%2C+S%3BFeolo%2C+M&rft.aulast=Jin&rft.aufirst=Y&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - A novel variant in tenascin-X may be associated with an Ehlers Danlos phenotype in patients with congenital adrenal hyperplasia T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167687; 6312417 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Morissette, R AU - Chen, W AU - Xu, Z. AU - McDonnell, N AU - Merke, D AU - Quezado, M AU - Dreiling, J Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Hyperplasia KW - Phenotypes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167687?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=A+novel+variant+in+tenascin-X+may+be+associated+with+an+Ehlers+Danlos+phenotype+in+patients+with+congenital+adrenal+hyperplasia&rft.au=Morissette%2C+R%3BChen%2C+W%3BXu%2C+Z.%3BMcDonnell%2C+N%3BMerke%2C+D%3BQuezado%2C+M%3BDreiling%2C+J&rft.aulast=Morissette&rft.aufirst=R&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Complex dynamics of meiotic recombination initiation in laboratory mouse strains T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167681; 6312508 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Brick, K AU - Smagulova, F AU - Camerini-Otero, R AU - Petukhova, G Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Recombination KW - Meiosis KW - Strains UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167681?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Complex+dynamics+of+meiotic+recombination+initiation+in+laboratory+mouse+strains&rft.au=Brick%2C+K%3BSmagulova%2C+F%3BCamerini-Otero%2C+R%3BPetukhova%2C+G&rft.aulast=Brick&rft.aufirst=K&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Genome: Unlocking Life's Code - A Museum Exhibition as a Model for Informal Genomics Education T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167516; 6312611 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Bonham, V AU - Easter, C AU - Schonman, E AU - Daulton, C AU - Wise, R AU - Hurle, B AU - Witherly, J Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Genomes KW - Education KW - Museums KW - genomics KW - Models UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167516?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Genome%3A+Unlocking+Life%27s+Code+-+A+Museum+Exhibition+as+a+Model+for+Informal+Genomics+Education&rft.au=Bonham%2C+V%3BEaster%2C+C%3BSchonman%2C+E%3BDaulton%2C+C%3BWise%2C+R%3BHurle%2C+B%3BWitherly%2C+J&rft.aulast=Bonham&rft.aufirst=V&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Using zebrafish to assess novel therapeutics and model the eye disease of cblC disease T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167507; 6312680 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Achilly, N AU - Sloan, J AU - Bishop, K AU - Jones, M AU - Sood, R AU - Venditti, C Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Eye diseases KW - Freshwater fish KW - Models KW - Danio rerio UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Using+zebrafish+to+assess+novel+therapeutics+and+model+the+eye+disease+of+cblC+disease&rft.au=Achilly%2C+N%3BSloan%2C+J%3BBishop%2C+K%3BJones%2C+M%3BSood%2C+R%3BVenditti%2C+C&rft.aulast=Achilly&rft.aufirst=N&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Genetic Heritability of Common Non-Hodgkin Lymphoma Subtypes T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167487; 6312587 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Berndt, S AU - Morton, L AU - Slager, S AU - Smedby, K AU - Miligi, L AU - Albanes, D AU - Brooks-Wilson, A AU - Monnereau, A AU - Birmann, B AU - Purdue, M AU - Vajdic, C AU - Skibola, C AU - Cerhan, J AU - Chanock, S Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Non-Hodgkin's lymphoma KW - Lymphoma KW - Heritability UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167487?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Genetic+Heritability+of+Common+Non-Hodgkin+Lymphoma+Subtypes&rft.au=Berndt%2C+S%3BMorton%2C+L%3BSlager%2C+S%3BSmedby%2C+K%3BMiligi%2C+L%3BAlbanes%2C+D%3BBrooks-Wilson%2C+A%3BMonnereau%2C+A%3BBirmann%2C+B%3BPurdue%2C+M%3BVajdic%2C+C%3BSkibola%2C+C%3BCerhan%2C+J%3BChanock%2C+S&rft.aulast=Berndt&rft.aufirst=S&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - A mutation in transferrin receptor 1 that disrupts iron internalization causes a novel immunodeficiency T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167432; 6312365 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Boyden, S AU - Jabara, H AU - Notarangelo, L AU - Fleming, M AU - Kunkel, L AU - Geha, R Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Transferrin receptors KW - Immunodeficiency KW - Iron KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167432?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=A+mutation+in+transferrin+receptor+1+that+disrupts+iron+internalization+causes+a+novel+immunodeficiency&rft.au=Boyden%2C+S%3BJabara%2C+H%3BNotarangelo%2C+L%3BFleming%2C+M%3BKunkel%2C+L%3BGeha%2C+R&rft.aulast=Boyden&rft.aufirst=S&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Aberrant DNA hypermethylation of SDHC: A novel mechanism of tumor development in Carney Triad T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167394; 6312669 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Faucz, F AU - Haller, F AU - Moskalev, E AU - Batthelmeb, S AU - Wiemann, S AU - Bieg, M AU - Bertherat, J AU - Schaefer, I.-M. AU - Maher, E AU - Werner, M AU - Carney, J AU - Hartmann, A AU - Agamy, A AU - Stratakis, C Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Tumors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167394?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Aberrant+DNA+hypermethylation+of+SDHC%3A+A+novel+mechanism+of+tumor+development+in+Carney+Triad&rft.au=Faucz%2C+F%3BHaller%2C+F%3BMoskalev%2C+E%3BBatthelmeb%2C+S%3BWiemann%2C+S%3BBieg%2C+M%3BBertherat%2C+J%3BSchaefer%2C+I.-M.%3BMaher%2C+E%3BWerner%2C+M%3BCarney%2C+J%3BHartmann%2C+A%3BAgamy%2C+A%3BStratakis%2C+C&rft.aulast=Faucz&rft.aufirst=F&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Using a population-based linkage analysis approach to identify transcript QTL in skeletal muscle tissues in a founder population T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167390; 6312310 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Hsueh, W.-C. AU - Kobes, S AU - Hanson, R Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Quantitative trait loci KW - Linkage analysis KW - Transcription KW - Skeletal muscle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167390?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Using+a+population-based+linkage+analysis+approach+to+identify+transcript+QTL+in+skeletal+muscle+tissues+in+a+founder+population&rft.au=Hsueh%2C+W.-C.%3BKobes%2C+S%3BHanson%2C+R&rft.aulast=Hsueh&rft.aufirst=W.-C.&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - A genome-wide scan identifies NFIB as important for metastasis in osteosarcoma patients T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167347; 6312588 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Mirabello, L AU - Spector, L AU - Meltzer, P AU - Largaespada, D AU - Gastier-Foster, J AU - Flanagan, A AU - Andrulis, I AU - Wunder, J AU - Lecanda, F AU - de Toledo, S. AU - Serra, M AU - Wacholder, S AU - Hoover, R AU - Savage, S AU - Helman, L Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Metastases KW - Osteosarcoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167347?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=A+genome-wide+scan+identifies+NFIB+as+important+for+metastasis+in+osteosarcoma+patients&rft.au=Mirabello%2C+L%3BSpector%2C+L%3BMeltzer%2C+P%3BLargaespada%2C+D%3BGastier-Foster%2C+J%3BFlanagan%2C+A%3BAndrulis%2C+I%3BWunder%2C+J%3BLecanda%2C+F%3Bde+Toledo%2C+S.%3BSerra%2C+M%3BWacholder%2C+S%3BHoover%2C+R%3BSavage%2C+S%3BHelman%2C+L&rft.aulast=Mirabello&rft.aufirst=L&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - RAB11FIP1 interacts with the BLOC-1 complex to retrieve melanogenic proteins from the recycling pathway and a dominant negative mutation in RAB11FIP1 causes Hermanksy-Pudlak Syndrome Type 10 (HPS-10) T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167283; 6312523 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Cullinane, A AU - Merideth, M AU - Datiles, M AU - Curry, J AU - Hansen, N AU - Teer, J AU - White, J AU - Mullikin, J AU - Huizing, M AU - Gahl, W Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Symptoms KW - Recycling KW - Mutation KW - Waste management UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=RAB11FIP1+interacts+with+the+BLOC-1+complex+to+retrieve+melanogenic+proteins+from+the+recycling+pathway+and+a+dominant+negative+mutation+in+RAB11FIP1+causes+Hermanksy-Pudlak+Syndrome+Type+10+%28HPS-10%29&rft.au=Cullinane%2C+A%3BMerideth%2C+M%3BDatiles%2C+M%3BCurry%2C+J%3BHansen%2C+N%3BTeer%2C+J%3BWhite%2C+J%3BMullikin%2C+J%3BHuizing%2C+M%3BGahl%2C+W&rft.aulast=Cullinane&rft.aufirst=A&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Data Sharing and dbGaP: A Survey of Practices and Opinions Among Human Geneticists T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645167230; 6312500 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Kaufman, D AU - Bollinger, J AU - Dvoskin, R Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Data processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167230?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Data+Sharing+and+dbGaP%3A+A+Survey+of+Practices+and+Opinions+Among+Human+Geneticists&rft.au=Kaufman%2C+D%3BBollinger%2C+J%3BDvoskin%2C+R&rft.aulast=Kaufman&rft.aufirst=D&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Individualized iterative phenotyping for genome-wide analysis of loss of function mutations T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645165351; 6312330 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Johnston, J AU - Singh, L AU - Brownell, I Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Phenotyping KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645165351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Individualized+iterative+phenotyping+for+genome-wide+analysis+of+loss+of+function+mutations&rft.au=Johnston%2C+J%3BSingh%2C+L%3BBrownell%2C+I&rft.aulast=Johnston&rft.aufirst=J&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - TRNT1 missense mutations define an autoinflammatory disease characterized by recurrent fever, severe anemia, and B-cell immunodeficiency T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645165341; 6312366 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Stoffels, M AU - Zhou, Q AU - Sediva, A AU - Pelletier, M AU - Sood, R AU - Kastner, D Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Fever KW - Missense mutation KW - Lymphocytes B KW - Immunodeficiency KW - Anemia UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645165341?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=TRNT1+missense+mutations+define+an+autoinflammatory+disease+characterized+by+recurrent+fever%2C+severe+anemia%2C+and+B-cell+immunodeficiency&rft.au=Stoffels%2C+M%3BZhou%2C+Q%3BSediva%2C+A%3BPelletier%2C+M%3BSood%2C+R%3BKastner%2C+D&rft.aulast=Stoffels&rft.aufirst=M&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Genome-Wide Analysis in Africans Provides Novel Insight into the Genetic Basis of the Metabolic Syndrome T2 - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AN - 1645165340; 6312564 JF - 2014 Annual Meeting of the American Society of Human Genetics (ASHG 2014) AU - Tekola-Ayele, F AU - Doumatey, A AU - Chen, G AU - Shriner, D AU - Bentley, A AU - Zhou, J AU - Adeyemo, A AU - Rotimi, C Y1 - 2014/10/18/ PY - 2014 DA - 2014 Oct 18 KW - Symptoms KW - Metabolic disorders KW - Africa UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645165340?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.atitle=Genome-Wide+Analysis+in+Africans+Provides+Novel+Insight+into+the+Genetic+Basis+of+the+Metabolic+Syndrome&rft.au=Tekola-Ayele%2C+F%3BDoumatey%2C+A%3BChen%2C+G%3BShriner%2C+D%3BBentley%2C+A%3BZhou%2C+J%3BAdeyemo%2C+A%3BRotimi%2C+C&rft.aulast=Tekola-Ayele&rft.aufirst=F&rft.date=2014-10-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Society+of+Human+Genetics+%28ASHG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/cgi-bin/2014/ashg14SOE.pl LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - JOUR T1 - Development of an immunologically tolerated combination of fluorescent proteins for in vivo two-photon imaging. AN - 1613941322; 25322934 AB - Combinations of fluorescent proteins (FPs) are routinely used for multi-parameter in vivo imaging experiments to visualize tagged proteins or cell populations of interest. Studies involving FPs are often limited by spectral overlap, toxicity, relative quantum efficiency, and the potential for immunological rejection upon transfer into a non-tolerant recipient. Here we evaluate the immunologic visibility of several commonly used FPs by the murine immune system and identify a spectrally compatible, immunologically tolerated combination of FPs well suited for in vivo two-photon imaging. JF - Scientific reports AU - Gossa, Selamawit AU - Nayak, Debasis AU - Zinselmeyer, Bernd H AU - McGavern, Dorian B AD - National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 2014/10/17/ PY - 2014 DA - 2014 Oct 17 SP - 6664 VL - 4 KW - Green Fluorescent Proteins KW - 147336-22-9 KW - Index Medicus KW - Animals KW - Photons KW - Fluorescence Resonance Energy Transfer KW - Mice KW - Immune Tolerance KW - Immune System -- ultrastructure KW - Green Fluorescent Proteins -- isolation & purification KW - Green Fluorescent Proteins -- immunology KW - Diagnostic Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1613941322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Development+of+an+immunologically+tolerated+combination+of+fluorescent+proteins+for+in+vivo+two-photon+imaging.&rft.au=Gossa%2C+Selamawit%3BNayak%2C+Debasis%3BZinselmeyer%2C+Bernd+H%3BMcGavern%2C+Dorian+B&rft.aulast=Gossa&rft.aufirst=Selamawit&rft.date=2014-10-17&rft.volume=4&rft.issue=&rft.spage=6664&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep06664 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-06 N1 - Date created - 2014-10-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Microsc Microanal. 2012 Aug;18(4):730-41 [22846498] Nat Methods. 2012 Aug;9(8):815-8 [22772730] J Exp Med. 2013 Apr 8;210(4):757-74 [23530125] FEBS Lett. 2000 Aug 18;479(3):131-5 [10981721] Proc Natl Acad Sci U S A. 2001 Jan 16;98(2):462-7 [11209050] FEBS Lett. 2002 Jan 30;511(1-3):11-4 [11821040] BMC Biotechnol. 2002 Jun 11;2:11 [12079497] J Exp Med. 1984 Aug 1;160(2):521-40 [6332167] Nature. 1989 Nov 30;342(6249):559-61 [2573841] Science. 1990 Apr 6;248(4951):73-6 [2321027] Gene. 1992 Feb 15;111(2):229-33 [1347277] Nature. 1995 Feb 23;373(6516):663-4 [7854443] Immunity. 1998 Feb;8(2):177-87 [9491999] Nat Biotechnol. 1999 Oct;17(10):969-73 [10504696] J Cell Comp Physiol. 1962 Jun;59:223-39 [13911999] Nat Immunol. 2004 Dec;5(12):1243-50 [15543150] Nat Biotechnol. 2004 Dec;22(12):1567-72 [15558047] Nat Methods. 2005 Dec;2(12):905-9 [16299475] Genesis. 2006 Mar;44(3):130-5 [16496331] AAPS J. 2006;8(3):E501-7 [17025268] Biochem J. 2006 Dec 15;400(3):531-40 [16859491] Nat Methods. 2008 May;5(5):373-4 [18446153] Nat Methods. 2008 Jun;5(6):545-51 [18454154] Nat Methods. 2009 May;6(5):355-8 [19363494] Methods Enzymol. 2009;461:349-78 [19480927] Nat Methods. 2011 May;8(5):393-9 [21527931] J Biomed Opt. 2011 Oct;16(10):106014 [22029361] Mol Immunol. 2013 Apr;53(4):450-2 [23142929] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep06664 ER - TY - CPAPER T1 - Exploiting anti-glycan immunity to improve cancer care T2 - 66th Southeastern Regional Meeting of the American Chemical Society (SERMACS 2014) AN - 1645167148; 6324702 JF - 66th Southeastern Regional Meeting of the American Chemical Society (SERMACS 2014) AU - Gildersleeve, Jeff Y1 - 2014/10/16/ PY - 2014 DA - 2014 Oct 16 KW - Immunity KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645167148?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=66th+Southeastern+Regional+Meeting+of+the+American+Chemical+Society+%28SERMACS+2014%29&rft.atitle=Exploiting+anti-glycan+immunity+to+improve+cancer+care&rft.au=Gildersleeve%2C+Jeff&rft.aulast=Gildersleeve&rft.aufirst=Jeff&rft.date=2014-10-16&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=66th+Southeastern+Regional+Meeting+of+the+American+Chemical+Society+%28SERMACS+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://abstracts.acs.org/chem/sermacs2014/program/divisionindex.php?act=session&val=289700&prog=289700 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - JOUR T1 - Lipoxin Generation Is Related to Soluble Epoxide Hydrolase Activity in Severe Asthma AN - 1614426148; 25162465 AB - Severe asthma is characterized by airway inflammatory responses associated with aberrant metabolism of arachidonic acid. Lipoxins (LX) are arachidonate-derived pro-resolving mediators that are decreased in severe asthma, yet mechanisms for defective LX biosynthesis and a means to increase LXs in severe asthma remain to be established. To determine if oxidative stress and soluble epoxide hydrolase (sEH) activity are linked to decreased LX biosynthesis in severe asthma. Aliquots of blood, sputum, and bronchoalveolar lavage fluid were obtained from asthma subjects for mediator determination. Select samples were exposed to t-butyl-hydroperoxide or sEH inhibitor (sEHI) before activation. Peripheral blood leukocyte-platelet aggregates were monitored by flow cytometry, and bronchial contraction was determined with cytokine-treated human lung sections. 8-Isoprostane levels in sputum supernatants were inversely related to LXA4 in severe asthma (r = -0.55; P = 0.03) and t-butyl-hydroperoxide decreased LXA4 and 15-epi-LXA4 biosynthesis by peripheral blood leukocytes. LXA4 and 15-epi-LXA4 levels were inversely related to sEH activity in sputum supernatants and sEHIs significantly increased 14,15-epoxy-eicosatrienoic acid and 15-epi-LXA4 generation by severe asthma whole blood and bronchoalveolar lavage fluid cells. The abundance of peripheral blood leukocyte-platelet aggregates was related to asthma severity. In a concentration-dependent manner, LXs significantly inhibited platelet-activating factor-induced increases in leukocyte-platelet aggregates (70.8% inhibition [LXA4 100 nM], 78.3% inhibition [15-epi-LXA4 100 nM]) and 15-epi-LXA4 markedly inhibited tumor necrosis factor-α-induced increases in bronchial contraction. LX levels were decreased by oxidative stress and sEH activity. Inhibitors of sEH increased LXs that mediated antiphlogistic actions, suggesting a new therapeutic approach for severe asthma. Clinical trial registered with www.clinicaltrials.gov (NCT 00595114). JF - American Journal of Respiratory and Critical Care Medicine AU - Ono, Emiko AU - Dutile, Stefanie AU - Kazani, Shamsah AU - Wechsler, Michael E AU - Yang, Jun AU - Hammock, Bruce D AU - Douda, David Nobuhiro AU - Tabet, Yacine AU - Khaddaj-Mallat, Rayan AU - Sirois, Marco AU - Sirois, Chantal AU - Rizcallah, Edmond AU - Rousseau, Éric AU - Martin, Richard AU - Sutherland, E Rand AU - Castro, Mario AU - Jarjour, Nizar N AU - Israel, Elliot AU - Levy, Bruce D Y1 - 2014/10/15/ PY - 2014 DA - 2014 Oct 15 SP - 886 EP - 97 CY - New York PB - American Thoracic Society VL - 190 IS - 8 SN - 1073449X KW - Medical Sciences--Respiratory Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1614426148?accountid=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=American+Journal+of+Respiratory+and+Critical+Care+Medicine&rft.atitle=Lipoxin+Generation+Is+Related+to+Soluble+Epoxide+Hydrolase+Activity+in+Severe+Asthma&rft.au=Ono%2C+Emiko%3BDutile%2C+Stefanie%3BKazani%2C+Shamsah%3BWechsler%2C+Michael+E%3BYang%2C+Jun%3BHammock%2C+Bruce+D%3BDouda%2C+David+Nobuhiro%3BTabet%2C+Yacine%3BKhaddaj-Mallat%2C+Rayan%3BSirois%2C+Marco%3BSirois%2C+Chantal%3BRizcallah%2C+Edmond%3BRousseau%2C+%C3%89ric%3BMartin%2C+Richard%3BSutherland%2C+E+Rand%3BCastro%2C+Mario%3BJarjour%2C+Nizar+N%3BIsrael%2C+Elliot%3BLevy%2C+Bruce+D&rft.aulast=Ono&rft.aufirst=Emiko&rft.date=2014-10-15&rft.volume=190&rft.issue=8&rft.spage=886&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Respiratory+and+Critical+Care+Medicine&rft.issn=1073449X&rft_id=info:doi/ LA - English DB - ProQuest Central N1 - Copyright - Copyright American Thoracic Society Oct 15, 2014 N1 - Last updated - 2017-01-07 ER - TY - JOUR T1 - CD47 signaling regulates the immunosuppressive activity of VEGF in T cells. AN - 1586100723; 25200950 AB - Thrombospondin-1 (TSP1) inhibits angiogenesis, in part, by interacting with the ubiquitous cell-surface receptor CD47. In endothelial cells, CD47 interacts directly with vascular endothelial growth factor receptor (VEGFR)-2, and TSP1 inhibits VEGFR2 phosphorylation and signaling by disrupting this association. We show that CD47 similarly associates with and regulates VEGFR2 in T cells. TSP1 inhibits phosphorylation of VEGFR2 and its downstream target Src in wild type but not in CD47-deficient human Jurkat and primary murine T cells. VEGFR2 signaling inhibits proliferation and TCR signaling in wild type T cells. However, ligation of CD47 by TSP1 or loss of CD47 expression reverses some inhibitory effects of VEGF on proliferation and T cell activation. We further found that VEGF and VEGFR2 expression are upregulated in CD47-deficient murine CD4(+) and human Jurkat T cells, and the resulting autocrine VEGFR2 signaling enhances proliferation and some TCR responses in the absence of CD47. Thus, CD47 signaling modulates the ability of VEGF to regulate proliferation and TCR signaling, and autocrine production of VEGF by T cells contributes to this regulation. This provides a mechanism to understand the context-dependent effects of TSP1 and VEGF on T cell activation, and reveals an important role for CD47 signaling in regulating T cell production of the major angiogenic factor VEGF. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kaur, Sukhbir AU - Chang, Tiffany AU - Singh, Satya P AU - Lim, Langston AU - Mannan, Poonam AU - Garfield, Susan H AU - Pendrak, Michael L AU - Soto-Pantoja, David R AU - Rosenberg, Avi Z AU - Jin, Shelly AU - Roberts, David D AD - Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20982; ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20982; and. ; Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. ; Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20982; droberts@helix.nih.gov. Y1 - 2014/10/15/ PY - 2014 DA - 2014 Oct 15 SP - 3914 EP - 3924 VL - 193 IS - 8 KW - Antigens, CD47 KW - 0 KW - CD47 protein, human KW - Receptors, Antigen, T-Cell KW - Thrombospondin 1 KW - VEGFA protein, human KW - Vascular Endothelial Growth Factor A KW - KDR protein, human KW - EC 2.7.10.1 KW - Vascular Endothelial Growth Factor Receptor-2 KW - src-Family Kinases KW - EC 2.7.10.2 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Humans KW - Jurkat Cells KW - Receptors, Antigen, T-Cell -- immunology KW - Cell Line, Tumor KW - Mice KW - Cell Proliferation KW - Mice, Knockout KW - Neovascularization, Pathologic -- immunology KW - Phosphorylation KW - CD8-Positive T-Lymphocytes -- immunology KW - Lymphocyte Activation -- immunology KW - src-Family Kinases -- metabolism KW - Signal Transduction -- immunology KW - Up-Regulation KW - Cell Communication -- immunology KW - Vascular Endothelial Growth Factor A -- biosynthesis KW - Antigens, CD47 -- genetics KW - Vascular Endothelial Growth Factor Receptor-2 -- biosynthesis KW - CD4-Positive T-Lymphocytes -- immunology KW - Antigens, CD47 -- immunology KW - Thrombospondin 1 -- immunology KW - Antigens, CD47 -- biosynthesis KW - Vascular Endothelial Growth Factor A -- immunology KW - Vascular Endothelial Growth Factor Receptor-2 -- metabolism KW - Immune Tolerance UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1586100723?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=CD47+signaling+regulates+the+immunosuppressive+activity+of+VEGF+in+T+cells.&rft.au=Kaur%2C+Sukhbir%3BChang%2C+Tiffany%3BSingh%2C+Satya+P%3BLim%2C+Langston%3BMannan%2C+Poonam%3BGarfield%2C+Susan+H%3BPendrak%2C+Michael+L%3BSoto-Pantoja%2C+David+R%3BRosenberg%2C+Avi+Z%3BJin%2C+Shelly%3BRoberts%2C+David+D&rft.aulast=Kaur&rft.aufirst=Sukhbir&rft.date=2014-10-15&rft.volume=193&rft.issue=8&rft.spage=3914&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.1303116 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-07 N1 - Date created - 2014-10-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Cancer Res. 1999 Oct;5(10):2963-70 [10537366] Matrix Biol. 2013 Aug 8;32(6):316-24 [23499828] J Immunol. 2000 Apr 15;164(8):3996-4002 [10754290] J Immunol. 2001 Feb 15;166(4):2427-36 [11160302] J Cell Biol. 2002 Apr 29;157(3):509-19 [11980922] Cancer Immunol Immunother. 2002 Aug;51(6):293-8 [12111117] J Clin Oncol. 2002 Nov 1;20(21):4368-80 [12409337] J Biol Chem. 2002 Nov 8;277(45):42859-66 [12218055] J Immunol. 2003 Apr 1;170(7):3544-53 [12646616] Nat Rev Cancer. 2003 Jun;3(6):401-10 [12778130] Clin Cancer Res. 2003 Nov 15;9(15):5721-8 [14654557] J Immunol. 2004 Apr 1;172(7):4618-23 [15034080] Nature. 1996 Apr 4;380(6573):435-9 [8602241] Nat Med. 1996 Oct;2(10):1096-103 [8837607] J Immunol. 1997 Jan 15;158(2):677-84 [8992983] J Exp Med. 1997 Jan 6;185(1):1-11 [8996237] J Immunol. 1998 Feb 1;160(3):1224-32 [9570538] Blood. 1998 Dec 1;92(11):4150-66 [9834220] Int Immunol. 1999 May;11(5):707-18 [10330276] EXS. 2005;(94):209-31 [15617481] J Biol Chem. 2006 Sep 8;281(36):26069-80 [16835222] J Immunol. 2006 Sep 15;177(6):3534-41 [16951312] Blood. 2006 Oct 15;108(8):2624-31 [16638931] Blood. 2006 Nov 1;108(9):3112-20 [16835379] J Immunol. 2007 May 1;178(9):5930-9 [17442977] J Immunol. 2007 Jun 1;178(11):6994-7005 [17513749] Mol Cancer Res. 2008 Mar;6(3):352-63 [18337445] Oncogene. 2008 Jun 26;27(28):3999-4007 [18278068] Nat Rev Cancer. 2009 Mar;9(3):182-94 [19194382] Cell Immunol. 2009;256(1-2):72-8 [19249018] J Immunol. 2010 Jan 15;184(2):545-9 [20008289] Exp Diabetes Res. 2009;2009:267107 [20111736] J Biol Chem. 2010 Dec 10;285(50):38923-32 [20923780] J Biol Chem. 2011 Jan 7;286(1):737-45 [20974861] Oncogene. 2011 Mar 10;30(10):1205-12 [21057529] J Biol Chem. 2011 Apr 29;286(17):14991-5002 [21343308] Cancer Lett. 2011 Oct 28;309(2):145-50 [21683519] Int J Cancer. 2012 Feb 15;130(4):857-64 [21445972] Matrix Biol. 2012 Apr;31(3):162-9 [22266027] J Exp Med. 2012 Mar 12;209(3):507-20 [22393126] Cancer Lett. 2012 May 28;318(2):221-5 [22182449] Nature. 2012 Apr 5;484(7392):44-6 [22481354] J Exp Med. 2012 Jul 2;209(7):1363-77 [22689825] Chin Med J (Engl). 2012 Jun;125(11):2025-31 [22884072] Cancer Res. 2012 Aug 15;72(16):3912-8 [22693250] Sci Rep. 2013;3:1673 [23591719] J Immunol. 2000 Mar 15;164(6):2947-54 [10706681] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4049/jimmunol.1303116 ER - TY - JOUR T1 - Perfluorinated compounds: emerging POPs with potential immunotoxicity. AN - 1563986924; 24503008 AB - Perfluorinated compounds (PFCs) have been recognized as an important class of environmental contaminants commonly detected in blood samples of both wildlife and humans. These compounds have been in use for more than 60 years as surface treatment chemicals, polymerization aids, and surfactants. They possess a strong carbon-fluorine bond, which leads to their environmental persistence. There is evidence from both epidemiology and laboratory studies that PFCs may be immunotoxic, affecting both cell-mediated and humoral immunity. Reported effects of PFCs include decreased spleen and thymus weights and cellularity, reduced specific antibody production, reduced survival after influenza infection, and altered cytokine production. Immunosuppression is a critical effect associated with exposure to PFCs, as it has been reported to reduce antibody responses to vaccination in children. Mounting evidence suggests that immunotoxicity in experimental animals can occur at serum concentrations below, within, or just above the reported range for highly exposed humans and wildlife. Considering bioaccumulation and exposure to multiple PFCs, the risk of immunotoxicity for humans and wildlife cannot be discounted. This review will discuss current and recently published work exploring the immunomodulatory effects of PFCs in experimental animals and humans. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Toxicology letters AU - Corsini, Emanuela AU - Luebke, Robert W AU - Germolec, Dori R AU - DeWitt, Jamie C AD - Laboratory of Toxicology, Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Italy. Electronic address: emanuela.corsini@unimi.it. ; U.S. Environmental Protection Agency/Office of Research and Development/National Health and Environmental Effects Research Laboratory, Research Triangle Park, NC, USA. ; National Toxicology Program, National Institute of Environmental Health Sciences, NIH, RTP, NC, USA. ; Department of Pharmacology and Toxicology, Brody School of Medicine, East Carolina University, Greenville, NC, USA. Y1 - 2014/10/15/ PY - 2014 DA - 2014 Oct 15 SP - 263 EP - 270 VL - 230 IS - 2 KW - Alkanesulfonic Acids KW - 0 KW - Caprylates KW - Fluorocarbons KW - PPAR alpha KW - perfluorooctanoic acid KW - 947VD76D3L KW - perfluorooctane sulfonic acid KW - 9H2MAI21CL KW - Index Medicus KW - Cytokine KW - PPAR-α receptor KW - Vaccination KW - Perfluorinated compounds KW - Immunosuppression KW - Animals KW - Humans KW - Alkanesulfonic Acids -- toxicity KW - Caprylates -- toxicity KW - PPAR alpha -- physiology KW - Immune System -- drug effects KW - Fluorocarbons -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1563986924?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Perfluorinated+compounds%3A+emerging+POPs+with+potential+immunotoxicity.&rft.au=Corsini%2C+Emanuela%3BLuebke%2C+Robert+W%3BGermolec%2C+Dori+R%3BDeWitt%2C+Jamie+C&rft.aulast=Corsini&rft.aufirst=Emanuela&rft.date=2014-10-15&rft.volume=230&rft.issue=2&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Toxicology+letters&rft.issn=1879-3169&rft_id=info:doi/10.1016%2Fj.toxlet.2014.01.038 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-25 N1 - Date created - 2014-09-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Toxicol Sci. 2009 Dec;34(6):687-91 [19952504] Toxicology. 2010 Jan 12;267(1-3):132-9 [19900501] Environ Health Perspect. 2010 Aug;118(8):1100-8 [20423814] Nephrol Dial Transplant. 2010 Nov;25(11):3593-9 [20501458] Environ Res. 2010 Nov;110(8):773-7 [20800832] Toxicol Appl Pharmacol. 2011 Jan 15;250(2):108-16 [21075133] Environ Sci Technol. 2011 Feb 1;45(3):1121-6 [21166449] J Immunotoxicol. 2011 Jan-Mar;8(1):17-29 [21261439] J Immunotoxicol. 2011 Jan-Mar;8(1):30-8 [21299352] Environ Int. 2011 May;37(4):687-93 [21334069] Toxicol In Vitro. 2011 Jun;25(4):960-8 [21397682] Environ Res. 2011 Aug;111(6):785-91 [21601844] Arch Toxicol. 2011 Oct;85(10):1235-44 [21327619] Fundam Appl Toxicol. 1996 Apr;30(2):220-8 [8812269] Fundam Appl Toxicol. 1996 Mar;30(1):102-8 [8812244] Mol Pharmacol. 1998 Jan;53(1):14-22 [9443928] J Natl Cancer Inst. 1998 Nov 18;90(22):1702-9 [9827524] J Occup Environ Med. 1999 Sep;41(9):799-806 [10491796] Toxicol Appl Pharmacol. 2005 Aug 7;206(2):229-36 [15967213] Toxicol Sci. 2009 Apr;108(2):367-76 [19196829] J Natl Cancer Inst. 2009 Apr 15;101(8):605-9 [19351918] J Immunotoxicol. 2008 Oct;5(4):401-12 [19404874] Toxicol Sci. 2009 May;109(1):106-12 [19240040] Environ Sci Technol. 2009 Apr 1;43(7):2641-7 [19452929] Environ Sci Technol. 2009 Jun 15;43(12):4547-54 [19603675] Environ Sci Technol. 2009 Aug 1;43(15):5565-75 [19731646] Toxicol Appl Pharmacol. 2012 Jan 15;258(2):248-55 [22119708] JAMA. 2012 Jan 25;307(4):391-7 [22274686] Environ Int. 2012 Apr;40:187-95 [21864910] Environ Res. 2012 Jan;112:118-25 [22030285] Toxicol Pathol. 2012;40(2):300-11 [22109712] PLoS One. 2013;8(2):e56969 [23441227] Chemosphere. 2013 May;91(6):725-32 [23498059] J Immunotoxicol. 2013 Oct-Dec;10(4):373-9 [23350954] Int J Androl. 2006 Feb;29(1):166-71; discussion 181-5 [16466536] Toxicol Sci. 2006 Apr;90(2):269-95 [16322072] J Occup Environ Med. 2006 Aug;48(8):771-9 [16902369] Toxicol Sci. 2007 Jan;95(1):108-17 [17047030] Chemosphere. 2007 May;67(10):2011-9 [17250873] Environ Sci Technol. 2007 Apr 1;41(7):2237-42 [17438769] Inflamm Res. 2000 Oct;49(10):497-505 [11089900] Clin Exp Immunol. 2000 Nov;122(2):219-26 [11091278] Toxicol Sci. 2001 Mar;60(1):44-55 [11222872] Trends Biochem Sci. 2001 Mar;26(3):186-90 [11246025] Biochem Pharmacol. 2001 Oct 15;62(8):1133-40 [11597582] Nat Immunol. 2002 Jan;3(1):69-75 [11743587] Int Immunopharmacol. 2002 Feb;2(2-3):389-97 [11811941] Biochem Pharmacol. 2002 May 15;63(10):1893-900 [12034374] Biochem Pharmacol. 2002 Sep;64(5-6):963-70 [12213593] EMBO J. 2003 Mar 17;22(6):1313-24 [12628924] Toxicol Lett. 2004 Apr 1;149(1-3):109-14 [15093255] Regul Toxicol Pharmacol. 2004 Jun;39(3):363-80 [15135214] Cancer Res. 2004 Jun 1;64(11):3849-54 [15172993] Toxicol Appl Pharmacol. 2004 Aug 15;199(1):61-70 [15289091] Crit Rev Toxicol. 2004 Jul-Aug;34(4):351-84 [15328768] Am Ind Hyg Assoc J. 1980 Aug;41(8):584-9 [7405826] Exp Mol Pathol. 1987 Aug;47(1):98-109 [3609246] Fundam Appl Toxicol. 1992 Feb;18(2):200-10 [1534777] Water Sci Technol. 2009;60(6):1533-44 [19759456] Epidemiology. 2009 Nov;20(6):921-8 [19797969] J Environ Sci Health A Tox Hazard Subst Environ Eng. 2009 Oct;44(12):1145-99 [19847705] Ann Epidemiol. 2007 Jun;17(6):471-8 [17448680] J Toxicol Environ Health A. 2007 Jul;70(13):1130-41 [17558808] Environ Health Perspect. 2007 Sep;115(9):1298-305 [17805419] Toxicol Sci. 2007 Oct;99(2):366-94 [17519394] Ann Epidemiol. 2008 Jan;18(1):15-22 [17900928] Environ Health Perspect. 2008 May;116(5):644-50 [18470313] Toxicol Sci. 2008 Jul;104(1):144-54 [18359764] Toxicol Sci. 2008 Sep;105(1):86-96 [18559402] Environ Sci Technol. 2008 Aug 15;42(16):6291-5 [18767701] J Toxicol Environ Health A. 2008;71(23):1516-25 [18923994] Crit Rev Toxicol. 2009;39(1):76-94 [18802816] J Occup Environ Med. 2009 Mar;51(3):364-72 [19225424] Int J Hyg Environ Health. 2009 May;212(3):239-70 [18565792] Fundam Appl Toxicol. 1993 Jul;21(1):71-82 [8365588] J Occup Med. 1993 Sep;35(9):950-4 [8229349] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.toxlet.2014.01.038 ER - TY - JOUR T1 - Profiling of the Tox21 Chemical Collection for Mitochondrial Function to Identify Compounds that Acutely Decrease Mitochondrial Membrane Potential AN - 1654685937; PQ0001052561 AB - Background: Mitochondrial dysfunction has been implicated in the pathogenesis of a variety of disorders including cancer, diabetes, and neurodegenerative and cardiovascular diseases. Understanding whether different environmental chemicals and druglike molecules impact mitochondrial function represents an initial step in predicting exposure-related toxicity and defining a possible role for such compounds in the onset of various diseases. Objectives: We sought to identify individual chemicals and general structural features associated with changes in mitochondrial membrane potential (MMP). Methods: We used a multiplexed [two end points in one screen; MMP and adenosine triphosphate (ATP) content] quantitative high throughput screening (qHTS) approach combined with informatics tools to screen the Tox21 library of 10,000 compounds (~ 8,300 unique chemicals) at 15 concentrations each in triplicate to identify chemicals and structural features that are associated with changes in MMP in HepG2 cells. Results: Approximately 11% of the compounds (913 unique compounds) decreased MMP after 1 hr of treatment without affecting cell viability (ATP content). In addition, 309 compounds decreased MMP over a concentration range that also produced measurable cytotoxicity [half maximal inhibitory concentration (IC50) in MMP assay/IC50 in viability assay less than or equal to 3; p < 0.05]. More than 11% of the structural clusters that constitute the Tox21 library (76 of 651 clusters) were significantly enriched for compounds that decreased the MMP. Conclusions: Our multiplexed qHTS approach allowed us to generate a robust and reliable data set to evaluate the ability of thousands of drugs and environmental compounds to decrease MMP. The use of structure-based clustering analysis allowed us to identify molecular features that are likely responsible for the observed activity. Citation: Attene-Ramos MS, Huang R, Michael S, Witt KL, Richard A, Tice RR, Simeonov A, Austin CP, Xia M. 2015. Profiling of the Tox21 chemical collection for mitochondrial function to identify compounds that acutely decrease mitochondrial membrane potential. Environ Health Perspect 123:49-56; http://dx.doi.org/10.1289/ehp.1408642 JF - Environmental Health Perspectives AU - Attene-Ramos, Matias S AU - Huang, Ruili AU - Michael, Sam AU - Witt, Kristine L AU - Richard, Ann AU - Tice, Raymond R AU - Simeonov, Anton AU - Austin, Christopher P AU - Xia, Menghang AD - National Center for Advancing Translational Sciences, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Bethesda, Maryland, USA Y1 - 2014/10/10/ PY - 2014 DA - 2014 Oct 10 SP - 49 EP - 56 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 123 IS - 1 SN - 0091-6765, 0091-6765 KW - Environment Abstracts; Health & Safety Science Abstracts KW - Diabetes mellitus KW - Cytotoxicity KW - Membranes KW - Informatics KW - Toxicity KW - Cardiovascular diseases KW - Drugs KW - H 4000:Food and Drugs KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654685937?accountid=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=Profiling+of+the+Tox21+Chemical+Collection+for+Mitochondrial+Function+to+Identify+Compounds+that+Acutely+Decrease+Mitochondrial+Membrane+Potential&rft.au=Attene-Ramos%2C+Matias+S%3BHuang%2C+Ruili%3BMichael%2C+Sam%3BWitt%2C+Kristine+L%3BRichard%2C+Ann%3BTice%2C+Raymond+R%3BSimeonov%2C+Anton%3BAustin%2C+Christopher+P%3BXia%2C+Menghang&rft.aulast=Attene-Ramos&rft.aufirst=Matias&rft.date=2014-10-10&rft.volume=123&rft.issue=1&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1408642 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Diabetes mellitus; Cytotoxicity; Membranes; Informatics; Cardiovascular diseases; Toxicity; Drugs DO - http://dx.doi.org/10.1289/ehp.1408642 ER - TY - JOUR T1 - Milestones in skin carcinogenesis: the biology of multistage carcinogenesis. AN - 1612289764; 25302469 JF - The Journal of investigative dermatology AU - Balmain, Allan AU - Yuspa, Stuart H AD - Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California, USA. ; Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA. Y1 - 2014/10/10/ PY - 2014 DA - 2014 Oct 10 SP - E2 EP - E7 VL - 134 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Genes, ras KW - Animals KW - Papilloma -- etiology KW - Humans KW - DNA -- metabolism KW - Mutation KW - Skin Neoplasms -- etiology KW - Carcinogenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1612289764?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Milestones+in+skin+carcinogenesis%3A+the+biology+of+multistage+carcinogenesis.&rft.au=Balmain%2C+Allan%3BYuspa%2C+Stuart+H&rft.aulast=Balmain&rft.aufirst=Allan&rft.date=2014-10-10&rft.volume=134&rft.issue=&rft.spage=E2&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+investigative+dermatology&rft.issn=1523-1747&rft_id=info:doi/10.1038%2Fskinbio.2014.2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-12 N1 - Date created - 2014-10-11 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/skinbio.2014.2 ER - TY - JOUR T1 - Disordered amyloidogenic peptides may insert into the membrane and assemble into common cyclic structural motifs. AN - 1561032680; 24566672 AB - Aggregation of disordered amyloidogenic peptides into oligomers is the causative agent of amyloid-related diseases. In solution, disordered protein states are characterized by heterogeneous ensembles. Among these, β-rich conformers self-assemble via a conformational selection mechanism to form energetically-favored cross-β structures, regardless of their precise sequences. These disordered peptides can also penetrate the membrane, and electrophysiological data indicate that they form ion-conducting channels. Based on these and additional data, including imaging and molecular dynamics simulations of a range of amyloid peptides, Alzheimer's amyloid-β (Aβ) peptide, its disease-related variants with point mutations and N-terminal truncated species, other amyloidogenic peptides, as well as a cytolytic peptide and a synthetic gel-forming peptide, we suggest that disordered amyloidogenic peptides can also present a common motif in the membrane. The motif consists of curved, moon-like β-rich oligomers associated into annular organizations. The motif is favored in the lipid bilayer since it permits hydrophobic side chains to face and interact with the membrane and the charged/polar residues to face the solvated channel pores. Such channels are toxic since their pores allow uncontrolled leakage of ions into/out of the cell, destabilizing cellular ionic homeostasis. Here we detail Aβ, whose aggregation is associated with Alzheimer's disease (AD) and for which there are the most abundant data. AD is a protein misfolding disease characterized by a build-up of Aβ peptide as senile plaques, neurodegeneration, and memory loss. Excessively produced Aβ peptides may directly induce cellular toxicity, even without the involvement of membrane receptors through Aβ peptide-plasma membrane interactions. JF - Chemical Society reviews AU - Jang, Hyunbum AU - Arce, Fernando Teran AU - Ramachandran, Srinivasan AU - Kagan, Bruce L AU - Lal, Ratnesh AU - Nussinov, Ruth AD - Cancer and Inflammation Program, National Cancer Institute at Frederick, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702, USA. jangh2@mail.nih.gov nussinor@helix.nih.gov. Y1 - 2014/10/07/ PY - 2014 DA - 2014 Oct 07 SP - 6750 EP - 6764 VL - 43 IS - 19 KW - Amyloid beta-Peptides KW - 0 KW - Lipid Bilayers KW - Index Medicus KW - Hydrophobic and Hydrophilic Interactions KW - Humans KW - Lipid Bilayers -- chemistry KW - Molecular Dynamics Simulation KW - Alzheimer Disease -- metabolism KW - Protein Structure, Tertiary KW - Lipid Bilayers -- metabolism KW - Alzheimer Disease -- pathology KW - Amyloid beta-Peptides -- metabolism KW - Amyloid beta-Peptides -- chemistry KW - Cell Membrane -- chemistry KW - Cell Membrane -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561032680?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Society+reviews&rft.atitle=Disordered+amyloidogenic+peptides+may+insert+into+the+membrane+and+assemble+into+common+cyclic+structural+motifs.&rft.au=Jang%2C+Hyunbum%3BArce%2C+Fernando+Teran%3BRamachandran%2C+Srinivasan%3BKagan%2C+Bruce+L%3BLal%2C+Ratnesh%3BNussinov%2C+Ruth&rft.aulast=Jang&rft.aufirst=Hyunbum&rft.date=2014-10-07&rft.volume=43&rft.issue=19&rft.spage=6750&rft.isbn=&rft.btitle=&rft.title=Chemical+Society+reviews&rft.issn=1460-4744&rft_id=info:doi/10.1039%2Fc3cs60459d LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-14 N1 - Date created - 2014-09-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10427-32 [16020533] J Comput Chem. 2005 Dec;26(16):1781-802 [16222654] Proc Natl 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AN - 1561967224; 25193297 AB - The neoclerodane diterpenoid salvinorin A is a major secondary metabolite isolated from the psychoactive plant Salvia divinorum. Salvinorin A has been shown to have high affinity and selectivity for the κ-opioid receptor (KOR). To study the ligand-receptor interactions that occur between salvinorin A and the KOR, a new series of salvinorin A derivatives bearing potentially reactive Michael acceptor functional groups at C-2 was synthesized and used to probe the salvinorin A binding site. The κ-, δ-, and μ-opioid receptor (KOR, DOR and MOR, respectively) binding affinities and KOR efficacies were measured for the new compounds. Although none showed wash-resistant irreversible binding, most of them showed high affinity for the KOR, and some exhibited dual affinity to KOR and MOR. Molecular modeling techniques based on the recently-determined crystal structure of the KOR combined with results from mutagenesis studies, competitive binding, functional assays and structure-activity relationships, and previous salvinorin A-KOR interaction models were used to identify putative interaction modes of the new compounds with the KOR and MOR. Copyright © 2014 Elsevier Masson SAS. All rights reserved. JF - European journal of medicinal chemistry AU - Polepally, Prabhakar R AU - Huben, Krzysztof AU - Vardy, Eyal AU - Setola, Vincent AU - Mosier, Philip D AU - Roth, Bryan L AU - Zjawiony, Jordan K AD - Department of BioMolecular Sciences, Division of Pharmacognosy, Research Institute of Pharmaceutical Sciences, School of Pharmacy, University of Mississippi, University, MS 38677-1848, USA. ; Department of BioMolecular Sciences, Division of Pharmacognosy, Research Institute of Pharmaceutical Sciences, School of Pharmacy, University of Mississippi, University, MS 38677-1848, USA; Institute of Organic Chemistry, Technical University of Lodz, 90-924 Lodz, Poland. ; Department of Pharmacology, Division of Chemical Biology and Medicinal Chemistry, Medical School, NIMH Psychoactive Drug Screening Program, University of North Carolina, Chapel Hill, NC 27599, USA. ; Department of Medicinal Chemistry and Institute for Structural Biology and Drug Discovery, Virginia Commonwealth University, Richmond, VA 23298-0540, USA. ; Department of BioMolecular Sciences, Division of Pharmacognosy, Research Institute of Pharmaceutical Sciences, School of Pharmacy, University of Mississippi, University, MS 38677-1848, USA. Electronic address: jordan@olemiss.edu. Y1 - 2014/10/06/ PY - 2014 DA - 2014 Oct 06 SP - 818 EP - 829 VL - 85 KW - Diterpenes, Clerodane KW - 0 KW - Ligands KW - Receptors, Opioid, kappa KW - salvinorin A KW - T56W91NG6J KW - Index Medicus KW - Kappa, delta, and mu opioid receptors KW - Salvinorin A and B KW - Michael acceptor-type ligands KW - Molecular modeling KW - Models, Molecular KW - Humans KW - HEK293 Cells KW - Protein Binding KW - Protein Conformation KW - Diterpenes, Clerodane -- metabolism KW - Diterpenes, Clerodane -- chemical synthesis KW - Receptors, Opioid, kappa -- metabolism KW - Diterpenes, Clerodane -- chemistry KW - Receptors, Opioid, kappa -- chemistry KW - Drug Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561967224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+medicinal+chemistry&rft.atitle=Michael+acceptor+approach+to+the+design+of+new+salvinorin+A-based+high+affinity+ligands+for+the+kappa-opioid+receptor.&rft.au=Polepally%2C+Prabhakar+R%3BHuben%2C+Krzysztof%3BVardy%2C+Eyal%3BSetola%2C+Vincent%3BMosier%2C+Philip+D%3BRoth%2C+Bryan+L%3BZjawiony%2C+Jordan+K&rft.aulast=Polepally&rft.aufirst=Prabhakar&rft.date=2014-10-06&rft.volume=85&rft.issue=&rft.spage=818&rft.isbn=&rft.btitle=&rft.title=European+journal+of+medicinal+chemistry&rft.issn=1768-3254&rft_id=info:doi/10.1016%2Fj.ejmech.2014.07.077 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-02 N1 - Date created - 2014-09-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Angew Chem Int Ed Engl. 2011 Jan 10;50(2):467-71 [21132828] Bioorg Med Chem Lett. 2011 Jan 1;21(1):160-3 [21115248] J Nat Prod. 2011 Apr 25;74(4):718-26 [21338114] Pharmacol Rev. 2011 Jun;63(2):316-47 [21444610] Top Curr Chem. 2011;299:141-85 [21630517] Trends Pharmacol Sci. 2012 Jan;33(1):17-27 [22032986] Nature. 2012 May 17;485(7398):327-32 [22437504] Bioorg Med Chem Lett. 2013 May 15;23(10):2860-2 [23587424] J Med Chem. 2013 May 9;56(9):3435-43 [23548164] J Biol Chem. 2013 Nov 29;288(48):34470-83 [24121503] J Chem Inf Model. 2013 Mar 25;53(3):521-6 [23461591] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11934-9 [12192085] Bioorg Med Chem Lett. 2004 Oct 18;14(20):5099-102 [15380207] J Med Chem. 1984 Dec;27(12):1718-23 [6209395] J Med Chem. 1989 Jan;32(1):96-100 [2535878] J Med Chem. 1992 Jun 12;35(12):2243-7 [1319495] Chem Commun (Camb). 2005 Feb 21;(7):886-8 [15700070] Bioorg Med Chem Lett. 2005 May 2;15(9):2215-9 [15837296] Biochemistry. 2005 Jun 21;44(24):8643-51 [15952771] J Med Chem. 2005 Jul 28;48(15):4765-71 [16033256] J Med Chem. 2007 Jul 26;50(15):3751-5 [17585855] J Med Chem. 2008 Apr 24;51(8):2421-31 [18380425] J Org Chem. 2008 Jun 20;73(12):4484-90 [18498197] Biochemistry. 2009 Jul 28;48(29):6898-908 [19555087] ChemMedChem. 2010 Mar 1;5(3):351-6 [20112330] Nat Rev Drug Discov. 2011 Apr;10(4):307-17 [21455239] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ejmech.2014.07.077 ER - TY - JOUR T1 - Cisplatin in cancer therapy: molecular mechanisms of action. AN - 1609507628; 25058905 AB - Cisplatin, cisplatinum, or cis-diamminedichloroplatinum (II), is a well-known chemotherapeutic drug. It has been used for treatment of numerous human cancers including bladder, head and neck, lung, ovarian, and testicular cancers. It is effective against various types of cancers, including carcinomas, germ cell tumors, lymphomas, and sarcomas. Its mode of action has been linked to its ability to crosslink with the purine bases on the DNA; interfering with DNA repair mechanisms, causing DNA damage, and subsequently inducing apoptosis in cancer cells. However, because of drug resistance and numerous undesirable side effects such as severe kidney problems, allergic reactions, decrease immunity to infections, gastrointestinal disorders, hemorrhage, and hearing loss especially in younger patients, other platinum-containing anti-cancer drugs such as carboplatin, oxaliplatin and others, have also been used. Furthermore, combination therapies of cisplatin with other drugs have been highly considered to overcome drug-resistance and reduce toxicity. This comprehensive review highlights the physicochemical properties of cisplatin and related platinum-based drugs, and discusses its uses (either alone or in combination with other drugs) for the treatment of various human cancers. A special attention is paid to its molecular mechanisms of action, and its undesirable side effects. Copyright © 2014 Elsevier B.V. All rights reserved. JF - European journal of pharmacology AU - Dasari, Shaloam AU - Tchounwou, Paul Bernard AD - Cellomics and Toxicogenomics Research Laboratory, NIH/NIMHD RCMI-Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, 1400 Lynch Street, Box 18750, Jackson, MS 39217, USA. ; Cellomics and Toxicogenomics Research Laboratory, NIH/NIMHD RCMI-Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, 1400 Lynch Street, Box 18750, Jackson, MS 39217, USA. Electronic address: paul.b.tchounwou@jsums.edu. Y1 - 2014/10/05/ PY - 2014 DA - 2014 Oct 05 SP - 364 EP - 378 VL - 740 KW - Antineoplastic Agents KW - 0 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Platinum-based drugs KW - Mechanisms of action KW - Cancer treatment KW - Drug Therapy, Combination KW - Animals KW - Humans KW - Neoplasms -- drug therapy KW - Cisplatin -- therapeutic use KW - Cisplatin -- pharmacology KW - Cisplatin -- adverse effects KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - Neoplasms -- metabolism KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1609507628?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmacology&rft.atitle=Cisplatin+in+cancer+therapy%3A+molecular+mechanisms+of+action.&rft.au=Dasari%2C+Shaloam%3BTchounwou%2C+Paul+Bernard&rft.aulast=Dasari&rft.aufirst=Shaloam&rft.date=2014-10-05&rft.volume=740&rft.issue=&rft.spage=364&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=1879-0712&rft_id=info:doi/10.1016%2Fj.ejphar.2014.07.025 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-30 N1 - Date created - 2014-08-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Cancer. 1999 Jun 21;84(3):234-8 [10371339] Nature. 1999 Jun 24;399(6738):806-9 [10391249] J Clin Oncol. 1999 Jan;17(1):409-22 [10458260] Nature. 1965 Feb 13;205:698-9 [14287410] Mol Cell. 2004 Nov 19;16(4):521-35 [15546613] Clin 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Cancer Prev. 2014;15(6):2911-6 [24761924] Sci Prog. 2014;97(Pt 1):20-40 [24800467] PLoS One. 2014;9(5):e98418 [24846322] Br J Cancer. 2014 May 27;110(11):2677-87 [24786604] Tumour Biol. 2014 Jul;35(7):7017-24 [24748236] Tumour Biol. 2014 Jul;35(7):7035-45 [24752576] J Biol Chem. 2014 Jun 13;289(24):17163-73 [24794870] BMC Pharmacol Toxicol. 2013;14:18 [23521834] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ejphar.2014.07.025 ER - TY - JOUR T1 - Evaluating the NIH Library Editing Service: Pilot Study Used to Analyze Service Impact AN - 1667947080; 201503151 AB - Evidence-based librarianship drives initiatives and priorities in today's research centers. To evaluate the effectiveness of the National Institutes of Health (NIH) Library's Editing Service, librarians conducted a pilot study comparing edited manuscripts with the published versions. Using a random number generator, five published journal articles were chosen for evaluation from a pool of NIH manuscripts (n = 147) edited between January 2008 and February 2012. A rubric delineating categories of frequently checked writing elements was used to facilitate quantitative analysis. Findings showed that 84 percent of editors' suggestions were accepted for three of the published papers that were submitted to the originally intended journal. Adapted from the source document. JF - Science & Technology Libraries AU - Clark, Cindy AU - Sullivan, Brigit AD - National Institutes of Health (NIH) Library, Bethesda, Maryland Y1 - 2014/10/02/ PY - 2014 DA - 2014 Oct 02 SP - 351 EP - 357 PB - Taylor & Francis, Philadelphia PA VL - 33 IS - 4 SN - 0194-262X, 0194-262X KW - Evaluation KW - Scholarly publishing KW - National libraries KW - Medicine KW - Editing KW - article KW - 4.15: USER SERVICES UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667947080?accountid=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=Science+%26+Technology+Libraries&rft.atitle=Evaluating+the+NIH+Library+Editing+Service%3A+Pilot+Study+Used+to+Analyze+Service+Impact&rft.au=Clark%2C+Cindy%3BSullivan%2C+Brigit&rft.aulast=Clark&rft.aufirst=Cindy&rft.date=2014-10-02&rft.volume=33&rft.issue=4&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=Science+%26+Technology+Libraries&rft.issn=0194262X&rft_id=info:doi/10.1080%2F0194262X.2014.950000 LA - English DB - Library & Information Science Abstracts (LISA) N1 - Date revised - 2015-06-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Evaluation; National libraries; Medicine; Editing; Scholarly publishing DO - http://dx.doi.org/10.1080/0194262X.2014.950000 ER - TY - JOUR T1 - Ten Years of Change: National Library of Medicine TOXMAP Gets a New Look AN - 1667945061; 201503265 AB - The United States National Library of Medicine (NLM) TOXNET(TM) databases provide broad coverage of environmental health information covering a wide variety of topics, including access to the U.S. Environment Protection Agency (EPA)'s Toxics Release Inventory (TRI) data. The NLM web-based geographic information system (GIS), TOXMAP(TM) , provides interactive maps which show where TRI chemicals are released into the environment and links to TOXNET for information about these chemicals. TOXMAP also displays locations of Superfund sites on the EPA National Priority List, as well as information about the chemical contaminants at these sites. This column focuses on a new version of TOXMAP which brings it up to date with current web GIS technologies and user expectations. Adapted from the source document. JF - Medical Reference Services Quarterly AU - Hochstein, Colette AU - Gemoets, Darren AU - Goshorn, Jeanne AD - Division of Specialized Information Services, National Library of Medicine, Bethesda, Maryland, USA colette@nlm.nih.gov Y1 - 2014/10/02/ PY - 2014 DA - 2014 Oct 02 SP - 428 EP - 437 PB - Taylor & Francis, Philadelphia PA VL - 33 IS - 4 SN - 0276-3869, 0276-3869 KW - Product design KW - Location KW - Environmental health KW - Online data bases KW - Pollution KW - article KW - 5.23: SCIENCE, TECHNOLOGY, MEDICINE MATERIALS UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667945061?accountid=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=Ten+Years+of+Change%3A+National+Library+of+Medicine+TOXMAP+Gets+a+New+Look&rft.au=Hochstein%2C+Colette%3BGemoets%2C+Darren%3BGoshorn%2C+Jeanne&rft.aulast=Hochstein&rft.aufirst=Colette&rft.date=2014-10-02&rft.volume=33&rft.issue=4&rft.spage=428&rft.isbn=&rft.btitle=&rft.title=Medical+Reference+Services+Quarterly&rft.issn=02763869&rft_id=info:doi/10.1080%2F02763869.2014.957090 LA - English DB - Library & Information Science Abstracts (LISA) N1 - Date revised - 2015-06-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Online data bases; Environmental health; Pollution; Product design; Location DO - http://dx.doi.org/10.1080/02763869.2014.957090 ER - TY - JOUR T1 - NLM Workshop Marks 20 Years of Community Outreach and Capacity Building in HIV/AIDS AN - 1667936759; 201503425 AB - The National Library of Medicine's (NLM) AIDS Community Information Outreach Program (ACIOP) was launched in 1994 to provide the HIV/AIDS affected community with access to vital health information resources increasingly becoming available on the Internet. Three hundred awards have been made mostly to community-based organizations. An evaluation in 2012 found that most program objectives are being met; a principal recommendation going forward was that NLM seek to enhance the capacity of community-based awardees to conduct evaluations of their own projects. This article reports on a workshop whose invitees were drawn from AIDS serving organizations, along with scientists, clinicians, and information technologists, to review the evaluation findings and recommendations. They considered alternatives for improving awardees' evaluation capabilities with the help of expert consultation, identified additional steps that could be taken to make individual project results more transparent and sharable, and looked at external influences ranging from mobile health devices to the latest HIV/AIDS scientific research findings that could be used to align future awards with unmet needs in the community. The paper identifies efforts subsequently made by ACIOP managers to prioritize and operationalize guidance from the evaluation and the workshop, and discusses the benefits of community engagement. Adapted from the source document. JF - Journal of Consumer Health on the Internet AU - Dancy-Scott, Nicole AU - Dutcher, Gale A AU - Keselman, Alla AU - Siegel, Elliot R AD - National Library of Medicine, Bethesda, Maryland, USA nicole.scott@nih.gov Y1 - 2014/10/02/ PY - 2014 DA - 2014 Oct 02 SP - 357 EP - 366 PB - Taylor & Francis, Philadelphia PA VL - 18 IS - 4 SN - 1539-8285, 1539-8285 KW - Communities KW - National libraries KW - Medicine KW - HIV KW - Outreach services KW - article KW - 10.13: INFORMATION COMMUNICATION - SCIENCE, TECHNOLOGY, MEDICINE UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667936759?accountid=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+Consumer+Health+on+the+Internet&rft.atitle=NLM+Workshop+Marks+20+Years+of+Community+Outreach+and+Capacity+Building+in+HIV%2FAIDS&rft.au=Dancy-Scott%2C+Nicole%3BDutcher%2C+Gale+A%3BKeselman%2C+Alla%3BSiegel%2C+Elliot+R&rft.aulast=Dancy-Scott&rft.aufirst=Nicole&rft.date=2014-10-02&rft.volume=18&rft.issue=4&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=Journal+of+Consumer+Health+on+the+Internet&rft.issn=15398285&rft_id=info:doi/10.1080%2F15398285.2014.952999 LA - English DB - Library & Information Science Abstracts (LISA) N1 - Date revised - 2015-04-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - National libraries; Medicine; Outreach services; HIV; Communities DO - http://dx.doi.org/10.1080/15398285.2014.952999 ER - TY - JOUR T1 - Sorafenib and locoregional deep electro-hyperthermia in advanced hepatocellular carcinoma: A phase II study. AN - 1826611459; 25202410 AB - The standard treatment for advanced hepatocellular carcinoma (HCC) is sorafenib, a multikinase inhibitor of tumor cell proliferation and angiogenesis. Hyperthermia inhibits angiogenesis and promotes apoptosis. Potential synergic antiangiogenic and proapoptotic effects represent the rationale for combining sorafenib with electro-hyperthermia (EHY) in HCC. A total of 21 patients (median age, 64 years; range, 55-73 years) with advanced HCC were enrolled in the current study between February 2009 and September 2010. EHY was achieved by arranging capacitive electrodes with a deep hypothermia radiofrequency field of 13.56 Mhz at 80 W for 60 min, three times per week for six weeks, followed by two weeks without treatment, in combination with sorafenib at a dose of 800 mg every other day. According to the modified Response Evaluation Criteria in Solid Tumors criteria, 50% achieved stable disease, 5% achieved partial response and 45% achieved progressive disease. No complete response was observed. The progression-free survival (PFS) rate at six months was 38%, while the median PFS and overall survival times were 5.2 [95% confidence interval (CI), 4.2-6.2) and 10.4 (95% CI, 10-11) months, respectively. The overall incidence of treatment-related adverse events was 80%, predominantly of grade 1 or 2. Grade 3 toxicity included fatigue, diarrhea, hand-foot skin reaction and hypertension. In the present study, the sorafenib plus EHY combination was feasible and well tolerated, and no major complications were observed. The initial findings indicated that this combination offers a promising option for advanced HCC. JF - Oncology letters AU - Gadaleta-Caldarola, Gennaro AU - Infusino, Stefania AU - Galise, Ida AU - Ranieri, Girolamo AU - Vinciarelli, Gianluca AU - Fazio, Vito AU - Divella, Rosa AU - Daniele, Antonella AU - Filippelli, Gianfranco AU - Gadaleta, Cosmo Damiano AD - Interventional Radiology and Medical Oncology Unit, National Cancer Research Centre, National Cancer Institute 'Giovanni Paolo II', Bari 70124, Italy. ; Medical Oncology Unit, 'S. Francesco di Paola' Hospital, Via Promintesta, Paola 87027, Italy. ; Apulia Cancer Registry, Statistic and Epidemiology Unit, National Cancer Research Centre, National Cancer Institute 'Giovanni Paolo II', Bari 70124, Italy. ; Clinical Pathology Laboratory, National Cancer Research Centre, National Cancer Institute 'Giovanni Paolo II', Bari 70124, Italy. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 1783 EP - 1787 VL - 8 IS - 4 SN - 1792-1074, 1792-1074 KW - electro-hyperthermia KW - sorafenib KW - hepatocellular KW - carcinoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826611459?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+letters&rft.atitle=Sorafenib+and+locoregional+deep+electro-hyperthermia+in+advanced+hepatocellular+carcinoma%3A+A+phase+II+study.&rft.au=Gadaleta-Caldarola%2C+Gennaro%3BInfusino%2C+Stefania%3BGalise%2C+Ida%3BRanieri%2C+Girolamo%3BVinciarelli%2C+Gianluca%3BFazio%2C+Vito%3BDivella%2C+Rosa%3BDaniele%2C+Antonella%3BFilippelli%2C+Gianfranco%3BGadaleta%2C+Cosmo+Damiano&rft.aulast=Gadaleta-Caldarola&rft.aufirst=Gennaro&rft.date=2014-10-01&rft.volume=8&rft.issue=4&rft.spage=1783&rft.isbn=&rft.btitle=&rft.title=Oncology+letters&rft.issn=17921074&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2014-09-09 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - The Yin: An adverse health perspective of nanoceria: uptake, distribution, accumulation, and mechanisms of its toxicity. AN - 1826601737; 25243070 AB - This critical review evolved from a SNO Special Workshop on Nanoceria panel presentation addressing the toxicological risks of nanoceria: accumulation, target organs, and issues of clearance; how exposure dose/concentration, exposure route, and experimental preparation/model influence the different reported effects of nanoceria; and how can safer by design concepts be applied to nanoceria? It focuses on the most relevant routes of human nanoceria exposure and uptake, disposition, persistence, and resultant adverse effects. The pulmonary, oral, dermal, and topical ocular exposure routes are addressed as well as the intravenous route, as the latter provides a reference for the pharmacokinetic fate of nanoceria once introduced into blood. Nanoceria reaching the blood is primarily distributed to mononuclear phagocytic system organs. Available data suggest nanoceria's distribution is not greatly affected by dose, shape, or dosing schedule. Significant attention has been paid to the inhalation exposure route. Nanoceria distribution from the lung to the rest of the body is less than 1% of the deposited dose, and from the gastrointestinal tract even less. Intracellular nanoceria and organ burdens persist for at least months, suggesting very slow clearance rates. The acute toxicity of nanoceria is very low. However, large/accumulated doses produce granuloma in the lung and liver, and fibrosis in the lung. Toxicity, including genotoxicity, increases with exposure time; the effects disappear slowly, possibly due to nanoceria's biopersistence. Nanoceria may exert toxicity through oxidative stress. Adverse effects seen at sites distal to exposure may be due to nanoceria translocation or released biomolecules. An example is elevated oxidative stress indicators in the brain, in the absence of appreciable brain nanoceria. Nanoceria may change its nature in biological environments and cause changes in biological molecules. Increased toxicity has been related to greater surface Ce3+, which becomes more relevant as particle size decreases and the ratio of surface area to volume increases. Given its biopersistence and resulting increased toxicity with time, there is a risk that long-term exposure to low nanoceria levels may eventually lead to adverse health effects. This critical review provides recommendations for research to resolve some of the many unknowns of nanoceria's fate and adverse effects. JF - Environmental science. Nano AU - Yokel, Robert A AU - Hussain, Salik AU - Garantziotis, Stavros AU - Demokritou, Philip AU - Castranova, Vincent AU - Cassee, Flemming R AD - Pharmaceutical Sciences, University of Kentucky, US ; Graduate Center for Toxicology, University of Kentucky, US. ; Clinical Research Unit, National Institute of Environmental Health Sciences, National Institutes of Health, US. ; Environmental Health, Harvard, US. ; National Institute for Occupational Safety and Health, US ; West Virginia University School of Pharmacy, Morgantown, WV, US. ; Centre for Sustainability, Environmental & Health, National Institute for Public Health and the Environment, Bilthoven, the Netherlands ; Institute of Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands. Y1 - 2014/10/01/ PY - 2014 DA - 2014 Oct 01 SP - 406 EP - 428 VL - 1 IS - 5 SN - 2051-8153, 2051-8153 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826601737?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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.+Nano&rft.atitle=The+Yin%3A+An+adverse+health+perspective+of+nanoceria%3A+uptake%2C+distribution%2C+accumulation%2C+and+mechanisms+of+its+toxicity.&rft.au=Yokel%2C+Robert+A%3BHussain%2C+Salik%3BGarantziotis%2C+Stavros%3BDemokritou%2C+Philip%3BCastranova%2C+Vincent%3BCassee%2C+Flemming+R&rft.aulast=Yokel&rft.aufirst=Robert&rft.date=2014-10-01&rft.volume=1&rft.issue=5&rft.spage=406&rft.isbn=&rft.btitle=&rft.title=Environmental+science.+Nano&rft.issn=20518153&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2014-09-22 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - THE FAMILY HOUSEHOLD AND INFORMAL OLD AGE CARE IN MEXICO: A RESEARCH NOTE AN - 1728661355; 201535886 AB - Mexican society has traditionally expected the family to care for of its older people but the current situation is being strained by demographic, social and economic changes. This research note outlines the situation and provides some basic information on current caretakers using data from the Mexican National Time Use Survey of 2009. The survey identifies six different caretaking tasks, three of which are performed predominantly by women. Since most health and personal care occurs within the household, the physical and psychological burdens, as well as opportunity costs involved, are seldom recognised by health and social development ministries. This remains a main challenge to be addressed in order to develop optimal targeted support for older adults and their caregivers. Adapted from the source document. JF - International Journal of Sociology of the Family AU - Lopez-Ortega, Mariana AD - National Institute of Geriatrics, National Institutes of Health, Mexico Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 235 EP - 246 PB - Serials Publications, Delhi, India VL - 40 IS - 2 SN - 0973-2039, 0973-2039 KW - Caregivers KW - Time KW - Mexico KW - Elderly KW - Social Development KW - Females KW - Health Care Costs KW - article KW - 1941: the family and socialization; sociology of the family, marriage, & divorce UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728661355?accountid=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=International+Journal+of+Sociology+of+the+Family&rft.atitle=THE+FAMILY+HOUSEHOLD+AND+INFORMAL+OLD+AGE+CARE+IN+MEXICO%3A+A+RESEARCH+NOTE&rft.au=Lopez-Ortega%2C+Mariana&rft.aulast=Lopez-Ortega&rft.aufirst=Mariana&rft.date=2014-10-01&rft.volume=40&rft.issue=2&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Sociology+of+the+Family&rft.issn=09732039&rft_id=info:doi/ LA - English DB - Sociological Abstracts N1 - Date revised - 2015-11-01 N1 - Number of references - 24 N1 - Last updated - 2016-09-28 N1 - CODEN - IJSFAK N1 - SubjectsTermNotLitGenreText - Elderly; Mexico; Health Care Costs; Caregivers; Time; Females; Social Development ER - TY - JOUR T1 - US state variation in Autism insurance mandates: Balancing access and fairness AN - 1698882292 AB - This article examines how nations split decision-making about health services between federal and sub-federal levels, creating variation between states or provinces. When is this variation ethically acceptable? We identify three sources of ethical acceptability—procedural fairness, value pluralism, and substantive fairness—and examine these sources with respect to a case study: the fact that only 30 out of 51 US states or territories passed mandates requiring private insurers to offer extensive coverage of Autism behavioral therapies, creating variation for privately insured children living in different US states. Is this variation ethically acceptable? To address this question, we need to analyze whether mandates go to more or less needy states and whether the mandates reflect value pluralism between states regarding government’s role in health care. Using time-series logistic regressions and data from National Survey of Children with Special Health Care Needs, Individual with Disabilities Education Act, legislature political composition, and American Board of Pediatrics workforce data, we find that the states in which mandates are passed are less needy than states in which mandates have not been passed, what we call a cumulative advantage outcome that increases between-state disparities rather than a compensatory outcome that decreases between-state disparities. Concluding, we discuss the implications of our analysis for broader discussions of variation in health services provision. JF - Autism AU - Johnson, Rebecca A AU - Danis, Marion AU - Hafner-Eaton, Chris AD - Department of Bioethics, National Institutes of Health, USA ; Division of Science Policy and Science Liaison, National Institutes of Health, USA ; Department of Bioethics, National Institutes of Health, USA Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 803 EP - 814 CY - London PB - SAGE PUBLICATIONS, INC. VL - 18 IS - 7 SN - 1362-3613 KW - Psychology KW - Autism KW - distributive justice KW - ethics KW - health policy KW - private insurance mandates KW - Autistic children KW - Health inequalities KW - Health insurance KW - Health services KW - Insurance KW - Labour force KW - Paediatrics KW - Pluralism KW - Procedural justice KW - Provinces KW - Service delivery KW - Service provision KW - Special needs children KW - Territories KW - Behaviour KW - Children KW - Composition KW - Coverage KW - Decision making KW - Distributive justice KW - Ethics KW - Fairness KW - Health care KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698882292?accountid=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=Autism&rft.atitle=US+state+variation+in+Autism+insurance+mandates%3A+Balancing+access+and+fairness&rft.au=Johnson%2C+Rebecca+A%3BDanis%2C+Marion%3BHafner-Eaton%2C+Chris&rft.aulast=Johnson&rft.aufirst=Rebecca&rft.date=2014-10-01&rft.volume=18&rft.issue=7&rft.spage=803&rft.isbn=&rft.btitle=&rft.title=Autism&rft.issn=13623613&rft_id=info:doi/10.1177%2F1362361314529191 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Name - American Board of Pediatrics N1 - Date revised - 2015-07-07 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1177/1362361314529191 ER - TY - JOUR T1 - Maternal hormonal contraceptive use and offspring overweight or obesity AN - 1680439030; 20867364 AB - Background/ objectives: Experiments in animal models have shown a positive association between in utero exposure to pharmacologic sex hormones and offspring obesity. The developmental effects of such hormones on human obesity are unknown.Subjects/ methods: Using data from a large, prospective pregnancy cohort study (n=19 652), with linkage to a national prescription registry, we evaluated the association between use of hormonal contraceptives before and after conception (defined from dispensed prescription data and characterized by last date of use relative to conception, 12 to >4 months before (n=3392), 4 to >1 months before (n=2541), 1 to >0 months before (n=2997) and 0-12 weeks after (n=567)) in relation to offspring overweight or obesity at age 3 years. Results: We observed a weak, inverse association between early pregnancy use of a combination oral contraceptive and offspring overweight or obesity at age 3 (adjusted odds ratio (OR): 0.75, 95% confidence interval (CI): 0.53, 1.08) and a positive, but imprecise, association with use of a progestin-only oral contraceptive in early pregnancy (adjusted OR: 1.26, 95% CI: 0.79, 2.02). In general, no association was observed between the use of a hormonal contraceptive before conception and offspring overweight or obesity. A sensitivity analysis comparing combination oral contraceptive users in early pregnancy to other unplanned pregnancies without hormonal contraceptive use further strengthened the inverse association (adjusted OR: 0.70, 95% CI: 0.48, 1.02). Other sensitivity analyses were conducted to evaluate the robustness of the associations observed given varying assumptions. Conclusions: Pharmacologic sex hormones in early pregnancy may be inversely or positively associated with offspring overweight or obesity at age 3, depending on the specific formulation used. The present study provides support for the potential for environmental sources of hormonally active agents to exert developmental effects. JF - International Journal of Obesity AU - Jensen, E T AU - Daniels, J L AU - Stuermer, T AU - Robinson, W R AU - Williams, C J AU - Moster, D AU - Juliusson, P B AU - Vejrup, K AU - Magnus, P AU - Longnecker, M P AD - 1] Department of Epidemiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA [2] Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 1275 EP - 1281 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 38 IS - 10 SN - 0307-0565, 0307-0565 KW - Physical Education Index KW - Human relations KW - Obesity KW - Analysis KW - Recruiting KW - Hormones KW - Pregnancy KW - Sex KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680439030?accountid=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=Maternal+hormonal+contraceptive+use+and+offspring+overweight+or+obesity&rft.au=Jensen%2C+E+T%3BDaniels%2C+J+L%3BStuermer%2C+T%3BRobinson%2C+W+R%3BWilliams%2C+C+J%3BMoster%2C+D%3BJuliusson%2C+P+B%3BVejrup%2C+K%3BMagnus%2C+P%3BLongnecker%2C+M+P&rft.aulast=Jensen&rft.aufirst=E&rft.date=2014-10-01&rft.volume=38&rft.issue=10&rft.spage=1275&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2014.114 LA - English DB - Physical Education Index N1 - Date revised - 2015-05-01 N1 - Last updated - 2015-06-12 N1 - SubjectsTermNotLitGenreText - Human relations; Obesity; Analysis; Recruiting; Hormones; Sex; Pregnancy DO - http://dx.doi.org/10.1038/ijo.2014.114 ER - TY - JOUR T1 - Liminality as a Conceptual Frame for Understanding the Family Caregiving Rite of Passage: An Integrative Review AN - 1665167736 AB - Family caregiving is a significant rite of passage experienced by family caregivers of individuals with protracted illness or injury. In an integrative review of 26 studies, we characterized family caregiving from the sociocultural perspective of liminality and explored associated psychosocial implications. Analysis of published evidence on this dynamic and formative transition produced a range of themes. While role ambiguity resolved for most, for others, uncertainty and suffering continued. The process of becoming a caregiver was transformative and can be viewed as a rebirth that is largely socially and culturally driven. The transition to family caregiving model produced by this review provides a holistic perspective on this phenomenon and draws attention to aspects of the experience previously underappreciated. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - Research in Nursing & Health AU - Gibbons, Susanne W AU - Ross, Alyson AU - Bevans, Margaret AD - Assistant Professor, Daniel K. Inouye Graduate School of Nursing, Uniformed Services University of the Health Sciences, Bethesda, MD. ; IRTA Postdoctoral Research Fellow, National Institutes of Health Clinical Center, Bethesda, MD. ; Clinical Nurse Scientist, National Institutes of Health Clinical Center, 10 Center Drive MSC 1151, Bethesda, MD, 20892. ; Assistant Professor, Daniel K. Inouye Graduate School of Nursing, Uniformed Services University of the Health Sciences, Bethesda, MD. Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 423 EP - 436 CY - New York PB - Wiley Subscription Services, Inc. VL - 37 IS - 5 SN - 0160-6891 KW - Medical Sciences--Nurses And Nursing KW - Ambiguity KW - Carers KW - Injuries KW - Psychosocial factors KW - Public domain KW - Role ambiguity KW - Sociocultural factors KW - Suffering KW - Uncertainty KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665167736?accountid=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=Research+in+Nursing+%26+Health&rft.atitle=Liminality+as+a+Conceptual+Frame+for+Understanding+the+Family+Caregiving+Rite+of+Passage%3A+An+Integrative+Review&rft.au=Gibbons%2C+Susanne+W%3BRoss%2C+Alyson%3BBevans%2C+Margaret&rft.aulast=Gibbons&rft.aufirst=Susanne&rft.date=2014-10-01&rft.volume=37&rft.issue=5&rft.spage=423&rft.isbn=&rft.btitle=&rft.title=Research+in+Nursing+%26+Health&rft.issn=01606891&rft_id=info:doi/10.1002%2Fnur.21622 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Copyright - Copyright Wiley Subscription Services, Inc. Oct 2014 N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-10-06 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1002/nur.21622 ER - TY - JOUR T1 - NETWORK STRUCTURE MODERATES INTERGROUP DIFFERENTIATION OF STEREOTYPED RUMORS AN - 1665157664 AB - The role of network structure in intergroup differentiation—the bipolarization of stereotypes that are defensive (ingroup-positive/outgroup-negative) and non-defensive (outgroup-positive/ingroup-negative)—was investigated using a Dynamic Social Impact Theory (DSIT) framework. Three computer-mediated laboratory social network experiments were pooled to test the interaction of network clustering (cliquish structure) and segregation (personal network homogeneity) on intergroup differentiation. Democrats and Republicans during the five months preceding the 2008 U.S. Presidential election, deaf and hearing persons, and women and men participated. Twenty-six 16-person groups (e.g., 8 Democrats, 8 Republicans) serially discussed nine controversial stereotyped rumors in lattice (unclustered) or "family" (clustered) network structures. Support was found on an Ingroup Echo Chamber Effect: segregation led to intergroup differentiation (stronger defensive belief, weaker non-defensive belief) in clustered, but not un-clustered, structures. At the individual level, network clustering amplified ingroup neighbor social ifluence, leading participants to think more positively of their ingroup and more negatively of their outgroup. JF - Social Cognition AU - DiFonzo, Nicholas AU - Suls, Jerry AU - Beckstead, Jason W AU - Bourgeois, Martin J AU - Homan, Christopher M AU - Brougher, Samuel AU - Younge, Andrew J AU - Terpstra-Schwab, Nicholas AD - Department of Psychology, Rochester Institute of Technology, 18 Lomb Memorial Drive, Rochester, NY 14623 ; National Cancer Institute ; University of South Florida ; Florida Gulf Coast University ; Rochester Institute of Technology ; University of Wyoming ; Department of Psychology, Rochester Institute of Technology, 18 Lomb Memorial Drive, Rochester, NY 14623 Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 409 EP - 448 CY - New York PB - Guilford Publications, Inc. VL - 32 IS - 5 SN - 0278-016X KW - Psychology KW - Intergroup differentiation KW - Hearing KW - Segregation KW - Deaf KW - Social networks KW - Clustering KW - Differentiation KW - Stereotypes KW - Social impact KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665157664?accountid=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+Cognition&rft.atitle=NETWORK+STRUCTURE+MODERATES+INTERGROUP+DIFFERENTIATION+OF+STEREOTYPED+RUMORS&rft.au=DiFonzo%2C+Nicholas%3BSuls%2C+Jerry%3BBeckstead%2C+Jason+W%3BBourgeois%2C+Martin+J%3BHoman%2C+Christopher+M%3BBrougher%2C+Samuel%3BYounge%2C+Andrew+J%3BTerpstra-Schwab%2C+Nicholas&rft.aulast=DiFonzo&rft.aufirst=Nicholas&rft.date=2014-10-01&rft.volume=32&rft.issue=5&rft.spage=409&rft.isbn=&rft.btitle=&rft.title=Social+Cognition&rft.issn=0278016X&rft_id=info:doi/ LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - United States--US ER - TY - JOUR T1 - Innate immunity is sufficient for the clearance of Chlamydia trachomatis from the female mouse genital tract AN - 1660408991; PQ0001030385 AB - Chlamydia muridarum and Chlamydia trachomatis, mouse and human strains, respectively, have been used to study immunity in a murine model of female genital tract infection. Despite evidence that unique genes of these otherwise genomically similar strains could play a role in innate immune evasion in their respective mouse and human hosts, there have been no animal model findings to directly support this conclusion. Here, we infected C57BL/6 and adaptive immune-deficient Rag1 super(-/-) female mice with these strains and evaluated their ability to spontaneously resolve genital infection. Predictably, C57BL/6 mice spontaneously cleared infection caused by both chlamydial strains. In contrast, Rag1 super(-/-) mice which lack mature T and B cell immunity but maintain functional innate immune effectors were incapable of resolving C. muridarum infection but spontaneously cleared C. trachomatis infection. This distinct dichotomy in adaptive and innate immune-mediated clearance between mouse and human strains has important cautionary implications for the study of natural immunity and vaccine development in the mouse model. We show using Rag1-deficient mice that genital tract infections caused by human and murine chlamydial strains are differentially resolved by innate and adaptive immune mechanisms. JF - Pathogens and Disease AU - Sturdevant, Gail L AU - Caldwell, Harlan D AD - Laboratory of Intracellular Parasites, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA. Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 70 EP - 73 PB - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801 England VL - 72 IS - 1 SN - 2049-632X, 2049-632X KW - Microbiology Abstracts B: Bacteriology KW - Lymphocytes B KW - Animal models KW - Chlamydia trachomatis KW - Genital tract KW - Immunity KW - Vaccines KW - Pathogens KW - Infection KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660408991?accountid=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=Pathogens+and+Disease&rft.atitle=Innate+immunity+is+sufficient+for+the+clearance+of+Chlamydia+trachomatis+from+the+female+mouse+genital+tract&rft.au=Sturdevant%2C+Gail+L%3BCaldwell%2C+Harlan+D&rft.aulast=Sturdevant&rft.aufirst=Gail&rft.date=2014-10-01&rft.volume=72&rft.issue=1&rft.spage=70&rft.isbn=&rft.btitle=&rft.title=Pathogens+and+Disease&rft.issn=2049632X&rft_id=info:doi/10.1111%2F2049-632X.12164 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Lymphocytes B; Animal models; Genital tract; Pathogens; Vaccines; Immunity; Infection; Chlamydia trachomatis DO - http://dx.doi.org/10.1111/2049-632X.12164 ER - TY - JOUR T1 - A combined prognostic serum interleukin-8 and interleukin-6 classifier for stage 1 lung cancer in the prostate, lung, colorectal, and ovarian cancer screening trial. AN - 1639978378; 25170636 AB - The advent of low-dose helical computed tomography for lung cancer screening will likely lead to an increase in the detection of stage I lung cancer. Presently, these patients are primarily treated with surgery alone and approximately 30% will develop recurrence and die. Biomarkers that can identify patients for whom adjuvant chemotherapy would be a benefit could significantly reduce both patient morbidity and mortality. Herein, we sought to build a prognostic inflammatory-based classifier for stage I lung cancer. We performed a retrospective analysis of 548 European American lung cancer cases prospectively enrolled in the Prostate, Lung, Colorectal and Ovarian study. C-reactive protein, interleukin (IL)-6, IL-8, tumor necrosis factor-α, and IL-1β were measured using an ultrasensitive electrochemiluminescence immunoassay in serum samples collected at the time of study entry. IL-6 and IL-8 were each associated with significantly shorter survival (hazard ratio [HR], 1.33; 95% confidence interval [CI], 1.08-1.64; p = 0.007; and HR, 1.3; 95% CI, 1.09-1.67; p = 0.005, respectively). Moreover, a combined classifier of IL-6 and IL-8 were significantly associated with poor outcome in stage I lung cancer patients (HR, 3.39; 95% CI, 1.54-7.48, p = 0.002) and in stage 1 patients with more than or equal to 30 pack-years of smoking (HR, 3.15; 95% CI, 1.54-6.46, p = 0.002). These results further support the association between inflammatory markers and lung cancer outcome and suggest that a combined serum IL-6/IL-8 classifier could be a useful tool for guiding therapeutic decisions in patients with stage I lung cancer. JF - Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer AU - Ryan, Bríd M AU - Pine, Sharon R AU - Chaturvedi, Anil K AU - Caporaso, Neil AU - Harris, Curtis C AD - *Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD; †Department of Medicine, Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, NJ; ‡Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD; and §Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 1494 EP - 1503 VL - 9 IS - 10 KW - Biomarkers, Tumor KW - 0 KW - Interleukin-6 KW - Interleukin-8 KW - Index Medicus KW - Neoplasm Staging KW - Risk Factors KW - Humans KW - Retrospective Studies KW - Prognosis KW - Aged KW - Middle Aged KW - Neoplasm Recurrence, Local KW - Early Detection of Cancer -- methods KW - Male KW - Female KW - Interleukin-6 -- blood KW - Lung Neoplasms -- blood KW - Biomarkers, Tumor -- blood KW - Interleukin-8 -- blood KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639978378?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+thoracic+oncology+%3A+official+publication+of+the+International+Association+for+the+Study+of+Lung+Cancer&rft.atitle=A+combined+prognostic+serum+interleukin-8+and+interleukin-6+classifier+for+stage+1+lung+cancer+in+the+prostate%2C+lung%2C+colorectal%2C+and+ovarian+cancer+screening+trial.&rft.au=Ryan%2C+Br%C3%ADd+M%3BPine%2C+Sharon+R%3BChaturvedi%2C+Anil+K%3BCaporaso%2C+Neil%3BHarris%2C+Curtis+C&rft.aulast=Ryan&rft.aufirst=Br%C3%ADd&rft.date=2014-10-01&rft.volume=9&rft.issue=10&rft.spage=1494&rft.isbn=&rft.btitle=&rft.title=Journal+of+thoracic+oncology+%3A+official+publication+of+the+International+Association+for+the+Study+of+Lung+Cancer&rft.issn=1556-1380&rft_id=info:doi/10.1097%2FJTO.0000000000000278 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-03 N1 - Date created - 2014-12-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncologist. 2007 Mar;12(3):331-7 [17405898] Circ J. 2007 Apr;71(4):495-8 [17384448] Hepatogastroenterology. 2007 Apr-May;54(75):858-61 [17591079] Circ J. 2007 Aug;71(8):1199-207 [17652881] Water Res. 2007 Aug;41(16):3615-28 [17507075] Nihon Naika Gakkai Zasshi. 2007 Jul 10;96(7):1476-8 [17682437] Dig Dis Sci. 2007 Sep;52(9):2095-103 [17429720] J Natl Cancer Inst. 2007 Aug 15;99(16):1257-69 [17686824] J Biol Chem. 2007 Sep 21;282(38):28164-74 [17623663] Eur J Epidemiol. 2007;22(10):691-8 [17680333] Cerebrovasc Dis. 2007;24(4):328-37 [17690544] Circ J. 2007 Oct;71(10):1617-21 [17895561] Int J Cancer. 2007 Nov 15;121(10):2205-11 [17657714] Bioinformatics. 2007 Nov 1;23(21):2934-41 [17893089] J Leukoc Biol. 2007 Dec;82(6):1481-90 [17881510] FEBS Lett. 2007 Dec 22;581(30):5879-84 [18067863] Cardiology. 2008;109(2):135-42 [17713329] J Am Soc Echocardiogr. 2008 Jun;21(6):756-60 [17928196] Int J Cardiol. 2008 Aug 1;128(1):69-76 [17692410] Eur J Clin Nutr. 2008 Oct;62(10):1187-93 [17622257] J Clin Oncol. 2008 Nov 1;26(31):5043-51 [18809614] Cancer. 2012 Nov 15;118(22):5630-6 [23044494] Chest. 2013 May;143(5 Suppl):e278S-313S [23649443] N Engl J Med. 2013 Jul 18;369(3):245-54 [23863051] Ann Oncol. 2013 Aug;24(8):2073-9 [23680692] Eur Urol. 2013 Sep;64(3):512 [23915461] J Natl Cancer Inst. 2013 Dec 18;105(24):1871-80 [24249745] JAMA Intern Med. 2014 Feb 1;174(2):269-74 [24322569] N Engl J Med. 2004 Apr 22;350(17):1713-21 [15102997] J Thorac Oncol. 2008 Dec;3(12):1468-81 [19057275] Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):215-22 [19124500] J Clin Oncol. 2010 Jan 1;28(1):29-34 [19933915] Ann Surg Oncol. 2010 Jun;17(6):1471-4 [20180029] J Clin Oncol. 2010 Jun 1;28(16):2719-26 [20421535] J Natl Cancer Inst. 2011 Jul 20;103(14):1112-22 [21685357] J Thorac Cardiovasc Surg. 2011 Nov;142(5):1161-7 [21872279] Oncology. 2011;81(2):113-8 [21986483] Ann Thorac Cardiovasc Surg. 2011;17(5):454-60 [21881374] Yonsei Med J. 2012 Jan;53(1):111-7 [22187240] J Med Assoc Thai. 2012 Feb;95 Suppl 2:S199-207 [22574550] Int J Cancer. 2013 Jan 1;132(1):9-18 [22618808] Lancet. 2000 Feb 5;355(9202):479-85 [10841143] Cancer Res. 2000 Jul 1;60(13):3333-7 [10910033] Clin Cancer Res. 2000 Dec;6(12):4739-44 [11156228] Control Clin Trials. 2000 Dec;21(6 Suppl):400S-406S [11189691] Br J Cancer. 2002 Jul 29;87(3):264-7 [12177792] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959] Nat Rev Cancer. 2003 Apr;3(4):276-85 [12671666] Stat Med. 1995 Aug 15;14(15):1707-23 [7481205] N Engl J Med. 2005 Jun 23;352(25):2589-97 [15972865] Int J Cancer. 2006 Aug 15;119(4):955-60 [16550600] Lancet Oncol. 2006 Sep;7(9):719-27 [16945766] Radiat Med. 2007 Jan;25(1):38-44 [17225052] J Clin Oncol. 2007 Jan 20;25(3):313-8 [17235046] Thromb Haemost. 2007 Jun;97(6):1052-3 [17549312] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/JTO.0000000000000278 ER - TY - JOUR T1 - Association of cancer worry and perceived risk with doctor avoidance: an analysis of information avoidance in a nationally representative US sample AN - 1627734018 AB - Fear of receiving bad news about one’s health can lead people to avoid seeking out health information that, ironically, may be crucial for health maintenance. Using a nationally representative US sample, the present study examined whether perceived likelihood of developing cancer and worry about cancer were associated with reports of avoiding visits to one’s doctor, in respondents under and over age 50. Cancer worry, but not perceived risk of cancer, predicted doctor avoidance in respondents aged 50 and older, whereas the opposite pattern held for respondents under age 50. Moreover, in respondents aged 50 and older, cancer worry and perceived cancer risk interacted such that cancer worry was linked to doctor avoidance only when respondents also perceived a high likelihood of cancer. The latter result is consistent with the notion that worry may motivate information seeking when people expect information to dispel worry and information avoidance when the information is seen as highly likely to confirm one’s fears. Findings suggest a need for communication strategies that can influence worry and perceived risk differentially. Research should also assess the effectiveness of other behavioral strategies (e.g., automatic scheduling of appointments) as a means for reducing doctor avoidance. JF - Journal of Behavioral Medicine AU - Persoskie, Alexander AU - Ferrer, Rebecca A AU - Klein, William M P AD - Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, 9609 Medical Center Drive, Floor 3 East Tower, Bethesda, MD, 20892–9761, USA persoskieai@mail.nih.gov persoskieai@mail.nih.gov persoskieai@mail.nih.gov; Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, 9609 Medical Center Drive, Floor 3 East Tower, Bethesda, MD, 20892–9761, USA Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 977 EP - 987 CY - New York PB - Springer Science & Business Media VL - 37 IS - 5 SN - 0160-7715 KW - Psychology KW - Appointments KW - Avoidance KW - Bad news KW - Cancer KW - Communication strategies KW - Fear KW - Health KW - Health information KW - News KW - Risk perception KW - Worry KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627734018?accountid=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=Association+of+cancer+worry+and+perceived+risk+with+doctor+avoidance%3A+an+analysis+of+information+avoidance+in+a+nationally+representative+US+sample&rft.au=Persoskie%2C+Alexander%3BFerrer%2C+Rebecca+A%3BKlein%2C+William+M+P&rft.aulast=Persoskie&rft.aufirst=Alexander&rft.date=2014-10-01&rft.volume=37&rft.issue=5&rft.spage=977&rft.isbn=&rft.btitle=&rft.title=Journal+of+Behavioral+Medicine&rft.issn=01607715&rft_id=info:doi/10.1007%2Fs10865-013-9537-2 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-11-10 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1007/s10865-013-9537-2 ER - TY - JOUR T1 - Attitudes About Internet Support Groups Among Adolescents and Young Adults with Neurofibromatosis Type 1 and their Parents AN - 1627732009 AB - Youth with neurofibromatosis type 1 (NF1) have multiple, complex symptoms associated with physical, social-emotional, and cognitive difficulties. In addition, caring for a child with NF1 can be extremely challenging for parents. Since research with other chronic illness populations suggests that social support, including internet support groups (ISGs), can be beneficial, this survey study aimed to determine the attitudes and preferences of adolescents and young adults with NF1 and parents of a child with NF1 regarding ISGs. Thirty patients and 30 caregivers completed a 24-item survey about ISGs. Many patients and parents are not aware of any ISGs for NF1, but are interested in using one in the future for a variety of reasons, including to get answers to their questions about NF1, to find out about research studies, and to discuss problems and concerns about NF1. Specific concerns of interest include physical, social-emotional, and cognitive aspects of NF1. ISGs have potential as a social support intervention within the NF1 community. ISGs for the NF1 population should include patients with NF1 (or parents of children with NF1) as well as a health professional, and both chat rooms and discussion boards likely would be well-received. JF - Journal of Genetic Counseling AU - Martin, Staci AU - Wolters, Pamela L AU - Baldwin, Andrea AU - Roderick, Marie Claire AU - Toledo-Tamula, Mary Anne AU - Gillespie, Andrea AU - Widemann, Brigitte AD - Pediatric Oncology Branch, National Cancer Institute, Building 82, Room 107 9030 Old Georgetown Road, Bethesda, MD, 20892-8200, USA martins@mail.nih.gov martins@mail.nih.gov martins@mail.nih.gov martins@mail.nih.gov martins@mail.nih.gov; Pediatric Oncology Branch, National Cancer Institute, Building 82, Room 107 9030 Old Georgetown Road, Bethesda, MD, 20892-8200, USA, Institute for Psychological Sciences, Arlington, VA, USA ; Clinical Research Directorate/CMRP, SAIC-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA ; Pediatric Oncology Branch, National Cancer Institute, Building 82, Room 107 9030 Old Georgetown Road, Bethesda, MD, 20892-8200, USA Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 796 EP - 804 CY - New York PB - Springer Science & Business Media VL - 23 IS - 5 SN - 1059-7700 KW - Psychology KW - Adolescents KW - Social support KW - Support groups KW - Young adults KW - Attitudes KW - Carers KW - Caring KW - Chat rooms KW - Children KW - Chronic sickness KW - Cognitive aspects KW - Health KW - Internet KW - Multiple symptoms KW - Neurofibromatosis KW - Parents KW - Physical symptoms KW - Preferences UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627732009?accountid=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+Genetic+Counseling&rft.atitle=Attitudes+About+Internet+Support+Groups+Among+Adolescents+and+Young+Adults+with+Neurofibromatosis+Type+1+and+their+Parents&rft.au=Martin%2C+Staci%3BWolters%2C+Pamela+L%3BBaldwin%2C+Andrea%3BRoderick%2C+Marie+Claire%3BToledo-Tamula%2C+Mary+Anne%3BGillespie%2C+Andrea%3BWidemann%2C+Brigitte&rft.aulast=Martin&rft.aufirst=Staci&rft.date=2014-10-01&rft.volume=23&rft.issue=5&rft.spage=796&rft.isbn=&rft.btitle=&rft.title=Journal+of+Genetic+Counseling&rft.issn=10597700&rft_id=info:doi/10.1007%2Fs10897-014-9688-5 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-11-10 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1007/s10897-014-9688-5 ER - TY - JOUR T1 - HIV Testing Histories and Risk Factors Among Migrants and Recent Immigrants Who Received Rapid HIV Testing from Three Community-Based Organizations AN - 1627731003 AB - Migrants and recent immigrants in the US constitute a large population that is vulnerable to HIV. From March 2005 to February 2007, three community-based organizations conducted rapid HIV testing among migrants in five states. Participants were asked to complete a survey on sociodemographics, HIV-risk behaviors, and HIV-testing histories with the aim of understanding factors associated with HIV testing. Among 5,247 persons tested, 6 (0.1 %) were HIV-positive. Among 3,135 persons who completed surveys, more than half had never been tested for HIV previously (59 %). Participants reported high levels of HIV-risk behaviors in the past year, including 2 or more sex partners (45 %), sex while high/drunk (30 %), and transactional sex (29 %). Multivariate analysis identified several factors independently associated with decreased likelihood of prior HIV testing, including poor spoken English. Continued efforts are needed to ensure that migrant populations have improved access to HIV testing and prevention services. Understanding factors associated with migrants’ lack of previous HIV testing may help focus these efforts. JF - Journal of Immigrant and Minority Health AU - Schulden, Jeffrey D AU - Painter, Thomas M AU - Song, Binwei AU - Valverde, Eduardo AU - Borman, Mary Ann AU - Monroe-Spencer, Kyle AU - Bautista, Greg AU - Saleheen, Hassan AU - Voetsch, Andrew C AU - Heffelfinger, James D AD - National Institute on Drug Abuse (NIDA), National Institutes of Health (NIH), 6001 Executive Blvd, MSC 9589, Bethesda, MD, 20892, USA schuldenj@nida.nih.gov; National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and Prevention (CDC), Atlanta, GA, USA ; United Migrant Opportunity Services, Milwaukee, WI, USA ; AIDGwinnett, Lawrenceville, GA, USA ; Connecticut Children’s Medical Center, Hartford, CT, USA ; National Institute on Drug Abuse (NIDA), National Institutes of Health (NIH), 6001 Executive Blvd, MSC 9589, Bethesda, MD, 20892, USA Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 798 EP - 810 CY - New York PB - Springer Science & Business Media VL - 16 IS - 5 SN - 1557-1912 KW - Medical Sciences KW - Community based KW - Risk behaviour KW - HIV KW - Immigrants KW - Migrants KW - Multivariate analysis KW - Preventive health care KW - Preventive programmes KW - Risk factors KW - Safe sexual practices KW - Sex education KW - Testing KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627731003?accountid=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=HIV+Testing+Histories+and+Risk+Factors+Among+Migrants+and+Recent+Immigrants+Who+Received+Rapid+HIV+Testing+from+Three+Community-Based+Organizations&rft.au=Schulden%2C+Jeffrey+D%3BPainter%2C+Thomas+M%3BSong%2C+Binwei%3BValverde%2C+Eduardo%3BBorman%2C+Mary+Ann%3BMonroe-Spencer%2C+Kyle%3BBautista%2C+Greg%3BSaleheen%2C+Hassan%3BVoetsch%2C+Andrew+C%3BHeffelfinger%2C+James+D&rft.aulast=Schulden&rft.aufirst=Jeffrey&rft.date=2014-10-01&rft.volume=16&rft.issue=5&rft.spage=798&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immigrant+and+Minority+Health&rft.issn=15571912&rft_id=info:doi/10.1007%2Fs10903-013-9811-y LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-11-10 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1007/s10903-013-9811-y ER - TY - JOUR T1 - Do Childhood Externalizing Disorders Predict Adult Depression? A Meta-Analysis AN - 1627730686 AB - Childhood externalizing disorders have been linked to adult affective disorders, although some studies fail to substantiate this finding. Multiple longitudinal cohort studies identifying childhood psychopathology and their association with adult psychiatric illness have been published. To examine the association between childhood externalizing symptoms or disorders and the development of adult depression across cohorts, a meta-analysis was performed. Potential studies were identified using a PubMed search through November 2013. All published, prospective, longitudinal, community-sampled cohort studies of children (≤ 13 years) with externalizing symptoms or disorders (aggression, conduct problems, oppositional defiant disorder, conduct disorder), reassessed in adulthood (≥ 18 years) for depressive disorders (major depressive disorder, depressive disorder NOS, or dysthymic disorder) were included. A random effects model was used to summarize the pooled effect sizes. Ancillary analyses considered covariates that could account for variance among studies. Ten studies representing eight cohorts of children initially assessed at age 13 or younger (N=17,712) were included in the meta-analysis. Childhood externalizing behavior was associated with adult depressive disorders (OR=1.52, 95 % confidence interval=1.27–1.80, p<0.0001). Utilizing Orwin’s Fail-safe N approach, 263 studies with a mean odds ratio of 1.0 would have to be added to the analysis before the cumulative effect would become trivial. Externalizing psychopathology in childhood is associated with the development of unipolar depressive disorders in adulthood. JF - Journal of Abnormal Child Psychology AU - Loth, Annemarie K AU - Drabick, Deborah A G AU - Leibenluft, Ellen AU - Hulvershorn, Leslie A AD - Department of Psychiatry, Indiana University School of Medicine, Riley Hospital for Children, 705 Riley Hospital Drive, Room 4300, Indianapolis, IN, 46202, USA lhulvers@iupui.edu lhulvers@iupui.edu; Department of Psychology, Temple University, Philadelphia, PA, USA ; Section on Bipolar Spectrum Disorders, Emotion and Development Branch, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA ; Department of Psychiatry, Indiana University School of Medicine, Riley Hospital for Children, 705 Riley Hospital Drive, Room 4300, Indianapolis, IN, 46202, USA Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 1103 EP - 1113 CY - New York PB - Springer Science & Business Media VL - 42 IS - 7 SN - 0091-0627 KW - Medical Sciences--Physical Medicine And Rehabilitation KW - Predictors KW - Adults KW - Analysis KW - Adulthood KW - Affective disorders KW - Aggression KW - Childhood KW - Children KW - Cohort analysis KW - Conduct disorders KW - Depression KW - Depressive personality disorders KW - Externalizing behaviour KW - Externalizing problems KW - Oppositional defiant disorder KW - Psychopathology KW - Random effects KW - Symptoms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627730686?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Abnormal+Child+Psychology&rft.atitle=Do+Childhood+Externalizing+Disorders+Predict+Adult+Depression%3F+A+Meta-Analysis&rft.au=Loth%2C+Annemarie+K%3BDrabick%2C+Deborah+A+G%3BLeibenluft%2C+Ellen%3BHulvershorn%2C+Leslie+A&rft.aulast=Loth&rft.aufirst=Annemarie&rft.date=2014-10-01&rft.volume=42&rft.issue=7&rft.spage=1103&rft.isbn=&rft.btitle=&rft.title=Journal+of+Abnormal+Child+Psychology&rft.issn=00910627&rft_id=info:doi/10.1007%2Fs10802-014-9867-8 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-11-10 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1007/s10802-014-9867-8 ER - TY - JOUR T1 - Approaches to integrating germline and tumor genomic data in cancer research. AN - 1623291726; 25115441 AB - Cancer is characterized by a diversity of genetic and epigenetic alterations occurring in both the germline and somatic (tumor) genomes. Hundreds of germline variants associated with cancer risk have been identified, and large amounts of data identifying mutations in the tumor genome that participate in tumorigenesis have been generated. Increasingly, these two genomes are being explored jointly to better understand how cancer risk alleles contribute to carcinogenesis and whether they influence development of specific tumor types or mutation profiles. To understand how data from germline risk studies and tumor genome profiling is being integrated, we reviewed 160 articles describing research that incorporated data from both genomes, published between January 2009 and December 2012, and summarized the current state of the field. We identified three principle types of research questions being addressed using these data: (i) use of tumor data to determine the putative function of germline risk variants; (ii) identification and analysis of relationships between host genetic background and particular tumor mutations or types; and (iii) use of tumor molecular profiling data to reduce genetic heterogeneity or refine phenotypes for germline association studies. We also found descriptive studies that compared germline and tumor genomic variation in a gene or gene family, and papers describing research methods, data sources, or analytical tools. We identified a large set of tools and data resources that can be used to analyze and integrate data from both genomes. Finally, we discuss opportunities and challenges for cancer research that integrates germline and tumor genomics data. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Feigelson, Heather Spencer AU - Goddard, Katrina A B AU - Hollombe, Celine AU - Tingle, Sharna R AU - Gillanders, Elizabeth M AU - Mechanic, Leah E AU - Nelson, Stefanie A AD - Institute for Health Research, Kaiser Permanente Colorado, Denver, CO, USA, Center for Health Research, Kaiser Permanente Northwest, Portland, OR, USA and Epidemiology and Genomics Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD, USA. ; Center for Health Research, Kaiser Permanente Northwest, Portland, OR, USA and. ; Epidemiology and Genomics Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD, USA. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 2157 EP - 2163 VL - 35 IS - 10 KW - Index Medicus KW - Gene Expression Regulation, Neoplastic KW - Humans KW - Genetic Predisposition to Disease KW - Databases, Genetic KW - Genomics -- methods KW - Germ-Line Mutation KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1623291726?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Approaches+to+integrating+germline+and+tumor+genomic+data+in+cancer+research.&rft.au=Feigelson%2C+Heather+Spencer%3BGoddard%2C+Katrina+A+B%3BHollombe%2C+Celine%3BTingle%2C+Sharna+R%3BGillanders%2C+Elizabeth+M%3BMechanic%2C+Leah+E%3BNelson%2C+Stefanie+A&rft.aulast=Feigelson&rft.aufirst=Heather&rft.date=2014-10-01&rft.volume=35&rft.issue=10&rft.spage=2157&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu165 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2014-09-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Genet. 2013 Apr;45(4):392-8, 398e1-2 [23535733] Nature. 2012 Nov 1;491(7422):56-65 [23128226] Nature. 2014 Jan 16;505(7483):302-8 [24429628] Nat Genet. 2014 Apr;46(4):318-9 [24675517] Nature. 2010 Apr 15;464(7291):993-8 [20393554] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8418-23 [12829800] Science. 2006 Jul 28;313(5786):521-2 [16809487] Nature. 2008 Oct 23;455(7216):1061-8 [18772890] Nat Genet. 2009 Apr;41(4):455-9 [19287384] Nat Genet. 2009 Sep;41(9):996-1000 [19648919] Methods Mol Biol. 2010;576:61-87 [19882258] Neoplasia. 2009 Dec;11(12):1340-7 [20019842] PLoS Genet. 2010 Apr;6(4):e1000888 [20369019] JAMA. 2010 Jul 28;304(4):426-34 [20664043] PLoS Genet. 2010 Sep;6(9):e1001086 [20824129] Cancer. 2010 Sep 15;116(18):4248-55 [20549826] PLoS Genet. 2010 Sep;6(9):e1001136 [20885788] Breast Cancer Res. 2010;12(4):R63 [20712882] Nature. 2010 Oct 28;467(7319):1061-73 [20981092] Nature. 2011 Feb 10;470(7333):204-13 [21307933] Breast Cancer Res. 2010;12(6):R93 [21062454] Genes Dev. 2011 Mar 15;25(6):534-55 [21406553] Cancer Res. 2011 Apr 1;71(7):2423-7 [21292812] Cancer Epidemiol Biomarkers Prev. 2011 May;20(5):793-8 [21415360] Nat Genet. 2011 Jun;43(6):513-8 [21614091] Nature. 2011 Jun 30;474(7353):609-15 [21720365] Cancer Sci. 2011 Oct;102(10):1874-81 [21740479] Cancer. 2011 Nov 15;117(22):5161-71 [21523770] Hum Mol Genet. 2011 Dec 1;20(23):4693-706 [21852249] Cancer. 2012 Jan 1;118(1):232-40 [21713760] Cell. 2012 Jan 20;148(1-2):59-71 [22265402] PLoS One. 2012;7(2):e30477 [22363440] Cancer Res. 2012 Mar 1;72(5):1064-9 [22282663] J Intern Med. 2012 Apr;271(4):366-78 [22443200] Proc Natl Acad Sci U S A. 2012 Mar 27;109(13):4974-9 [22416122] Carcinogenesis. 2012 May;33(5):1059-64 [22382497] Hum Mutat. 2012 Jul;33(7):1123-32 [22461340] Proc Natl Acad Sci U S A. 2012 Jul 10;109(28):11252-7 [22730461] Nature. 2012 Aug 2;488(7409):100-5 [22832583] J Gastroenterol Hepatol. 2012 Sep;27(9):1423-31 [22694276] Nature. 2012 Oct 4;490(7418):61-70 [23000897] Cancer Epidemiol Biomarkers Prev. 2012 Oct;21(10):1783-91 [22859399] Nature. 2013 Jul 11;499(7457):214-8 [23770567] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu165 ER - TY - JOUR T1 - An analysis of genetic factors related to risk of inflammatory bowel disease and colon cancer AN - 1622607920; 20875936 AB - Background and aims Patients with inflammatory bowel disease (IBD) have a higher risk of developing colorectal cancer than the general population. Genome-wide association studies have identified and replicated several loci associated with risk of IBD; however, it is currently unknown whether these loci are also associated with colon cancer risk. Methods We selected 15 validated SNPs associated with risk of either Crohn's disease, ulcerative colitis, or both in previous GWAS and tested whether these loci were also associated with colon cancer risk in a two-stage study design. Results We found that rs744166 in STAT3 was associated with colon cancer risk in two studies; however, the direction of the observation was reversed in TP53 mutant tumors possibly due to a nullification of the effect by mutant p53. The SNP, which lies within intron 1 of the STAT3 gene, was associated with lower expression of STAT3 mRNA in TP53 wild-type, but not mutant, tumors. Conclusions These data suggest that the STAT3 locus is associated with both IBD and cancer. Further understanding the function of this variant in relation to TP53 could possibly explain the role of this gene in autoimmunity and cancer. Furthermore, an analysis of this locus, specifically in a population with IBD, could help to resolve the relationship between this SNP and cancer. JF - Cancer Epidemiology AU - Ryan, Brid M AU - Wolff, Roger K AU - Valeri, Nicola AU - Khan, Mohammed AU - Robinson, Dillon AU - Paone, Alessio AU - Bowman, Elise D AU - Lundgreen, Abbie AU - Caan, Bette AU - Potter, John AU - Brown, Derek AU - Croce, Carlo AU - Slattery, Martha L AU - Harris, Curtis C AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 583 EP - 590 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 38 IS - 5 SN - 1877-7821, 1877-7821 KW - Genetics Abstracts; Risk Abstracts KW - Inflammatory bowel disease KW - Colon cancer KW - STAT3 KW - Genetic factors KW - Ulcerative colitis KW - Colorectal cancer KW - Autoimmunity KW - Mutants KW - Gene expression KW - Risk factors KW - Crohn's disease KW - Data processing KW - Stat3 protein KW - Tumors KW - Cancer KW - mRNA KW - p53 protein KW - Health risks KW - Inflammatory bowel diseases KW - Single-nucleotide polymorphism KW - Introns KW - Colorectal carcinoma 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/1622607920?accountid=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=An+analysis+of+genetic+factors+related+to+risk+of+inflammatory+bowel+disease+and+colon+cancer&rft.au=Ryan%2C+Brid+M%3BWolff%2C+Roger+K%3BValeri%2C+Nicola%3BKhan%2C+Mohammed%3BRobinson%2C+Dillon%3BPaone%2C+Alessio%3BBowman%2C+Elise+D%3BLundgreen%2C+Abbie%3BCaan%2C+Bette%3BPotter%2C+John%3BBrown%2C+Derek%3BCroce%2C+Carlo%3BSlattery%2C+Martha+L%3BHarris%2C+Curtis+C&rft.aulast=Ryan&rft.aufirst=Brid&rft.date=2014-10-01&rft.volume=38&rft.issue=5&rft.spage=583&rft.isbn=&rft.btitle=&rft.title=Cancer+Epidemiology&rft.issn=18777821&rft_id=info:doi/10.1016%2Fj.canep.2014.07.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2015-01-07 N1 - SubjectsTermNotLitGenreText - Crohn's disease; Genetic factors; Data processing; Stat3 protein; Ulcerative colitis; Colorectal cancer; Autoimmunity; Colon cancer; Tumors; p53 protein; mRNA; Gene expression; Inflammatory bowel diseases; Single-nucleotide polymorphism; Risk factors; Introns; Health risks; Colorectal carcinoma; Cancer; Mutants DO - http://dx.doi.org/10.1016/j.canep.2014.07.003 ER - TY - JOUR T1 - NUCLEAR MEDICINE PRACTICES IN THE 1950s THROUGH THE MID-1970S AND OCCUPATIONAL RADIATION DOSES TO TECHNOLOGISTS FROM DIAGNOSTIC RADIOISOTOPE PROCEDURES AN - 1622607874; 20802508 AB - Data on occupational radiation exposure from nuclear medicine procedures for the time period of the 1950s through the 1970s is important for retrospective health risk studies of medical personnel who conducted those activities. To better understand and characterize historical radiation exposures to technologists, the authors collected information on nuclear medicine practices in the 1950s, 1960s, and 1970s. To collect historical data needed to reconstruct doses to technologists, a focus group interview was held with experts who began using radioisotopes in medicine in the 1950s and the 1960s. The doses estimated in this study show that the introduction of [sup 99m]Tc resulted in an increase in occupational doses per procedure. JF - Health Physics AU - Drozdovitch, Vladimir AU - Brill, Aaron B AU - Mettler, Fred A, Jr AU - Beckner, William M AU - Goldsmith, Stanley J AU - Gross, Milton D AU - Hays, Marguerite T AU - Kirchner, Peter T AU - Langan, James K AU - Reba, Richard C AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 9609 Medical Center Drive, Room 7E548, MSC 9778, Bethesda, MD 20892-9778, drozdovv@mail.nih.gov Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 300 EP - 310 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 107 IS - 4 SN - 0017-9078, 0017-9078 KW - Risk Abstracts; Health & Safety Science Abstracts KW - dose assessment KW - historical profiles KW - nuclear medicine KW - radiation, medical KW - Historical account KW - Health risks KW - Radiation KW - Radioisotopes KW - Occupational exposure KW - Medical personnel 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/1622607874?accountid=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=NUCLEAR+MEDICINE+PRACTICES+IN+THE+1950s+THROUGH+THE+MID-1970S+AND+OCCUPATIONAL+RADIATION+DOSES+TO+TECHNOLOGISTS+FROM+DIAGNOSTIC+RADIOISOTOPE+PROCEDURES&rft.au=Drozdovitch%2C+Vladimir%3BBrill%2C+Aaron+B%3BMettler%2C+Fred+A%2C+Jr%3BBeckner%2C+William+M%3BGoldsmith%2C+Stanley+J%3BGross%2C+Milton+D%3BHays%2C+Marguerite+T%3BKirchner%2C+Peter+T%3BLangan%2C+James+K%3BReba%2C+Richard+C&rft.aulast=Drozdovitch&rft.aufirst=Vladimir&rft.date=2014-10-01&rft.volume=107&rft.issue=4&rft.spage=300&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000107 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2015-05-27 N1 - SubjectsTermNotLitGenreText - Health risks; Historical account; Radiation; Radioisotopes; Medical personnel; Occupational exposure DO - http://dx.doi.org/10.1097/HP.0000000000000107 ER - TY - JOUR T1 - Alterations in leukocyte telomere length in workers occupationally exposed to benzene AN - 1622606180; 20840744 AB - Exposure to benzene, a known leukemogen and probable lymphomagen, has been demonstrated to result in oxidative stress, which has previously been associated with altered telomere length (TL). TL specifically has been associated with several health outcomes in epidemiologic studies, including cancer risk, and has been demonstrated to be altered following exposure to a variety of chemical agents. To evaluate the association between benzene exposure and TL, we measured TL by monochrome multiplex quantitative PCR in 43 workers exposed to high levels of benzene and 43 age and sex-matched unexposed workers in Shanghai, China. Benzene exposure levels were monitored using organic vapor passive dosimetry badges before phlebotomy. The median benzene exposure level in exposed workers was 31 ppm. The mean TL in controls, workers exposed to levels of benzene below the median ( less than or equal to 31 ppm), and above the median (>31 ppm) was 1.26 plus or minus 0.17, 1.25 plus or minus 0.16, and 1.37 plus or minus 0.23, respectively. Mean TL was significantly elevated in workers exposed to >31 ppm of benzene compared with controls (P=0.03). Our findings provide evidence that high levels of occupational benzene exposure are associated with TL. Environ. Mol. Mutagen. 55:673-678, 2014. Published [2014]. This article is a U.S. Government work and is in the public domain in the USA. JF - Environmental and Molecular Mutagenesis AU - Bassig, Bryan A AU - Zhang, Luoping AU - Cawthon, Richard M AU - Smith, Martyn T AU - Yin, Songnian AU - Li, Guilan AU - Hu, Wei AU - Shen, Min AU - Rappaport, Stephen AU - Barone-Adesi, Francesco AU - Rothman, Nathaniel AU - Vermeulen, Roel AU - Lan, Qing AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland. Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 673 EP - 678 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 55 IS - 8 SN - 0893-6692, 0893-6692 KW - Health & Safety Science Abstracts; Risk Abstracts; Toxicology Abstracts; Genetics Abstracts KW - Mutagens KW - Age KW - Dosimetry KW - Leukocytes KW - Benzene KW - Cancer KW - Mutagenesis KW - Health risks KW - Telomeres KW - USA KW - Vapors KW - Oxidative stress KW - Polymerase chain reaction KW - China, People's Rep. KW - China, People's Rep., Shanghai KW - Occupational exposure KW - H 1000:Occupational Safety and Health KW - R2 23060:Medical and environmental health KW - G 07730:Development & Cell Cycle KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622606180?accountid=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+and+Molecular+Mutagenesis&rft.atitle=Alterations+in+leukocyte+telomere+length+in+workers+occupationally+exposed+to+benzene&rft.au=Bassig%2C+Bryan+A%3BZhang%2C+Luoping%3BCawthon%2C+Richard+M%3BSmith%2C+Martyn+T%3BYin%2C+Songnian%3BLi%2C+Guilan%3BHu%2C+Wei%3BShen%2C+Min%3BRappaport%2C+Stephen%3BBarone-Adesi%2C+Francesco%3BRothman%2C+Nathaniel%3BVermeulen%2C+Roel%3BLan%2C+Qing&rft.aulast=Bassig&rft.aufirst=Bryan&rft.date=2014-10-01&rft.volume=55&rft.issue=8&rft.spage=673&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/10.1002%2Fem.21880 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Mutagens; Telomeres; Age; Vapors; Oxidative stress; Leukocytes; Dosimetry; Polymerase chain reaction; Cancer; Occupational exposure; Benzene; Mutagenesis; Health risks; USA; China, People's Rep., Shanghai; China, People's Rep. DO - http://dx.doi.org/10.1002/em.21880 ER - TY - JOUR T1 - Statin use and risk of hepatocellular carcinoma in a U.S. population AN - 1622603586; 20875946 AB - Purpose Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are medications widely prescribed to reduce cholesterol levels. Observational studies in high-risk populations, mostly in Asia, have suggested that statins are associated with a reduced risk of hepatocellular carcinoma (HCC). The current study sought to evaluate the association of statin use and HCC in a U.S.-based, low-risk, general population. Methods A nested case-control study was conducted among members of the Health Alliance Plan HMO of the Henry Ford Health System enrolled between 1999 and 2010. Electronic pharmacy records of statin use were compared among tumor registry-confirmed cases of HCC (n=94) and controls (n=468) matched on age, sex, diagnosis date, and length of HMO enrolment. Results In multivariate analyses, ever-use of statins was significantly inversely associated with development of HCC (Odds ratio (OR): 0.32, 95%CI: 0.15-0.67). No clear dose-response relationship was evident as statin use for 2 years (OR=0.31, 95CI%=0.12-9.81) resulted in very similar ORs. Conclusions The use of statins among populations in low-risk HCC areas may be associated with decreased risk of HCC. JF - Cancer Epidemiology AU - McGlynn, Katherine A AU - Divine, George W AU - Sahasrabuddhe, Vikrant V AU - Engel, Lawrence S AU - VanSlooten, Ashley AU - Wells, Karen AU - Yood, Marianne Ulcickas AU - Alford, Sharon Hensley AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, United States Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 523 EP - 527 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 38 IS - 5 SN - 1877-7821, 1877-7821 KW - Risk Abstracts KW - Statins KW - Liver cancer KW - Epidemiology KW - Health risks KW - Age KW - Dose-response effects KW - Risk reduction KW - Tumors KW - Cholesterol KW - Asia KW - Drugs KW - Cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622603586?accountid=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=Statin+use+and+risk+of+hepatocellular+carcinoma+in+a+U.S.+population&rft.au=McGlynn%2C+Katherine+A%3BDivine%2C+George+W%3BSahasrabuddhe%2C+Vikrant+V%3BEngel%2C+Lawrence+S%3BVanSlooten%2C+Ashley%3BWells%2C+Karen%3BYood%2C+Marianne+Ulcickas%3BAlford%2C+Sharon+Hensley&rft.aulast=McGlynn&rft.aufirst=Katherine&rft.date=2014-10-01&rft.volume=38&rft.issue=5&rft.spage=523&rft.isbn=&rft.btitle=&rft.title=Cancer+Epidemiology&rft.issn=18777821&rft_id=info:doi/10.1016%2Fj.canep.2014.06.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2014-11-26 N1 - SubjectsTermNotLitGenreText - Health risks; Age; Statins; Dose-response effects; Cholesterol; Tumors; Risk reduction; Drugs; Cancer; Asia DO - http://dx.doi.org/10.1016/j.canep.2014.06.009 ER - TY - JOUR T1 - Chloroquine Remains Effective for Treating Plasmodium vivax Malaria in Pursat Province, Western Cambodia AN - 1622601429; 20856093 AB - Chloroquine (CQ) is used to treat Plasmodium vivax malaria in areas where CQ resistance has not been reported. The use of artemisinin (ART)-based combination therapies (ACTs) to treat CQ-sensitive P. vivax infections is effective and convenient but may promote the emergence and worsening of ART resistance in sympatric Plasmodium falciparum populations. Here, we show that CQ effectively treats P. vivax malaria in Pursat Province, western Cambodia, where ART-resistant P. falciparum is highly prevalent and spreading. (This study has been registered at ClinicalTrials.gov under registration no. NCT00663546.) JF - Antimicrobial Agents & Chemotherapy AU - Amaratunga, Chanaki AU - Sreng, Sokunthea AU - Mao, Sivanna AU - Tullo, Gregory S AU - Anderson, Jennifer M AU - Chuor, Char Meng AU - Suon, Seila AU - Fairhurst, Rick M AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, rfairhurst@niaid.nih.gov. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 6270 EP - 6272 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 58 IS - 10 SN - 0066-4804, 0066-4804 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Parasites KW - Human diseases KW - Spreading KW - Sympatric populations KW - Therapy KW - Chloroquine KW - Plasmodium vivax KW - Malaria KW - Plasmodium falciparum KW - Infection KW - Public health KW - Cambodia KW - artemisinin KW - K 03340:Effects of Physical & Chemical Factors KW - A 01340:Antibiotics & Antimicrobials 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/1622601429?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Chloroquine+Remains+Effective+for+Treating+Plasmodium+vivax+Malaria+in+Pursat+Province%2C+Western+Cambodia&rft.au=Amaratunga%2C+Chanaki%3BSreng%2C+Sokunthea%3BMao%2C+Sivanna%3BTullo%2C+Gregory+S%3BAnderson%2C+Jennifer+M%3BChuor%2C+Char+Meng%3BSuon%2C+Seila%3BFairhurst%2C+Rick+M&rft.aulast=Amaratunga&rft.aufirst=Chanaki&rft.date=2014-10-01&rft.volume=58&rft.issue=10&rft.spage=6270&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.03026-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Number of references - 17 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Therapy; Malaria; Public health; Spreading; Sympatric populations; Chloroquine; artemisinin; Infection; Plasmodium vivax; Plasmodium falciparum; Cambodia DO - http://dx.doi.org/10.1128/AAC.03026-14 ER - TY - JOUR T1 - Combined Effects of the Structural Heterogeneity and Dynamics of Flaviviruses on Antibody Recognition AN - 1622598932; 20856421 AB - Flaviviruses are thought to sample an ensemble of structures at equilibrium. One consequence of a structurally dynamic virion is the observed time-dependent increases in neutralization sensitivity that can occur after prolonged incubation with antibody. Differences in how virus strains "breathe" may affect epitope exposure and contribute to the underlying mechanisms of strain-dependent neutralization sensitivity. Beyond the contribution of structural dynamics, flaviviruses exist as a structurally heterogeneous population due to an inefficient virion maturation process. Here, we investigate the interplay between virion maturation and structural dynamics that contributes to antibody-mediated neutralization. Using West Nile (WNV) and dengue (DENV) viruses produced under conditions that modify the extent of virion maturation, we investigated time-dependent changes in neutralization sensitivity associated with structural dynamics. Our results identify distinct patterns of neutralization against viruses that vary markedly with respect to the extent of virion maturation. Reducing the efficiency of virion maturation resulted in greater time-dependent changes in neutralization potency and a marked reduction in the stability of the particle at 37 degree C compared to more mature virus. The fact that the neutralization sensitivity of WNV and DENV did not increase after prolonged incubation in the absence of antibody, regardless of virion maturation, suggests that the dynamic processes that govern epitope accessibility on infectious viruses are reversible. Against the backdrop of heterogeneous flavivirus structures, differences in the pathways by which viruses "breathe" represent an additional layer of complexity in understanding maturation state-dependent patterns of antibody recognition. IMPORTANCE Flaviviruses exist as a group of related structures at equilibrium that arise from the dynamic motion of E proteins that comprise the antigenic surface of the mature virion. This process has been characterized for numerous viruses and is referred to as viral "breathing." Additionally, flaviviruses are structurally heterogeneous due to an inefficient maturation process responsible for cleaving prM on the virion surface. Both of these mechanisms vary the exposure of antigenic sites available for antibody binding and impact the ability of antibodies to neutralize infection. We demonstrate that virions with inefficient prM cleavage "breathe" differently than their more mature counterparts, resulting in distinct patterns of neutralization sensitivity. Additionally, the maturation state was found to impact virus stability in solution. Our findings provide insight into the complex flavivirus structures that contribute to infection with the potential to impact antibody recognition. JF - Journal of Virology AU - Dowd, Kimberly A AU - Mukherjee, Swati AU - Kuhn, Richard J AU - Pierson, Theodore C AD - Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, piersontc@mail.nih.gov. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 11726 EP - 11737 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 88 IS - 20 SN - 0022-538X, 0022-538X KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Virology & AIDS Abstracts KW - Virions KW - Virology KW - Respiration KW - Viruses KW - Environmental impact KW - Infection KW - E protein KW - Flavivirus KW - Antibodies KW - Viral diseases KW - Dengue KW - Sexual maturity KW - Structural dynamics KW - Epitopes KW - Q1 08442:Population dynamics KW - V 22320:Replication KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622598932?accountid=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=Combined+Effects+of+the+Structural+Heterogeneity+and+Dynamics+of+Flaviviruses+on+Antibody+Recognition&rft.au=Dowd%2C+Kimberly+A%3BMukherjee%2C+Swati%3BKuhn%2C+Richard+J%3BPierson%2C+Theodore+C&rft.aulast=Dowd&rft.aufirst=Kimberly&rft.date=2014-10-01&rft.volume=88&rft.issue=20&rft.spage=11726&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.01140-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Number of references - 56 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Virology; Antibodies; Viral diseases; Structural dynamics; Sexual maturity; Viruses; Environmental impact; Virions; Dengue; Respiration; Infection; E protein; Epitopes; Flavivirus DO - http://dx.doi.org/10.1128/JVI.01140-14 ER - TY - JOUR T1 - The role of acculturation and collectivism in cancer screening for Vietnamese American women AN - 1622301416; 4614933 AB - The aim of this study was to examine the influence of demographic variables and the interplay between collectivism and acculturation on breast and cervical cancer screening outcomes among Vietnamese American women. Convenience sampling was used to recruit 111 Vietnamese women from the Richmond, VA, metropolitan area, who participated in a larger cancer screening intervention. All participants completed measures on demographic variables, collectivism, acculturation, and cancer-screening- related variables (i.e., attitudes, self-efficacy, and screening behavior). Findings indicated that collectivism predicted both positive attitudes and higher levels of self-efficacy with regard to breast and cervical cancer screening. Collectivism also moderated the relationship between acculturation and attitudes toward breast cancer screening such that for women with low levels of collectivistic orientation, increasing acculturation predicted less positive attitudes towards breast cancer screening. This relationship was not found for women with high levels of collectivistic orientation. The current findings highlight the important roles that sociodemographic and cultural variables play in affecting health attitudes, self- efficacy, and behavior among Vietnamese women. The findings potentially inform screening programs that rely on culturally relevant values in helping increase Vietnamese women's motivation to screen. Reprinted by permission of Taylor & Francis Ltd. JF - Health care for women international AU - Nguyen, Anh B AU - Clark, Trenette T AD - US National Cancer Institute ; University of North Carolina, Chapel Hill Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 1162 EP - 1180 VL - 35 IS - 10 SN - 0739-9332, 0739-9332 KW - Sociology KW - Acculturation KW - Health care KW - Motivation KW - Collectivism KW - Women KW - U.S.A. KW - Cancer KW - Vietnam UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622301416?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+care+for+women+international&rft.atitle=The+role+of+acculturation+and+collectivism+in+cancer+screening+for+Vietnamese+American+women&rft.au=Nguyen%2C+Anh+B%3BClark%2C+Trenette+T&rft.aulast=Nguyen&rft.aufirst=Anh&rft.date=2014-10-01&rft.volume=35&rft.issue=10&rft.spage=1162&rft.isbn=&rft.btitle=&rft.title=Health+care+for+women+international&rft.issn=07399332&rft_id=info:doi/10.1080%2F07399332.2013.863317 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-11-10 N1 - Last updated - 2014-11-11 N1 - SubjectsTermNotLitGenreText - 1939 3617 6220; 2491 5676; 8322; 13598 5421 6091; 5775 13521; 539 3105 3198; 449 393 30; 433 293 14 DO - http://dx.doi.org/10.1080/07399332.2013.863317 ER - TY - JOUR T1 - MMS exposure promotes increased MtDNA mutagenesis in the presence of replication-defective disease-associated DNA polymerase γ variants. AN - 1618161204; 25340760 AB - Mitochondrial DNA (mtDNA) encodes proteins essential for ATP production. Mutant variants of the mtDNA polymerase cause mutagenesis that contributes to aging, genetic diseases, and sensitivity to environmental agents. We interrogated mtDNA replication in Saccharomyces cerevisiae strains with disease-associated mutations affecting conserved regions of the mtDNA polymerase, Mip1, in the presence of the wild type Mip1. Mutant frequency arising from mtDNA base substitutions that confer erythromycin resistance and deletions between 21-nucleotide direct repeats was determined. Previously, increased mutagenesis was observed in strains encoding mutant variants that were insufficient to maintain mtDNA and that were not expected to reduce polymerase fidelity or exonuclease proofreading. Increased mutagenesis could be explained by mutant variants stalling the replication fork, thereby predisposing the template DNA to irreparable damage that is bypassed with poor fidelity. This hypothesis suggests that the exogenous base-alkylating agent, methyl methanesulfonate (MMS), would further increase mtDNA mutagenesis. Mitochondrial mutagenesis associated with MMS exposure was increased up to 30-fold in mip1 mutants containing disease-associated alterations that affect polymerase activity. Disrupting exonuclease activity of mutant variants was not associated with increased spontaneous mutagenesis compared with exonuclease-proficient alleles, suggesting that most or all of the mtDNA was replicated by wild type Mip1. A novel subset of C to G transversions was responsible for about half of the mutants arising after MMS exposure implicating error-prone bypass of methylated cytosines as the predominant mutational mechanism. Exposure to MMS does not disrupt exonuclease activity that suppresses deletions between 21-nucleotide direct repeats, suggesting the MMS-induce mutagenesis is not explained by inactivated exonuclease activity. Further, trace amounts of CdCl2 inhibit mtDNA replication but suppresses MMS-induced mutagenesis. These results suggest a novel mechanism wherein mutations that lead to hypermutation by DNA base-damaging agents and associate with mitochondrial disease may contribute to previously unexplained phenomena, such as the wide variation of age of disease onset and acquired mitochondrial toxicities. JF - PLoS genetics AU - Stumpf, Jeffrey D AU - Copeland, William C AD - Mitochondrial DNA Replication Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina, United States of America. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 1 VL - 10 IS - 10 KW - DNA, Mitochondrial KW - 0 KW - Saccharomyces cerevisiae Proteins KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Methyl Methanesulfonate KW - AT5C31J09G KW - DNA Polymerase I KW - EC 2.7.7.- KW - DNA polymerase gamma KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - MIP1 protein, S cerevisiae KW - Index Medicus KW - DNA Repair -- genetics KW - DNA Replication -- genetics KW - Humans KW - Point Mutation KW - Mutagenesis -- genetics KW - DNA Replication -- drug effects KW - DNA Repair -- drug effects KW - Adenosine Triphosphate -- biosynthesis KW - Sequence Deletion KW - Saccharomyces cerevisiae KW - Methyl Methanesulfonate -- pharmacology KW - Mitochondrial Diseases -- genetics KW - Mitochondrial Diseases -- metabolism KW - Saccharomyces cerevisiae Proteins -- genetics KW - Mitochondrial Diseases -- etiology KW - DNA Polymerase I -- genetics KW - DNA-Directed DNA Polymerase -- genetics KW - DNA, Mitochondrial -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618161204?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+genetics&rft.atitle=MMS+exposure+promotes+increased+MtDNA+mutagenesis+in+the+presence+of+replication-defective+disease-associated+DNA+polymerase+%CE%B3+variants.&rft.au=Stumpf%2C+Jeffrey+D%3BCopeland%2C+William+C&rft.aulast=Stumpf&rft.aufirst=Jeffrey&rft.date=2014-10-01&rft.volume=10&rft.issue=10&rft.spage=e1004748&rft.isbn=&rft.btitle=&rft.title=PLoS+genetics&rft.issn=1553-7404&rft_id=info:doi/10.1371%2Fjournal.pgen.1004748 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-30 N1 - Date created - 2014-10-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2002 May 3;277(18):15225-8 [11897778] J Biol Chem. 2001 Oct 12;276(41):38097-107 [11477094] Eukaryot Cell. 2003 Aug;2(4):809-20 [12912900] Nature. 2004 May 27;429(6990):417-23 [15164064] Nat Struct Mol Biol. 2004 Aug;11(8):770-6 [15258572] Cell. 1982 Apr;28(4):693-705 [6178513] Nucleic Acids Res. 1984 Nov 26;12(22):8313-8 [6095195] J Biol Chem. 1989 Dec 5;264(34):20552-60 [2684980] EMBO J. 1992 Jul;11(7):2717-26 [1321035] J Biol Chem. 1993 May 25;268(15):11028-40 [8496164] Carcinogenesis. 1993 Oct;14(10):2105-8 [8222061] Genomics. 1996 Sep 15;36(3):449-58 [8884268] Mol Cell Biol. 1997 May;17(5):2859-65 [9111358] Biochemistry. 1998 Jul 21;37(29):10529-39 [9671525] J Biol Chem. 1998 Sep 11;273(37):23690-7 [9726974] Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12244-8 [9770471] Biochemistry. 1999 Aug 31;38(35):11298-306 [10471279] Arch Dis Child. 1963 Jun;38:193-204 [13971413] Mol Cell Biol. 2005 Jun;25(12):5196-204 [15923634] Science. 2005 Jul 15;309(5733):481-4 [16020738] J Biol Chem. 2005 Sep 9;280(36):31341-6 [16024923] DNA Repair (Amst). 2005 Dec 8;4(12):1381-9 [16181814] Hum Mol Genet. 2006 Jan 15;15(2):363-74 [16368709] Am J Hum Genet. 2006 Jun;78(6):1026-34 [16685652] DNA Repair (Amst). 2006 Jul 13;5(7):829-39 [16730479] Neuromuscul Disord. 2006 Aug;16(8):507-9 [16919951] Hum Mol Genet. 2006 Oct 1;15(19):2846-55 [16940310] Hum Mol Genet. 2006 Dec 1;15(23):3473-83 [17088268] Lab Invest. 2007 Apr;87(4):326-35 [17310215] Nat Genet. 2007 Apr;39(4):540-3 [17334366] Hum Mol Genet. 2007 Nov 15;16(22):2729-39 [17725985] DNA Repair (Amst). 2007 Dec 1;6(12):1732-9 [17689152] Biochim Biophys Acta. 2007 Dec;1772(11-12):1225-35 [17980715] Nat Genet. 2008 Apr;40(4):392-4 [18311139] PLoS Genet. 2008 Nov;4(11):e1000264 [19023402] Environ Mol Mutagen. 2009 May;50(4):317-27 [19197988] J Biol Chem. 2009 Jul 17;284(29):19501-10 [19478085] Genetics. 2009 Jul;182(3):699-709 [19398768] DNA Repair (Amst). 2009 Oct 2;8(10):1242-9 [19699691] Mitochondrion. 2009 Sep;9(5):340-5 [19501198] Cell. 2009 Oct 16;139(2):312-24 [19837034] Hum Mol Genet. 2010 Jun 1;19(11):2123-33 [20185557] DNA Repair (Amst). 2010 Aug 5;9(8):914-21 [20663718] Methods. 2010 Aug;51(4):426-36 [20206271] Hum Mol Genet. 2010 Sep 15;19(18):3516-29 [20601675] Cell Mol Life Sci. 2011 Jan;68(2):219-33 [20927567] Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4135-40 [21368114] Mol Cell. 2012 May 25;46(4):424-35 [22607975] DNA Repair (Amst). 2012 Aug 1;11(8):684-92 [22766155] Cold Spring Harb Perspect Biol. 2013 Apr;5(4):a011395 [23545419] Genetics. 2013 Jun;194(2):519-22 [23589460] Nat Genet. 2001 Jul;28(3):211-2 [11431686] Clin Ther. 2000 Jun;22(6):685-708 [10929917] Prog Nucleic Acid Res Mol Biol. 2001;68:257-71 [11554302] Nat Genet. 2003 Jul;34(3):326-9 [12796780] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pgen.1004748 ER - TY - JOUR T1 - Lessons from a BACE1 inhibitor trial: off-site but not off base. AN - 1618140880; 24530026 AB - Alzheimer's disease (AD) is characterized by formation of neuritic plaque primarily composed of a small filamentous protein called amyloid-β peptide (Aβ). The rate-limiting step in the production of Aβ is the processing of Aβ precursor protein (APP) by β-site APP-cleaving enzyme (BACE1). Hence, BACE1 activity plausibly plays a rate-limiting role in the generation of potentially toxic Aβ within brain and the development of AD, thereby making it an interesting drug target. A phase II trial of the promising LY2886721 inhibitor of BACE1 was suspended in June 2013 by Eli Lilly and Co., due to possible liver toxicity. This outcome was apparently a surprise to the study's team, particularly since BACE1 knockout mice and mice treated with the drug did not show such liver toxicity. Lilly proposed that the problem was not due to LY2886721 anti-BACE1 activity. We offer an alternative hypothesis, whereby anti-BACE1 activity may induce apparent hepatotoxicity through inhibiting BACE1's processing of β-galactoside α-2,6-sialyltransferase I (STGal6 I). In knockout mice, paralogues, such as BACE2 or cathepsin D, could partially compensate. Furthermore, the short duration of animal studies and short lifespan of study animals could mask effects that would require several decades to accumulate in humans. Inhibition of hepatic BACE1 activity in middle-aged humans would produce effects not detectable in mice. We present a testable model to explain the off-target effects of LY2886721 and highlight more broadly that so-called off-target drug effects might actually represent off-site effects that are not necessarily off-target. Consideration of this concept in forthcoming drug design, screening, and testing programs may prevent such failures in the future. Copyright © 2014 The Alzheimer's Association. All rights reserved. JF - Alzheimer's & dementia : the journal of the Alzheimer's Association AU - Lahiri, Debomoy K AU - Maloney, Bryan AU - Long, Justin M AU - Greig, Nigel H AD - Laboratory of Molecular Neurogenetics, Department of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA. Electronic address: dlahiri@iupui.edu. ; Laboratory of Molecular Neurogenetics, Department of Psychiatry, Institute of Psychiatric Research, Indiana University School of Medicine, Indianapolis, IN, USA. ; Laboratory of Translational Gerontology, Intramural Research Program, National Institute of Aging, National Institutes of Health, Baltimore, MD, USA. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - S411 EP - S419 VL - 10 IS - 5 Suppl KW - Heterocyclic Compounds, 2-Ring KW - 0 KW - N-(3-(2-amino-4a,5,7,7a-tetrahydro-4H-furo(3,4-d)(1,3)thiazin-7a-yl)-4-fluorophenyl)-5-fluoropicolinamide KW - Nootropic Agents KW - Picolinic Acids KW - Protease Inhibitors KW - Amyloid Precursor Protein Secretases KW - EC 3.4.- KW - Aspartic Acid Endopeptidases KW - EC 3.4.23.- KW - BACE1 protein, human KW - EC 3.4.23.46 KW - Bace1 protein, mouse KW - Index Medicus KW - Liver damage KW - ROS KW - Neuronal death KW - CNS KW - Aging KW - Human studies KW - Demyelination KW - Drug trial KW - Brain disorder KW - Animal model KW - Sialylation KW - Melatonin KW - Secretase KW - Dementia KW - Side effects KW - Heterocyclic Compounds, 2-Ring -- therapeutic use KW - Animals KW - Picolinic Acids -- therapeutic use KW - Picolinic Acids -- adverse effects KW - Alzheimer Disease -- drug therapy KW - Alzheimer Disease -- physiopathology KW - Brain -- drug effects KW - Humans KW - Clinical Trials as Topic KW - Disease Models, Animal KW - Heterocyclic Compounds, 2-Ring -- adverse effects KW - Nootropic Agents -- pharmacology KW - Nootropic Agents -- adverse effects KW - Models, Biological KW - Heterocyclic Compounds, 2-Ring -- pharmacology KW - Mice, Knockout KW - Brain -- physiopathology KW - Liver -- physiopathology KW - Liver -- drug effects KW - Nootropic Agents -- therapeutic use KW - Picolinic Acids -- pharmacology KW - Protease Inhibitors -- therapeutic use KW - Protease Inhibitors -- pharmacology KW - Protease Inhibitors -- adverse effects KW - Aspartic Acid Endopeptidases -- genetics KW - Amyloid Precursor Protein Secretases -- antagonists & inhibitors KW - Aspartic Acid Endopeptidases -- metabolism KW - Aspartic Acid Endopeptidases -- antagonists & inhibitors KW - Amyloid Precursor Protein Secretases -- metabolism KW - Amyloid Precursor Protein Secretases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618140880?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alzheimer%27s+%26+dementia+%3A+the+journal+of+the+Alzheimer%27s+Association&rft.atitle=Lessons+from+a+BACE1+inhibitor+trial%3A+off-site+but+not+off+base.&rft.au=Lahiri%2C+Debomoy+K%3BMaloney%2C+Bryan%3BLong%2C+Justin+M%3BGreig%2C+Nigel+H&rft.aulast=Lahiri&rft.aufirst=Debomoy&rft.date=2014-10-01&rft.volume=10&rft.issue=5+Suppl&rft.spage=S411&rft.isbn=&rft.btitle=&rft.title=Alzheimer%27s+%26+dementia+%3A+the+journal+of+the+Alzheimer%27s+Association&rft.issn=1552-5279&rft_id=info:doi/10.1016%2Fj.jalz.2013.11.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-13 N1 - Date created - 2014-10-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Neurosci. 2013 May 1;33(18):7856-69 [23637177] Alzheimers Dement. 2013 Mar;9(2):208-45 [23507120] Curr Med Chem. 2013;20(24):3011-21 [23746274] J Neurochem. 2013 Nov;127(4):471-81 [23406323] Expert Opin Drug Saf. 2014 Jan;13(1):67-81 [24073714] Science. 1999 Oct 22;286(5440):735-41 [10531052] Chem Res Toxicol. 2000 Mar;13(3):135-60 [10725110] Cytogenet Cell Genet. 2000;89(3-4):177-84 [10965118] Nat Neurosci. 2001 Mar;4(3):231-2 [11224535] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13554-9 [11698669] Curr Drug Metab. 2002 Aug;3(4):425-38 [12093358] Mol Cell Neurosci. 2003 Nov;24(3):646-55 [14664815] J Pineal Res. 2004 May;36(4):217-23 [15066045] FASEB J. 2004 Jun;18(9):1034-6 [15059975] FASEB J. 2004 Jun;18(9):1037-9 [15059977] J Clin Endocrinol Metab. 1999 Jan;84(1):323-7 [9920102] J Biol Chem. 2005 Mar 4;280(9):8589-95 [15364953] Curr Drug Metab. 2005 Jun;6(3):161-225 [15975040] Toxicol Sci. 2006 Jan;89(1):31-41 [16177235] FASEB J. 2006 Feb;20(2):285-92 [16449801] J Mol Neurosci. 2006;28(2):193-210 [16679558] J Clin Gastroenterol. 2006 Aug;40(7):629-32 [16917407] Toxicology. 2006 Sep 1;226(1):1-11 [16860917] Science. 2006 Oct 27;314(5799):664-6 [16990514] Nat Neurosci. 2006 Dec;9(12):1520-5 [17099708] Curr Alzheimer Res. 2006 Dec;3(5):475-83 [17168646] Curr Alzheimer Res. 2007 Apr;4(2):219-28 [17430250] Surgery. 2007 Aug;142(2):262-9 [17689694] J Neurosci. 2008 Jan 2;28(1):3-9 [18171917] Biol Chem. 2008 Mar;389(3):313-20 [18177262] Neuron. 2008 Mar 13;57(5):680-90 [18341989] Curr Opin Gastroenterol. 2008 May;24(3):287-97 [18408456] Curr Drug Metab. 2008 May;9(4):344-51 [18473753] J Neurosci. 2011 Nov 16;31(46):16507-16 [22090477] Biochem J. 2012 Jan 1;441(1):285-96 [21880018] Drug Metab Rev. 2012 Feb;44(1):18-33 [21939431] Cell. 2012 Mar 16;148(6):1204-22 [22424230] Exp Neurol. 2012 Jun;235(2):402-18 [22245616] Expert Opin Emerg Drugs. 2012 Jun;17(2):147-56 [22439621] Science. 2012 Sep 7;337(6099):1172 [22955815] Mol Cancer Res. 2008 Aug;6(8):1316-25 [18708363] J Pathol. 2008 Dec;216(4):387-93 [18853439] Cell. 2009 Jan 23;136(2):215-33 [19167326] Curr Alzheimer Res. 2009 Feb;6(1):77-8 [19199878] Glycobiology. 2009 May;19(5):479-87 [19150807] J Neurochem. 2009 Aug;110(4):1129-34 [19457065] Mol Psychiatry. 2009 Nov;14(11):992-1003 [19851280] Expert Opin Drug Metab Toxicol. 2010 May;6(5):519-31 [20166853] Curr Alzheimer Res. 2010 Nov;7(7):642-51 [20704560] Biochem Biophys Res Commun. 2011 Jan 28;404(4):889-95 [21172309] Expert Opin Investig Drugs. 2011 Mar;20(3):325-41 [21222550] Nat Biotechnol. 2011 Apr;29(4):341-5 [21423189] J Neurochem. 2011 May;117(3):359-74 [21320126] PLoS One. 2011;6(7):e21954 [21799757] J Biol Chem. 2012 Sep 7;287(37):31298-310 [22733824] Drug Saf. 2012 Dec 1;35(12):1099-117 [23137150] EMBO J. 2013 Jul 17;32(14):2015-28 [23792428] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jalz.2013.11.004 ER - TY - JOUR T1 - Cross-national comparison of prenatal methamphetamine exposure on infant and early child physical growth: a natural experiment AN - 1610988995; 4605836 AB - The current study seeks to compare the effects of prenatal methamphetamine exposure (PME) on infant and child physical growth between the USA and New Zealand (NZ). This cross-national comparison provides a unique opportunity to examine the potential impact of services provided to drug using mothers on child health. The longitudinal Infant Development, Environment and Lifestyle study of PME from birth to 36_months was conducted in the USA and NZ. The US cohort included 204 children with PME and 212 non-PME matched comparisons (NPME); the NZ cohort included 108 children with PME and 115 NPME matched comparisons. Latent growth curve models were used to examine effects of PME, country of origin, and the country × PME interaction on growth in length/height and weight. In regard to length/height, PME and country of origin were associated with initial length and growth over time. There was also a significant interaction effect, such that children with PME in the USA were shorter at birth than children with PME in NZ after controlling for other prenatal exposures, infant set, socioeconomic status, and maternal height. In regard to weight, there was only an effect of country of origin. Effects of PME on infant and child growth were shown to differ across countries, with exposed children in NZ faring better than exposed children in the USA. Implications for prevention programs and public policy are discussed. Reprinted by permission of Springer JF - Prevention science AU - Abar, Beau AU - LaGasse, Linda L AU - Wouldes, Trecia AU - Derauf, Chris AU - Newman, Elana AU - Shah, Rizwan AU - Smith, Lynne M AU - Arria, Amelia M AU - Huestis, Marilyn A AU - DellaGrotta, Sheri AU - Dansereau, Lynne M AU - Wilcox, Tara AU - Neal, Charles R AU - Lester, Barry M AD - Brown University ; University of Auckland ; University of Hawaii ; University of Tulsa ; Harbor-UCLA Medical Center ; University of Maryland School of Public Health ; National Institute on Drug Abuse Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 767 EP - 776 VL - 15 IS - 5 SN - 1389-4986, 1389-4986 KW - Sociology KW - Prevention KW - Socioeconomic status KW - U.S.A. KW - Drugs KW - New Zealand KW - Child health KW - Infants KW - Cross-national analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1610988995?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Prevention+science&rft.atitle=Cross-national+comparison+of+prenatal+methamphetamine+exposure+on+infant+and+early+child+physical+growth%3A+a+natural+experiment&rft.au=Abar%2C+Beau%3BLaGasse%2C+Linda+L%3BWouldes%2C+Trecia%3BDerauf%2C+Chris%3BNewman%2C+Elana%3BShah%2C+Rizwan%3BSmith%2C+Lynne+M%3BArria%2C+Amelia+M%3BHuestis%2C+Marilyn+A%3BDellaGrotta%2C+Sheri%3BDansereau%2C+Lynne+M%3BWilcox%2C+Tara%3BNeal%2C+Charles+R%3BLester%2C+Barry+M&rft.aulast=Abar&rft.aufirst=Beau&rft.date=2014-10-01&rft.volume=15&rft.issue=5&rft.spage=767&rft.isbn=&rft.btitle=&rft.title=Prevention+science&rft.issn=13894986&rft_id=info:doi/10.1007%2Fs11121-013-0431-5 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-10-14 N1 - Last updated - 2014-10-14 N1 - SubjectsTermNotLitGenreText - 3060 971; 6495 2212; 10072; 2199 5772; 3755; 11988 4011 3974 9390 11932 2328 11935 5837 2360 2688 2449 10404 11936; 286 309; 433 293 14 DO - http://dx.doi.org/10.1007/s11121-013-0431-5 ER - TY - JOUR T1 - TRIM28 regulates RNA polymerase II promoter-proximal pausing and pause release. AN - 1609505644; 25173174 AB - Promoter-proximal pausing of RNA polymerase II (Pol II) is a major checkpoint in transcription. An unbiased search for new human proteins that could regulate paused Pol II at the HSPA1B gene identified TRIM28. In vitro analyses indicated HSF1-dependent attenuation of Pol II pausing upon TRIM28 depletion, whereas in vivo data revealed de novo expression of HSPA1B and other known genes regulated by paused Pol II upon TRIM28 knockdown. These results were supported by genome-wide ChIP-sequencing analyses of Pol II occupancy that revealed a global role for TRIM28 in regulating Pol II pausing and pause release. Furthermore, in vivo and in vitro mechanistic studies suggest that transcription-coupled phosphorylation regulates Pol II pause release by TRIM28. Collectively, our findings identify TRIM28 as a new factor that modulates Pol II pausing and transcriptional elongation at a large number of mammalian genes. JF - Nature structural & molecular biology AU - Bunch, Heeyoun AU - Zheng, Xiaofeng AU - Burkholder, Adam AU - Dillon, Simon T AU - Motola, Shmulik AU - Birrane, Gabriel AU - Ebmeier, Christopher C AU - Levine, Stuart AU - Fargo, David AU - Hu, Guang AU - Taatjes, Dylan J AU - Calderwood, Stuart K AD - Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. ; 1] Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. [2]. ; 1] Integrative Bioinformatics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. [2]. ; 1] Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. [2] Genomics and Proteomics Center, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. ; BioMicro Center, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. ; 1] Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. [2] Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA. ; Department of Chemistry and Biochemistry, University of Colorado, Boulder, Boulder, Colorado, USA. ; Integrative Bioinformatics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. ; Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 876 EP - 883 VL - 21 IS - 10 KW - DNA-Binding Proteins KW - 0 KW - HSP70 Heat-Shock Proteins KW - HSPA1B protein, human KW - Repressor Proteins KW - TRIM28 protein, human KW - Transcription Factors KW - heat shock transcription factor KW - ATM protein, human KW - EC 2.7.11.1 KW - Ataxia Telangiectasia Mutated Proteins KW - DNA-Activated Protein Kinase KW - RNA Polymerase II KW - EC 2.7.7.- KW - Index Medicus KW - DNA-Activated Protein Kinase -- antagonists & inhibitors KW - Transcription Factors -- antagonists & inhibitors KW - Phosphorylation KW - HeLa Cells KW - Humans KW - HEK293 Cells KW - DNA-Binding Proteins -- genetics KW - Transcription, Genetic -- genetics KW - DNA-Binding Proteins -- antagonists & inhibitors KW - Cell Line, Tumor KW - Transcription Factors -- genetics KW - Ataxia Telangiectasia Mutated Proteins -- antagonists & inhibitors KW - HSP70 Heat-Shock Proteins -- genetics KW - HSP70 Heat-Shock Proteins -- biosynthesis KW - RNA Polymerase II -- genetics KW - Repressor Proteins -- metabolism KW - Promoter Regions, Genetic -- genetics KW - Repressor Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1609505644?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+structural+%26+molecular+biology&rft.atitle=TRIM28+regulates+RNA+polymerase+II+promoter-proximal+pausing+and+pause+release.&rft.au=Bunch%2C+Heeyoun%3BZheng%2C+Xiaofeng%3BBurkholder%2C+Adam%3BDillon%2C+Simon+T%3BMotola%2C+Shmulik%3BBirrane%2C+Gabriel%3BEbmeier%2C+Christopher+C%3BLevine%2C+Stuart%3BFargo%2C+David%3BHu%2C+Guang%3BTaatjes%2C+Dylan+J%3BCalderwood%2C+Stuart+K&rft.aulast=Bunch&rft.aufirst=Heeyoun&rft.date=2014-10-01&rft.volume=21&rft.issue=10&rft.spage=876&rft.isbn=&rft.btitle=&rft.title=Nature+structural+%26+molecular+biology&rft.issn=1545-9985&rft_id=info:doi/10.1038%2Fnsmb.2878 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-07 N1 - Date created - 2014-10-08 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE48253; GEO N1 - SuppNotes - Cited By: Science. 2008 Dec 19;322(5909):1849-51 [19056940] Cell Rep. 2012 Dec 27;2(6):1670-83 [23260668] Mol Cell Biol. 2009 Mar;29(5):1123-33 [19103744] Genes Dev. 2009 Apr 1;23(7):837-48 [19339689] Science. 2010 Jan 15;327(5963):335-8 [20007866] J Biol Chem. 2010 Feb 26;285(9):6443-52 [20028984] Cell. 2010 Apr 30;141(3):432-45 [20434984] Mol Cell. 2010 Dec 22;40(6):965-75 [21172661] J Biol Chem. 2011 Jan 21;286(3):1737-47 [21078672] Mol Cell Biol. 2011 May;31(9):1833-47 [21343339] Proc Natl Acad Sci U S A. 2011 May 17;108(20):8212-7 [21531907] Mol Cell. 2012 Jan 13;45(1):38-50 [22244331] Nat Commun. 2012;3:633 [22252557] Mol Cancer Res. 2012 Mar;10(3):401-14 [22205726] Genes Dev. 2003 Jun 1;17(11):1402-14 [12782658] Proc Natl Acad Sci U S A. 1991 Aug 15;88(16):6906-10 [1871105] Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):7923-7 [8367444] Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9407-12 [9689093] Med Chem. 2005 Mar;1(2):199-208 [16787315] Nat Cell Biol. 2006 Aug;8(8):870-6 [16862143] Mol Cell. 2006 Aug 4;23(3):297-305 [16885020] Genes Dev. 2007 Feb 15;21(4):385-90 [17322397] J Biol Chem. 2007 Mar 2;282(9):6582-7 [17189255] Nature. 2007 Jul 12;448(7150):163-8 [17581591] Nat Genet. 2007 Oct;39(10):1235-44 [17873876] Cell. 2007 Oct 5;131(1):46-57 [17923087] Nat Genet. 2007 Dec;39(12):1507-11 [17994021] J Biol Chem. 2007 Dec 14;282(50):36177-89 [17942393] Mol Cell. 2007 Dec 14;28(5):823-37 [18082607] Mol Cell Biol. 2008 May;28(10):3290-300 [18332113] Proc Natl Acad Sci U S A. 2008 Jun 3;105(22):7762-7 [18505835] Genes Dev. 2008 Jul 15;22(14):1921-33 [18628398] Science. 2012 Mar 23;335(6075):1499-502 [22442485] Genes Dev. 2012 May 1;26(9):933-44 [22549956] EMBO J. 2012 May 16;31(10):2403-15 [22491012] Nat Immunol. 2012 Jun;13(6):596-603 [22544392] Nat Rev Genet. 2012 Oct;13(10):720-31 [22986266] J Biol Chem. 2012 Nov 23;287(48):40106-18 [23060449] Science. 2008 Dec 19;322(5909):1845-8 [19056941] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nsmb.2878 ER - TY - JOUR T1 - The crystal structure of the phosphatidylinositol 4-kinase IIα. AN - 1586095389; 25168678 AB - Phosphoinositides are a class of phospholipids generated by the action of phosphoinositide kinases with key regulatory functions in eukaryotic cells. Here, we present the atomic structure of phosphatidylinositol 4-kinase type IIα (PI4K IIα), in complex with ATP solved by X-ray crystallography at 2.8 Å resolution. The structure revealed a non-typical kinase fold that could be divided into N- and C-lobes with the ATP binding groove located in between. Surprisingly, a second ATP was found in a lateral hydrophobic pocket of the C-lobe. Molecular simulations and mutagenesis analysis revealed the membrane binding mode and the putative function of the hydrophobic pocket. Taken together, our results suggest a mechanism of PI4K IIα recruitment, regulation, and function at the membrane. © 2014 The Authors. JF - EMBO reports AU - Baumlova, Adriana AU - Chalupska, Dominika AU - Róźycki, Bartosz AU - Jovic, Marko AU - Wisniewski, Eva AU - Klima, Martin AU - Dubankova, Anna AU - Kloer, Daniel P AU - Nencka, Radim AU - Balla, Tamas AU - Boura, Evzen AD - Institute of Organic Chemistry and Biochemistry AS CR, Prague, Czech Republic. ; Institute of Physics Polish Academy of Sciences, Warsaw, Poland. ; Section on Molecular Signal Transduction, Program for Developmental Neuroscience, NICHD NIH, Bethesda, MD, USA. ; Syngenta Jealott's Hill Internation Research Centre, Bracknell, UK. ; Institute of Organic Chemistry and Biochemistry AS CR, Prague, Czech Republic boura@uochb.cas.cz. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 1085 EP - 1092 VL - 15 IS - 10 KW - Minor Histocompatibility Antigens KW - 0 KW - Phosphatidylinositols KW - Inositol KW - 4L6452S749 KW - Phosphotransferases (Alcohol Group Acceptor) KW - EC 2.7.1.- KW - phosphatidylinositol phosphate 4-kinase KW - EC 2.7.1.67 KW - Index Medicus KW - kinase KW - Monte Carlo simulations KW - membrane KW - crystal structure KW - phosphatidyl inositol KW - Membranes -- chemistry KW - Humans KW - Monte Carlo Method KW - Inositol -- chemistry KW - Protein Binding KW - Signal Transduction KW - Binding Sites KW - Phosphotransferases (Alcohol Group Acceptor) -- chemistry KW - Phosphatidylinositols -- chemistry KW - Phosphatidylinositols -- metabolism KW - Crystallography, X-Ray KW - Phosphotransferases (Alcohol Group Acceptor) -- ultrastructure KW - Phosphotransferases (Alcohol Group Acceptor) -- metabolism KW - Protein Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1586095389?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=EMBO+reports&rft.atitle=The+crystal+structure+of+the+phosphatidylinositol+4-kinase+II%CE%B1.&rft.au=Baumlova%2C+Adriana%3BChalupska%2C+Dominika%3BR%C3%B3%C5%BAycki%2C+Bartosz%3BJovic%2C+Marko%3BWisniewski%2C+Eva%3BKlima%2C+Martin%3BDubankova%2C+Anna%3BKloer%2C+Daniel+P%3BNencka%2C+Radim%3BBalla%2C+Tamas%3BBoura%2C+Evzen&rft.aulast=Baumlova&rft.aufirst=Adriana&rft.date=2014-10-01&rft.volume=15&rft.issue=10&rft.spage=1085&rft.isbn=&rft.btitle=&rft.title=EMBO+reports&rft.issn=1469-3178&rft_id=info:doi/10.15252%2Fembr.201438841 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-11 N1 - Date created - 2014-10-02 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4PLA; PDB N1 - SuppNotes - Cited By: J Biol Chem. 2001 May 18;276(20):16635-40 [11279162] J Cell Sci. 2014 Sep 1;127(Pt 17):3745-56 [25002402] J Biol Chem. 2002 May 31;277(22):20041-50 [11923287] J Biol Chem. 2002 Nov 15;277(46):44366-75 [12215430] Cell. 2003 Aug 8;114(3):299-310 [12914695] Nature. 1984 Nov 22-28;312(5992):315-21 [6095092] Curr Opin Cell Biol. 1996 Apr;8(2):153-8 [8791418] Cell. 1998 Sep 18;94(6):829-39 [9753329] Mol Biol Cell. 2005 Mar;16(3):1282-95 [15635101] J Cell Sci. 2006 Feb 1;119(Pt 3):571-81 [16443754] J Biol Chem. 2006 Feb 17;281(7):3757-63 [16249177] Biochim Biophys Acta. 2007 Mar;1771(3):353-404 [17382260] Mol Biol Cell. 2007 Jul;18(7):2646-55 [17494868] Biochem J. 2008 Jan 15;409(2):501-9 [17927563] J Mol Biol. 2008 Feb 1;375(5):1416-33 [18083189] Mol Biol Cell. 2008 Apr;19(4):1415-26 [18256276] J Biol Chem. 2009 Apr 10;284(15):9994-10003 [19211550] J Struct Biol. 2010 Jun;170(3):451-61 [20347994] Acta Crystallogr D Biol Crystallogr. 2010 Dec;66(Pt 12):1351-7 [21123876] Cell. 2010 Dec 10;143(6):875-87 [21145455] Proc Natl Acad Sci U S A. 2010 Dec 14;107(50):21418-23 [21098302] Anal Biochem. 2011 Oct 1;417(1):97-102 [21704602] Proc Natl Acad Sci U S A. 2012 Feb 7;109(6):1901-6 [22232651] Subcell Biochem. 2012;59:255-70 [22374093] Subcell Biochem. 2012;58:1-24 [22403072] Mol Biol Cell. 2012 Apr;23(8):1533-45 [22337770] J Biol Chem. 2012 Jun 22;287(26):21856-65 [22535966] Trends Biochem Sci. 2012 Jul;37(7):293-302 [22633842] Science. 2012 Aug 10;337(6095):727-30 [22722250] EMBO Rep. 2012 Dec;13(12):1087-94 [23146885] Physiol Rev. 2013 Jul;93(3):1019-137 [23899561] Structure. 2013 Aug 6;21(8):1374-83 [23891288] Nat Commun. 2014;5:3552 [24675427] Science. 2014 May 30;344(6187):1035-8 [24876499] J Biol Chem. 2001 Mar 16;276(11):7705-8 [11244087] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.15252/embr.201438841 ER - TY - JOUR T1 - Smoothness of in vivo spectral baseline determined by mean-square error AN - 1566849715; 20749130 AB - Purpose A nonparametric smooth line is usually added to the spectral model to account for background signals in vivo magnetic resonance spectroscopy (MRS). The assumed smoothness of the baseline significantly influences quantitative spectral fitting. In this paper, a method is proposed to minimize baseline influences on the estimated spectral parameters. Methods The nonparametric baseline function with a given smoothness was treated as a function of spectral parameters. Its uncertainty was measured by root-mean-square error (RMSE). The proposed method was demonstrated with a simulated spectrum and in vivo spectra of both short echo time and averaged echo times. The estimated in vivo baselines were compared with the metabolite-nulled spectra and the LCModel-estimated baselines. The accuracies of estimated baseline and metabolite concentrations were further verified via cross-validation. Results An optimal smoothness condition was found that led to the minimal baseline RMSE. In this condition, the best fit was balanced against minimal baseline influences on metabolite concentration estimates. Conclusion Baseline RMSE can be used to indicate estimated baseline uncertainties and serve as the criterion for determining the baseline smoothness of in vivo MRS. Magn Reson Med 72:913-922, 2014. copyright 2013 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Zhang, Yan AU - Shen, Jun AD - MR Spectroscopy Core Facility, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 913 EP - 922 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 72 IS - 4 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Magnetic resonance spectroscopy KW - Metabolites KW - N.M.R. KW - Models KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566849715?accountid=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=Smoothness+of+in+vivo+spectral+baseline+determined+by+mean-square+error&rft.au=Zhang%2C+Yan%3BShen%2C+Jun&rft.aulast=Zhang&rft.aufirst=Yan&rft.date=2014-10-01&rft.volume=72&rft.issue=4&rft.spage=913&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25013 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-10-15 N1 - SubjectsTermNotLitGenreText - Magnetic resonance spectroscopy; N.M.R.; Metabolites; Models DO - http://dx.doi.org/10.1002/mrm.25013 ER - TY - JOUR T1 - N-acetyl-aspartyl-glutamate detection in the human brain at 7 Tesla by echo time optimization and improved Wiener filtering AN - 1566845802; 20749125 AB - Purpose To report enhanced signal detection for measuring N-acetyl-aspartyl-glutamate (NAAG) in the human brain at 7 Tesla by echo time (TE) -optimized point-resolved spectroscopy (PRESS) and improved Wiener filtering. Methods Using a highly efficient in-house developed numerical simulation program, a PRESS sequence with (TE sub(1), TE sub(2))=(26, 72) ms was found to maximize the NAAG signals relative to the overlapping Glu signals. A new Wiener filtering water reference deconvolution method was developed to reduce broadening and distortions of metabolite peaks caused by B sub(0) inhomogeneity and eddy currents. Results Monte Carlo simulation results demonstrated that the new Wiener filtering method offered higher spectral resolution, reduced spectral artifacts, and higher accuracy in NAAG quantification compared with the original Wiener filtering method. In vivo spectra and point spread functions of signal distortion confirmed that the new Wiener filtering method lead to improved spectral resolution and reduced spectral artifacts. Conclusion TE-optimized PRESS in combination with a new Wiener filtering method made it possible to fully use both the NAAG singlet signal at 2.05 ppm and the NAAG multiplet signal at 2.18 ppm in the quantification of NAAG. A more accurate characterization of lineshape distortion for Wiener filtering needs B sub(0) field maps and segmented anatomical images to exclude contribution from cerebral spinal fluid. Magn Reson Med 72:903-912, 2014. copyright 2013 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - An, Li AU - Li, Shizhe AU - Wood, Emily T AU - Reich, Daniel S AU - Shen, Jun AD - National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 903 EP - 912 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 72 IS - 4 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Monte Carlo simulation KW - N-Acetylaspartylglutamic acid KW - Cerebrospinal fluid KW - Mathematical models KW - Brain KW - N.M.R. KW - Metabolites KW - Maps KW - Spectroscopy KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566845802?accountid=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=N-acetyl-aspartyl-glutamate+detection+in+the+human+brain+at+7+Tesla+by+echo+time+optimization+and+improved+Wiener+filtering&rft.au=An%2C+Li%3BLi%2C+Shizhe%3BWood%2C+Emily+T%3BReich%2C+Daniel+S%3BShen%2C+Jun&rft.aulast=An&rft.aufirst=Li&rft.date=2014-10-01&rft.volume=72&rft.issue=4&rft.spage=903&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25007 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-10-15 N1 - SubjectsTermNotLitGenreText - Monte Carlo simulation; Cerebrospinal fluid; N-Acetylaspartylglutamic acid; Mathematical models; Brain; Metabolites; N.M.R.; Spectroscopy; Maps DO - http://dx.doi.org/10.1002/mrm.25007 ER - TY - JOUR T1 - NIH Workshop on Clinical Translation of Molecular Imaging Probes and Technology-Meeting Report AN - 1566844270; 20740778 AB - A workshop on "Clinical Translation of Molecular Imaging Probes and Technology" was held August 2, 2013 in Bethesda, Maryland, organized and supported by the National Institute of Biomedical Imaging and Bioengineering (NIBIB). This workshop brought together researchers, clinicians, representatives from pharmaceutical companies, molecular probe developers, and regulatory science experts. Attendees met to talk over current challenges in the discovery, validation, and translation of molecular imaging (MI) probes for key clinical applications. Participants also discussed potential strategies to address these challenges. The workshop consisted of 4 sessions, with 14 presentations and 2 panel discussions. Topics of discussion included (1) challenges and opportunities for clinical research and patient care, (2) advances in molecular probe design, (3) current approaches used by industry and pharmaceutical companies, and (4) clinical translation of MI probes. In the presentations and discussions, there were general agreement that while the barriers for validation and translation of MI probes remain high, there are pressing clinical needs and development opportunities for targets in cardiovascular, cancer, endocrine, neurological, and inflammatory diseases. The strengths of different imaging modalities, and the synergy of multimodality imaging, were highlighted. Participants also underscored the continuing need for close interactions and collaborations between academic and industrial partners, and federal agencies in the imaging probe development process. JF - Molecular Imaging and Biology AU - Liu, Christina H AU - Sastre, Antonio AU - Conroy, Richard AU - Seto, Belinda AU - Pettigrew, Roderic I AD - National Institute of Biomedical Imaging and Bioengineering, 6707 Democracy Blvd., Suite 200, Bethesda, MD, 20892, USA, Christina.liu@nih.gov Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 595 EP - 604 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 16 IS - 5 SN - 1536-1632, 1536-1632 KW - Biotechnology and Bioengineering Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566844270?accountid=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=NIH+Workshop+on+Clinical+Translation+of+Molecular+Imaging+Probes+and+Technology-Meeting+Report&rft.au=Liu%2C+Christina+H%3BSastre%2C+Antonio%3BConroy%2C+Richard%3BSeto%2C+Belinda%3BPettigrew%2C+Roderic+I&rft.aulast=Liu&rft.aufirst=Christina&rft.date=2014-10-01&rft.volume=16&rft.issue=5&rft.spage=595&rft.isbn=&rft.btitle=&rft.title=Molecular+Imaging+and+Biology&rft.issn=15361632&rft_id=info:doi/10.1007%2Fs11307-014-0746-z LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 95 N1 - Last updated - 2014-10-02 DO - http://dx.doi.org/10.1007/s11307-014-0746-z ER - TY - JOUR T1 - The evidence base for the use of internal dosimetry in the clinical practice of molecular radiotherapy AN - 1566838182; 20719981 AB - Molecular radiotherapy (MRT) has demonstrated unique therapeutic advantages in the treatment of an increasing number of cancers. As with other treatment modalities, there is related toxicity to a number of organs at risk. Despite the large number of clinical trials over the past several decades, considerable uncertainties still remain regarding the optimization of this therapeutic approach and one of the vital issues to be answered is whether an absorbed radiation dose-response exists that could be used to guide personalized treatment. There are only limited and sporadic data investigating MRT dosimetry. The determination of dose-effect relationships for MRT has yet to be the explicit aim of a clinical trial. The aim of this article was to collate and discuss the available evidence for an absorbed radiation dose-effect relationships in MRT through a review of published data. Based on a PubMed search, 92 papers were found. Out of 79 studies investigating dosimetry, an absorbed dose-effect correlation was found in 48. The application of radiobiological modelling to clinical data is of increasing importance and the limited published data on absorbed dose-effect relationships based on these models are also reviewed. Based on National Cancer Institute guideline definition, the studies had a moderate or low rate of clinical relevance due to the limited number of studies investigating overall survival and absorbed dose. Nevertheless, the evidence strongly implies a correlation between the absorbed doses delivered and the response and toxicity, indicating that dosimetry-based personalized treatments would improve outcome and increase survival. JF - European Journal of Nuclear Medicine and Molecular Imaging AU - Strigari, Lidia AU - Konijnenberg, Mark AU - Chiesa, Carlo AU - Bardies, Manuel AU - Du, Yong AU - Gleisner, Katarina Sjogreen AU - Lassmann, Michael AU - Flux, Glenn AD - Laboratory of Medical Physics and Expert Systems, Regina Elena National Cancer Institute, via E. Chianesi 53, 00144, Rome, Italy, strigari@ifo.it Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 1976 EP - 1988 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 41 IS - 10 SN - 1619-7070, 1619-7070 KW - Biotechnology and Bioengineering Abstracts KW - Data processing KW - Radiation KW - Reviews KW - Dosimetry KW - Survival KW - Radiotherapy KW - Nuclear medicine KW - Toxicity KW - Clinical trials KW - Cancer KW - Models KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566838182?accountid=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=The+evidence+base+for+the+use+of+internal+dosimetry+in+the+clinical+practice+of+molecular+radiotherapy&rft.au=Strigari%2C+Lidia%3BKonijnenberg%2C+Mark%3BChiesa%2C+Carlo%3BBardies%2C+Manuel%3BDu%2C+Yong%3BGleisner%2C+Katarina+Sjogreen%3BLassmann%2C+Michael%3BFlux%2C+Glenn&rft.aulast=Strigari&rft.aufirst=Lidia&rft.date=2014-10-01&rft.volume=41&rft.issue=10&rft.spage=1976&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-014-2824-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 75 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Data processing; Radiation; Reviews; Dosimetry; Nuclear medicine; Radiotherapy; Survival; Toxicity; Clinical trials; Cancer; Models DO - http://dx.doi.org/10.1007/s00259-014-2824-5 ER - TY - JOUR T1 - [ super(18)F]Fluciclatide in the in vivo evaluation of human melanoma and renal tumors expressing alpha sub(v) beta sub(3) and alpha sub(v) beta sub(5) integrins AN - 1566837864; 20719972 AB - Purpose: [ super(18)F]Fluciclatide is an integrin-targeted PET radiopharmaceutical. alpha sub(v) beta sub(3) and alpha sub(v) beta sub(5) are upregulated in tumor angiogenesis as well as on some tumor cell surfaces. Our aim was to use [ super(18)F]fluciclatide (formerly known as [ super(18)F]AH111585) for PET imaging of angiogenesis in melanoma and renal tumors and compare with tumor integrin expression. Methods: Eighteen evaluable patients with solid tumors greater than or equal to 2.0 cm underwent [ super(18)F]fluciclatide PET/CT. All patients underwent surgery and tumor tissue samples were obtained. Immunohistochemical (IHC) staining with mouse monoclonal antibodies and diaminobenzidine (DAB) was applied to snap-frozen tumor specimens, and additional IHC was done on formalin-fixed paraffin-embedded samples. DAB optical density (OD) data from digitized whole-tissue sections were compared with PET SUV sub(80% max), and Patlak influx rate constant (K sub(i)) data, tumor by tumor. Results: Tumors from all 18 patients demonstrated measurable [ super(18)F]fluciclatide uptake. At the final dynamic time-point (55 min after injection), renal malignancies (in 11 patients) demonstrated an average SUV sub(80% max) of 6.4 plus or minus 2.0 (range 3.8 - 10.0), while the average SUV sub(80% max) for metastatic melanoma lesions (in 6 patients) was 3.0 plus or minus 2.0 (range 0.7 - 6.5). There was a statistically significant difference in [ super(18)F]fluciclatide uptake between chromophobe and nonchromophobe renal cell carcinoma (RCCs, with SUV sub(80% max) of 8.2 plus or minus 1.8 and 5.4 plus or minus 1.4 (P=0.020) and tumor-to-normal kidney (T/N) ratios of 1.5 plus or minus 0.4 and 0.9 plus or minus 0.2, respectively (P=0.029). The highest Pearson's correlation coefficients were obtained when comparing Patlak K sub(i) and alpha sub(v) beta sub(5) OD when segregating the patient population between melanoma and RCC (r=0.83 for K sub(i) vs. melanoma and r=0.91 for K sub(i) vs. RCC). SUV sub(80% max) showed a moderate correlation with alpha sub(v) beta sub(5) and alpha sub(v) beta sub(3) OD. Conclusion: [ super(18)F]Fluciclatide PET imaging was well tolerated and demonstrated favorable characteristics for imaging alpha sub(v) beta sub(3) and alpha sub(v) beta sub(5) expression in melanoma and RCC. Higher uptake was observed in chromophobe than in nonchromophobe RCC. [ super(18)F]Fluciclatide may be a useful radiotracer to improve knowledge of integrin expression. JF - European Journal of Nuclear Medicine and Molecular Imaging AU - Mena, Esther AU - Owenius, Rikard AU - Turkbey, Baris AU - Sherry, Richard AU - Bratslavsky, Gennady AU - Macholl, Sven AU - Miller, Matthew P AU - Somer, Ed J AU - Lindenberg, Liza AU - Adler, Stephen AU - Shih, Joanna AU - Choyke, Peter AU - Kurdziel, Karen AD - Molecular Imaging Program, NCI, NIH, Bethesda, MD, USA, liza.lindenberg@nih.gov Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 1879 EP - 1888 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 41 IS - 10 SN - 1619-7070, 1619-7070 KW - Biotechnology and Bioengineering Abstracts KW - Data processing KW - Monoclonal antibodies KW - Solid tumors KW - Statistical analysis KW - Angiogenesis KW - Tumors KW - Tumor cells KW - Melanoma KW - Metastases KW - Malignancy KW - renal cell carcinoma KW - Integrins KW - Surgery KW - Optical density KW - Computed tomography KW - Radioisotopes KW - Kidney KW - Pharmaceuticals KW - Nuclear medicine KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566837864?accountid=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=%5B+super%2818%29F%5DFluciclatide+in+the+in+vivo+evaluation+of+human+melanoma+and+renal+tumors+expressing+alpha+sub%28v%29+beta+sub%283%29+and+alpha+sub%28v%29+beta+sub%285%29+integrins&rft.au=Mena%2C+Esther%3BOwenius%2C+Rikard%3BTurkbey%2C+Baris%3BSherry%2C+Richard%3BBratslavsky%2C+Gennady%3BMacholl%2C+Sven%3BMiller%2C+Matthew+P%3BSomer%2C+Ed+J%3BLindenberg%2C+Liza%3BAdler%2C+Stephen%3BShih%2C+Joanna%3BChoyke%2C+Peter%3BKurdziel%2C+Karen&rft.aulast=Mena&rft.aufirst=Esther&rft.date=2014-10-01&rft.volume=41&rft.issue=10&rft.spage=1879&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-014-2791-x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 36 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Data processing; Solid tumors; Monoclonal antibodies; Angiogenesis; Statistical analysis; Tumors; Tumor cells; Melanoma; Metastases; Malignancy; renal cell carcinoma; Integrins; Surgery; Computed tomography; Optical density; Kidney; Radioisotopes; Nuclear medicine; Pharmaceuticals DO - http://dx.doi.org/10.1007/s00259-014-2791-x ER - TY - JOUR T1 - Value of super(18)F-FDG uptake on PET/CT and CEA level to predict epidermal growth factor receptor mutations in pulmonary adenocarcinoma AN - 1566828838; 20719976 AB - Purpose: The identification of the mutation status of the epidermal growth factor receptor (EGFR) is important for the optimization of treatment in patients with pulmonary adenocarcinoma. The acquisition of adequate tissues for EGFR mutational analysis is sometimes not feasible, especially in advanced-stage patients. The aim of this study was to predict EGFR mutation status in patients with pulmonary adenocarcinoma based on super(18)F-fluorodeoxyglucose (FDG) uptake and imaging features in positron emission tomography/computed tomography (PET/CT), as well as on the serum carcinoembryonic antigen (CEA) level. Methods: We retrospectively reviewed 132 pulmonary adenocarcinoma patients who underwent EGFR mutation testing, pretreatment FDG PET/CT and serum CEA analysis. The associations between EGFR mutations and patient characteristics, maximal standard uptake value (SUVmax) of primary tumors, serum CEA level and CT imaging features were analyzed. Receiver-operating characteristic (ROC) curve analysis was performed to quantify the predictive value of these factors. Results: EGFR mutations were identified in 69 patients (52.2 %). Patients with SUVmax greater than or equal to 6 (p=0.002) and CEA level greater than or equal to 5 (p=0.013) were more likely to have EGFR mutations. The CT characteristics of larger tumors ( greater than or equal to 3 cm) (p=0.023) and tumors with a nonspiculated margin (p=0.026) were also associated with EGFR mutations. Multivariate analysis showed that higher SUVmax and CEA level, never smoking and a nonspiculated tumor margin were the most significant predictors of EGFR mutation. The combined use of these four criteria yielded a higher area under the ROC curve (0.82), suggesting a good discrimination. Conclusion: The combined evaluation of FDG uptake, CEA level, smoking status and tumor margins may be helpful in predicting EGFR mutation status in patients with pulmonary adenocarcinoma, especially when the tumor sample is inadequate for genetic analysis or genetic testing is not available. Further large-scale prospective studies are needed to validate these results. JF - European Journal of Nuclear Medicine and Molecular Imaging AU - Ko, Kai-Hsiung AU - Hsu, Hsian-He AU - Huang, Tsai-Wang AU - Gao, Hong-Wei AU - Shen, Daniel HY AU - Chang, Wei-Chou AU - Hsu, Yi-Chih AU - Chang, Tsun-Hou AU - Chu, Chi-Ming AU - Ho, Ching-Liang AU - Chang, Hung AD - Department of Radiology, Tri-Service General Hospital and National Defense Medical Center, 325, Section 2, Cheng-Gong Road, Nei-Hu, Taipei 114, Taiwan, Republic of China, hsianhe@yahoo.com.tw Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 1889 EP - 1897 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 41 IS - 10 SN - 1619-7070, 1619-7070 KW - Biotechnology and Bioengineering Abstracts KW - Genetic analysis KW - Carcinoembryonic antigen KW - Epidermal growth factor receptors KW - Tumors KW - Smoking KW - Multivariate analysis KW - Lung KW - Computed tomography KW - Positron emission tomography KW - Genetic screening KW - Nuclear medicine KW - Adenocarcinoma KW - Mutation KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566828838?accountid=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=Value+of+super%2818%29F-FDG+uptake+on+PET%2FCT+and+CEA+level+to+predict+epidermal+growth+factor+receptor+mutations+in+pulmonary+adenocarcinoma&rft.au=Ko%2C+Kai-Hsiung%3BHsu%2C+Hsian-He%3BHuang%2C+Tsai-Wang%3BGao%2C+Hong-Wei%3BShen%2C+Daniel+HY%3BChang%2C+Wei-Chou%3BHsu%2C+Yi-Chih%3BChang%2C+Tsun-Hou%3BChu%2C+Chi-Ming%3BHo%2C+Ching-Liang%3BChang%2C+Hung&rft.aulast=Ko&rft.aufirst=Kai-Hsiung&rft.date=2014-10-01&rft.volume=41&rft.issue=10&rft.spage=1889&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-014-2802-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 30 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Carcinoembryonic antigen; Genetic analysis; Epidermal growth factor receptors; Tumors; Smoking; Lung; Multivariate analysis; Computed tomography; Positron emission tomography; Nuclear medicine; Genetic screening; Adenocarcinoma; Mutation DO - http://dx.doi.org/10.1007/s00259-014-2802-y ER - TY - JOUR T1 - N-methylnicotinamide and nicotinamide N-methyltransferase are associated with microRNA-1291-altered pancreatic carcinoma cell metabolome and suppressed tumorigenesis. AN - 1566824134; 25115443 AB - The cell metabolome comprises abundant information that may be predictive of cell functions in response to epigenetic or genetic changes at different stages of cell proliferation and metastasis. An unbiased ultra-performance liquid chromatography-mass spectrometry-based metabolomics study revealed a significantly altered metabolome for human pancreatic carcinoma PANC-1 cells with gain-of-function non-coding microRNA-1291 (miR-1291), which led to a lower migration and invasion capacity as well as suppressed tumorigenesis in a xenograft tumor mouse model. A number of metabolites, including N-methylnicotinamide, involved in nicotinamide metabolism, and l-carnitine, isobutyryl-carnitine and isovaleryl-carnitine, involved in fatty acid metabolism, were elevated in miR-1291-expressing PANC-1. Notably, N-methylnicotinamide was elevated to the greatest extent, and this was associated with a sharp increase in nicotinamide N-methyltransferase (NNMT) mRNA level in miR-1291-expressing PANC-1 cells. In addition, expression of NNMT mRNA was inversely correlated with pancreatic tumor size in the xenograft mouse model. These results indicate that miR-1291-altered PANC-1 cell function is associated with the increase in N-methylnicotinamide level and NNMT expression, and in turn NNMT may be indicative of the extent of pancreatic carcinogenesis. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Bi, Hui-Chang AU - Pan, Yu-Zhuo AU - Qiu, Jing-Xin AU - Krausz, Kristopher W AU - Li, Fei AU - Johnson, Caroline H AU - Jiang, Chang-Tao AU - Gonzalez, Frank J AU - Yu, Ai-Ming AD - School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Pharmaceutical Sciences, SUNY-Buffalo, Buffalo, NY 14214, USA, Department of Biochemistry & Molecular Medicine, UC Davis Medical Center, Sacramento, CA 95817, USA and. ; Department of Pathology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. ; Department of Pharmaceutical Sciences, SUNY-Buffalo, Buffalo, NY 14214, USA, Department of Biochemistry & Molecular Medicine, UC Davis Medical Center, Sacramento, CA 95817, USA and aimyu@ucdavis.edu. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 2264 EP - 2272 VL - 35 IS - 10 KW - Biomarkers, Tumor KW - 0 KW - MIRN1291 microRNA, human KW - MicroRNAs KW - Niacinamide KW - 25X51I8RD4 KW - NNMT protein, human KW - EC 2.1.1.1 KW - Nicotinamide N-Methyltransferase KW - N-methylnicotinamide KW - X3I82S5L8I KW - Index Medicus KW - Cell Movement KW - Animals KW - Humans KW - Aged KW - Mice, Nude KW - Mice KW - Cell Line, Tumor KW - Biomarkers, Tumor -- metabolism KW - Gene Expression Regulation, Neoplastic KW - Metabolome KW - Aged, 80 and over KW - Adult KW - Xenograft Model Antitumor Assays KW - Middle Aged KW - Female KW - Male KW - Nicotinamide N-Methyltransferase -- genetics KW - Pancreatic Neoplasms -- pathology KW - Pancreatic Neoplasms -- mortality KW - Pancreatic Neoplasms -- metabolism KW - MicroRNAs -- genetics KW - Nicotinamide N-Methyltransferase -- metabolism KW - Niacinamide -- analogs & derivatives KW - Pancreatic Neoplasms -- genetics KW - Niacinamide -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566824134?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=N-methylnicotinamide+and+nicotinamide+N-methyltransferase+are+associated+with+microRNA-1291-altered+pancreatic+carcinoma+cell+metabolome+and+suppressed+tumorigenesis.&rft.au=Bi%2C+Hui-Chang%3BPan%2C+Yu-Zhuo%3BQiu%2C+Jing-Xin%3BKrausz%2C+Kristopher+W%3BLi%2C+Fei%3BJohnson%2C+Caroline+H%3BJiang%2C+Chang-Tao%3BGonzalez%2C+Frank+J%3BYu%2C+Ai-Ming&rft.aulast=Bi&rft.aufirst=Hui-Chang&rft.date=2014-10-01&rft.volume=35&rft.issue=10&rft.spage=2264&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu174 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2014-09-30 N1 - 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Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu174 ER - TY - JOUR T1 - Household air pollution and lung cancer in China: a review of studies in Xuanwei. AN - 1566822185; 25223911 AB - Over half of the world's population is exposed to household air pollution from the burning of solid fuels at home. Household air pollution from solid fuel use is a leading risk factor for global disease and remains a major public health problem, especially in low- and mid-income countries. This is a particularly serious problem in China, where many people in rural areas still use coal for household heating and cooking. This review focuses on several decades of research carried out in Xuanwei County, Yunnan Province, where household coal use is a major source of household air pollution and where studies have linked household air pollution exposure to high rates of lung cancer. We conducted a series of case-control and cohort studies in Xuanwei to characterize the lung cancer risk in this population and the factors associated with it. We found lung cancer risk to vary substantially between different coal types, with a higher risk associated with smoky (i.e., bituminous) coal use compared to smokeless (i.e., anthracite) coal use. The installation of a chimney in homes resulted in a substantial reduction in lung cancer incidence and mortality. Overall, our research underscores the need among existing coal users to improve ventilation, use the least toxic fuel, and eventually move toward the use of cleaner fuels, such as gas and electricity. JF - Chinese journal of cancer AU - Seow, Wei Jie AU - Hu, Wei AU - Vermeulen, Roel AU - Hosgood Iii, H Dean AU - Downward, George S AU - Chapman, Robert S AU - He, Xingzhou AU - Bassig, Bryan A AU - Kim, Christopher AU - Wen, Cuiju AU - Rothman, Nathaniel AU - Lan, Qing AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA. weijie.seow2@nih.gov. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 471 EP - 475 VL - 33 IS - 10 SN - 1000-467X, 1000-467X KW - Coal KW - 0 KW - Fossil Fuels KW - Smoke KW - Index Medicus KW - Smoking KW - Heating KW - Risk Factors KW - Humans KW - Cooking KW - Cohort Studies KW - Incidence KW - China KW - Smoke -- adverse effects KW - Air Pollution, Indoor -- adverse effects KW - Lung Neoplasms -- etiology KW - Coal -- adverse effects KW - Coal -- classification KW - Lung Neoplasms -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566822185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chinese+journal+of+cancer&rft.atitle=Household+air+pollution+and+lung+cancer+in+China%3A+a+review+of+studies+in+Xuanwei.&rft.au=Seow%2C+Wei+Jie%3BHu%2C+Wei%3BVermeulen%2C+Roel%3BHosgood+Iii%2C+H+Dean%3BDownward%2C+George+S%3BChapman%2C+Robert+S%3BHe%2C+Xingzhou%3BBassig%2C+Bryan+A%3BKim%2C+Christopher%3BWen%2C+Cuiju%3BRothman%2C+Nathaniel%3BLan%2C+Qing&rft.aulast=Seow&rft.aufirst=Wei&rft.date=2014-10-01&rft.volume=33&rft.issue=10&rft.spage=471&rft.isbn=&rft.btitle=&rft.title=Chinese+journal+of+cancer&rft.issn=1000467X&rft_id=info:doi/10.5732%2Fcjc.014.10132 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-01 N1 - Date created - 2014-09-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):605-8 [10868696] Chin J Cancer. 2014 Apr;33(4):176-88 [24636232] Int J Hyg Environ Health. 2003 Aug;206(4-5):279-89 [12971683] Science. 1987 Jan 9;235(4785):217-20 [3798109] Environ Health Perspect. 1991 Aug;94:9-13 [1954946] Carcinogenesis. 1995 Dec;16(12):3031-6 [8603481] BMJ. 2005 Nov 5;331(7524):1050 [16234255] Environ Health Perspect. 2007 Jun;115(6):848-55 [17589590] Paediatr Respir Rev. 2007 Dec;8(4):281-6 [18005895] Mutat Res. 2007 Nov-Dec;636(1-3):134-43 [17428724] Int J Cancer. 2008 Nov 1;123(9):2164-9 [18712724] Br J Cancer. 2008 Dec 2;99(11):1934-9 [19034286] Environ Health Perspect. 2009 Feb;117(2):261-6 [19270797] PLoS Genet. 2010 Aug;6(8). pii: e1001051. doi: 10.1371/journal.pgen.1001051 [20700438] Br J Cancer. 2010 Aug 24;103(5):727-9 [20648014] Int J Epidemiol. 2011 Jun;40(3):719-28 [21278196] J Natl Cancer Inst. 2012 Jun 6;104(11):855-68 [22393209] Ann Oncol. 2012 Oct;23(10):2755-62 [22492700] Nat Genet. 2012 Dec;44(12):1330-5 [23143601] Lancet. 2012 Dec 15;380(9859):2224-60 [23245609] Environ Health Perspect. 2013 Jul;121(7):751-5 [23665813] Lancet. 2014 Mar 8;383(9920):845 [24607085] Lung Cancer. 2014 Apr;84(1):31-5 [24506909] Annu Rev Public Health. 2014;35:185-206 [24641558] J Natl Cancer Inst. 2002 Jun 5;94(11):826-35 [12048270] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.5732/cjc.014.10132 ER - TY - JOUR T1 - Assay of lapatinib in murine models of cigarette smoke carcinogenesis. AN - 1566821174; 25053627 AB - Lapatinib, a dual tyrosine kinase inhibitor targeting the epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER-2), is prescribed for the treatment of patients with metastatic breast cancer overexpressing HER-2. Involvement of this drug in pulmonary carcinogenesis has been poorly investigated. We used murine models suitable to evaluate cigarette smoke-related molecular and histopathological alterations. A total of 481 Swiss H mice were used. The mice were exposed to mainstream cigarette smoke (MCS) during the first four months of life. After 10 weeks, MCS caused an elevation of bulky DNA adducts, oxidative DNA damage and an extensive downregulation of microRNAs in lung. After four months, an increase in micronucleus frequency was observed in peripheral blood erythrocytes. After 7.5 months, histopathological alterations were detected in the lung, also including benign tumors and malignant tumors, and in the urinary tract. A subchronic toxicity study assessed the non-toxic doses of lapatinib, administered daily with the diet after weaning. After 10 weeks, lapatinib significantly attenuated the MCS-related nucleotide changes and upregulated several low-intensity microRNAs in lung. The drug poorly affected the MCS systemic genotoxicity and had modest protective effects on MCS-induced preneoplastic lesions in lung and kidney, when administered under conditions that temporarily mimicked interventions either in current smokers or ex-smokers. On the other hand, it caused some toxicity to the liver. Thus, on the whole, lapatinib appears to have a low impact in the smoke-related lung carcinogenesis models used, especially in terms of tumorigenic response. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Balansky, Roumen AU - Izzotti, Alberto AU - D'Agostini, Francesco AU - Longobardi, Mariagrazia AU - Micale, Rosanna T AU - La Maestra, Sebastiano AU - Camoirano, Anna AU - Ganchev, Gancho AU - Iltcheva, Marietta AU - Steele, Vernon E AU - De Flora, Silvio AD - Department of Health Sciences, University of Genoa, Via A. Pastore 1, 16132 Genoa, Italy, National Center of Oncology, Sofia-1756, Bulgaria. ; Department of Health Sciences, University of Genoa, Via A. Pastore 1, 16132 Genoa, Italy, IRCCS AOU San Martino - IST, 16132 Genoa, Italy and. ; Department of Health Sciences, University of Genoa, Via A. Pastore 1, 16132 Genoa, Italy. ; National Center of Oncology, Sofia-1756, Bulgaria. ; Division of Cancer Prevention, National Cancer Institute, Rockville, MD 20892, USA. ; Department of Health Sciences, University of Genoa, Via A. Pastore 1, 16132 Genoa, Italy, sdf@unige.it. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 2300 EP - 2307 VL - 35 IS - 10 KW - Antineoplastic Agents KW - 0 KW - DNA Adducts KW - MicroRNAs KW - Protein Kinase Inhibitors KW - Quinazolines KW - Tobacco Smoke Pollution KW - lapatinib KW - 0VUA21238F KW - Index Medicus KW - Erythrocytes -- drug effects KW - Animals KW - Toxicity Tests, Subchronic KW - Protein Kinase Inhibitors -- pharmacology KW - Body Weight -- drug effects KW - Disease Models, Animal KW - Mice KW - Gene Expression Regulation -- drug effects KW - DNA Damage -- drug effects KW - Lung Neoplasms -- drug therapy KW - Tobacco Smoke Pollution -- adverse effects KW - Lung -- drug effects KW - Lung Neoplasms -- mortality KW - Lung Neoplasms -- chemically induced KW - Lung -- pathology KW - Lung -- metabolism KW - Antineoplastic Agents -- pharmacology KW - Quinazolines -- pharmacology KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566821174?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Assay+of+lapatinib+in+murine+models+of+cigarette+smoke+carcinogenesis.&rft.au=Balansky%2C+Roumen%3BIzzotti%2C+Alberto%3BD%27Agostini%2C+Francesco%3BLongobardi%2C+Mariagrazia%3BMicale%2C+Rosanna+T%3BLa+Maestra%2C+Sebastiano%3BCamoirano%2C+Anna%3BGanchev%2C+Gancho%3BIltcheva%2C+Marietta%3BSteele%2C+Vernon+E%3BDe+Flora%2C+Silvio&rft.aulast=Balansky&rft.aufirst=Roumen&rft.date=2014-10-01&rft.volume=35&rft.issue=10&rft.spage=2300&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu154 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2014-09-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mutat Res. 2011 Dec 1;717(1-2):9-16 [21185844] Gastroenterology. 2011 Dec;141(6):2076-2087.e6 [21925125] Int J Cancer. 2012 Mar 1;130(5):1001-10 [21484788] Eur J Cancer. 2012 Jan;48(2):279-85 [22100178] Curr Cancer Drug Targets. 2012 Feb;12(2):164-9 [22165969] Curr Top Med Chem. 2012;12(8):920-6 [22352917] Mol Cancer Ther. 2012 Apr;11(4):795-804 [22302097] Int Immunopharmacol. 2012 May;13(1):73-81 [22465384] Breast Cancer Res Treat. 2012 Jun;133(2):703-11 [22370628] Ann N Y Acad Sci. 2012 Jul;1259:26-32 [22758633] Int J Cancer. 2012 Nov 1;131(9):1991-7 [22328465] Expert Opin Investig Drugs. 2012 Nov;21(11):1727-32 [22876762] Int J Cancer. 2012 Dec 15;131(12):2763-73 [22945459] Carcinogenesis. 2013 Jan;34(1):183-9 [23042096] Drug Saf. 2013 Jul;36(7):491-503 [23620168] Carcinogenesis. 2013 Oct;34(10):2322-9 [23708261] Expert Rev Anticancer Ther. 2013 Oct;13(10):1219-28 [24134423] Pharmacol Res. 2014 Jan;79:34-74 [24269963] J Clin Pathol. 2014 Mar;67(3):198-203 [24098024] PLoS One. 2014;9(2):e89105 [24551227] Genes Dev. 2014 Mar 1;28(5):438-50 [24532687] Pharm Res. 2014 Mar;31(3):780-94 [24078287] Biochem Pharmacol. 2000 Jan 1;59(1):13-23 [10605930] Cancer Res. 2001 Mar 15;61(6):2472-9 [11289117] Chest. 2004 May;125(5 Suppl):154S-5S [15136480] J Natl Cancer Inst. 1998 Aug 19;90(16):1198-205 [9719080] Thorax. 2004 Dec;59(12):1032-40 [15563701] Cancer Lett. 2006 Sep 28;241(2):197-202 [16337739] Carcinogenesis. 2007 Oct;28(10):2236-43 [17522065] Am J Pathol. 2008 Jan;172(1):59-67 [18079438] J Cell Biol. 2008 Aug 11;182(3):509-17 [18695042] Clin Ther. 2008 Aug;30(8):1426-47 [18803986] J Natl Cancer Inst. 2009 Jan 21;101(2):107-13 [19141783] Oncol Rep. 2009 Sep;22(3):469-74 [19639190] Carcinogenesis. 2009 Aug;30(8):1398-401 [19458036] FASEB J. 2009 Sep;23(9):3243-50 [19465468] Int J Cancer. 2010 Mar 1;126(5):1047-54 [19816928] Cancer Prev Res (Phila). 2010 Jan;3(1):62-72 [20051373] Cancer Cell. 2010 Jan 19;17(1):89-97 [20129250] Clin Cancer Res. 2010 Mar 15;16(6):1938-49 [20215545] Carcinogenesis. 2010 May;31(5):894-901 [20145010] BMC Cancer. 2010;10:188 [20459769] J Clin Oncol. 2010 Sep 20;28(27):4221-7 [20713864] Mol Pharmacol. 2010 Oct;78(4):693-703 [20624855] J Clin Oncol. 2011 Feb 20;29(6):667-73 [21245432] Cancer Prev Res (Phila). 2011 Aug;4(8):1181-9 [21685235] Cancer Prev Res (Phila). 2011 Aug;4(8):1190-7 [21791570] Cancer Prev Res (Phila). 2011 Aug;4(8):1149-57 [21816844] J Clin Oncol. 2011 Sep 10;29(26):3529-34 [21825264] Mutat Res. 2011 Dec 1;717(1-2):17-24 [20974155] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu154 ER - TY - JOUR T1 - An improved recombinant Fab-immunotoxin targeting CD22 expressing malignancies. AN - 1566820524; 25127689 AB - Moxetumomab pasudotox (HA22) is a recombinant immunotoxin, now in clinical trials, that combines an anti-CD22-Fv with a 38-kDa fragment of Pseudomonas exotoxin A. To produce a less immunogenic molecule without reducing the half-life in circulation, we constructed LMB11 combining an anti-CD22 Fab with a less immunogenic version of PE38. We found that LMB11 retains full activity toward CD22-expressing cells. In mice, the half-life of LMB11 is 29 min and the antitumor activity of LMB11 is better than that of HA22. Because it can be safely given at much higher doses, LMB11 produced complete tumor remissions in 7/7 mice. Published by Elsevier Ltd. JF - Leukemia research AU - Bera, Tapan K AU - Onda, Masanori AU - Kreitman, Robert J AU - Pastan, Ira AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 5106, Bethesda, MD 20892-4264, USA. ; Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Room 5106, Bethesda, MD 20892-4264, USA. Electronic address: pastani@mail.nih.gov. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 1224 EP - 1229 VL - 38 IS - 10 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunoglobulin Fab Fragments KW - Immunotoxins KW - Sialic Acid Binding Ig-like Lectin 2 KW - immunotoxin HA22 KW - Index Medicus KW - B-cell malignancies KW - Less immunogenic PE38 KW - Moxetumomab pasudotox KW - Animals KW - Half-Life KW - Humans KW - Xenograft Model Antitumor Assays KW - Mice KW - Mice, Inbred BALB C KW - Female KW - Leukemia KW - Sialic Acid Binding Ig-like Lectin 2 -- immunology KW - Immunotoxins -- pharmacology KW - Immunoglobulin Fab Fragments -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566820524?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=An+improved+recombinant+Fab-immunotoxin+targeting+CD22+expressing+malignancies.&rft.au=Bera%2C+Tapan+K%3BOnda%2C+Masanori%3BKreitman%2C+Robert+J%3BPastan%2C+Ira&rft.aulast=Bera&rft.aufirst=Tapan&rft.date=2014-10-01&rft.volume=38&rft.issue=10&rft.spage=1224&rft.isbn=&rft.btitle=&rft.title=Leukemia+research&rft.issn=1873-5835&rft_id=info:doi/10.1016%2Fj.leukres.2014.06.014 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-18 N1 - Date created - 2014-09-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Methods Mol Biol. 2004;248:503-18 [14970517] Br Med Bull. 2012;104:41-59 [23118261] Bioconjug Chem. 1998 Nov-Dec;9(6):736-43 [9815167] Int J Cancer. 1999 Mar 31;81(1):148-55 [10077166] Clin Cancer Res. 2005 Feb 15;11(4):1545-50 [15746059] Annu Rev Med. 2007;58:221-37 [17059365] Blood. 2009 Apr 16;113(16):3792-800 [18988862] J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673] Clin Cancer Res. 2010 Mar 15;16(6):1894-903 [20215554] J Immunother. 2010 Apr;33(3):297-304 [20445350] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054] Cancer Res. 2011 Oct 15;71(20):6300-9 [21998010] J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053] Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11782-7 [22753489] Cancer Immun. 2012;12:14 [22896759] Nature. 1989 Jun 1;339(6223):394-7 [2498664] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.leukres.2014.06.014 ER - TY - JOUR T1 - Activation of invariant natural killer T cells impedes liver regeneration by way of both IFN-γ- and IL-4-dependent mechanisms. AN - 1566107791; 24623351 AB - Invariant natural killer T (iNKT) cells are a major subset of lymphocytes found in the liver. These cells mediate various functions, including hepatic injury, fibrogenesis, and carcinogenesis. However, the function of iNKT cells in liver regeneration remains unclear. In the present study, partial hepatectomy (PHx) was used to study liver regeneration. α-Galactosylceramide (α-GalCer), a specific ligand for iNKT cells, was used to induce iNKT cell activation. After PHx, two strains of iNKT cell-deficient mice, CD1d(-/-) and Jα281(-/-) mice, showed normal liver regeneration. Injection of α-GalCer before or after PHx, which rapidly stimulated interferon-gamma (IFN-γ) and interleukin (IL)-4 production by iNKT cells, markedly inhibited liver regeneration. In vitro treatment with IFN-γ inhibited hepatocyte proliferation. In agreement with this in vitro finding, genetic disruption of IFN-γ or its downstream signaling molecule signal transducer and activator of transcription (STAT)1 significantly abolished the α-GalCer-mediated inhibition of liver regeneration. In vitro exposure to IL-4 did not affect hepatocyte proliferation, but surprisingly, genetic ablation of IL-4 or its downstream signaling molecule STAT6 partially eliminated the inhibitory effect of α-GalCer on liver regeneration. Further studies revealed that IL-4 contributed to α-GalCer-induced iNKT cell expansion and IFN-γ production, thereby inhibiting liver regeneration. iNKT cells play a minor role in controlling liver regeneration after PHx under healthy conditions. Activation of iNKT cells by α-GalCer induces the production of IFN-γ, which directly inhibits liver regeneration, and IL-4, which indirectly attenuates liver regeneration by stimulating iNKT cell expansion and IFN-γ production. © 2014 by the American Association for the Study of Liver Diseases. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA. JF - Hepatology (Baltimore, Md.) AU - Yin, Shi AU - Wang, Hua AU - Bertola, Adeline AU - Feng, Dechun AU - Xu, Ming-Jiang AU - Wang, Yan AU - Gao, Bin AD - Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA; Department of Geriatrics, Affiliated Provincial Hospital of Anhui Medical University, Hefei, China. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 1356 EP - 1366 VL - 60 IS - 4 KW - Antigens, CD1d KW - 0 KW - CD1d antigen, mouse KW - Galactosylceramides KW - STAT6 Transcription Factor KW - Stat6 protein, mouse KW - alpha-galactosylceramide KW - Interleukin-4 KW - 207137-56-2 KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Models, Animal KW - Cell Proliferation -- drug effects KW - Animals KW - Galactosylceramides -- pharmacology KW - Antigens, CD1d -- genetics KW - Hepatocytes -- drug effects KW - STAT6 Transcription Factor -- physiology KW - Mice KW - Hepatocytes -- pathology KW - Mice, Knockout KW - Antigens, CD1d -- physiology KW - STAT6 Transcription Factor -- genetics KW - STAT6 Transcription Factor -- deficiency KW - Hepatectomy KW - In Vitro Techniques KW - Mice, Inbred C57BL KW - Male KW - Interleukin-4 -- genetics KW - Liver Regeneration -- drug effects KW - Interferon-gamma -- genetics KW - Liver -- surgery KW - Liver -- drug effects KW - Interferon-gamma -- deficiency KW - Interleukin-4 -- deficiency KW - Natural Killer T-Cells -- physiology KW - Interferon-gamma -- physiology KW - Natural Killer T-Cells -- pathology KW - Liver Regeneration -- physiology KW - Interleukin-4 -- physiology KW - Liver -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566107791?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Activation+of+invariant+natural+killer+T+cells+impedes+liver+regeneration+by+way+of+both+IFN-%CE%B3-+and+IL-4-dependent+mechanisms.&rft.au=Yin%2C+Shi%3BWang%2C+Hua%3BBertola%2C+Adeline%3BFeng%2C+Dechun%3BXu%2C+Ming-Jiang%3BWang%2C+Yan%3BGao%2C+Bin&rft.aulast=Yin&rft.aufirst=Shi&rft.date=2014-10-01&rft.volume=60&rft.issue=4&rft.spage=1356&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.27128 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2014-09-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hepatology. 2003 Nov;38(5):1116-24 [14578850] Nat Rev Immunol. 2002 Aug;2(8):557-68 [12154375] J Hepatol. 2006 Sep;45(3):347-9 [16854494] Hepatology. 2006 Oct;44(4):955-66 [17006930] Gastroenterology. 2006 Nov;131(5):1573-83 [17064698] Hepatology. 2007 Jan;45(1):22-30 [17187419] Hepatology. 2007 Jun;45(6):1400-12 [17523147] Nat Protoc. 2008;3(7):1167-70 [18600221] Curr Mol Med. 2008 Aug;8(5):384-92 [18691065] J Leukoc Biol. 2009 Sep;86(3):513-28 [19542050] Am J Pathol. 2010 Jan;176(1):2-13 [20019184] Hepatology. 2010 Apr;51(4):1354-62 [20041412] Cytokine Growth Factor Rev. 2011 Feb;22(1):35-43 [21334249] Expert Opin Ther Targets. 2011 Aug;15(8):973-88 [21564001] Clin Immunol. 2011 Aug;140(2):130-41 [21169066] Hepatology. 2011 Oct;54(4):1445-53 [21626524] Autoimmun Rev. 2011 Oct;10(12):793-800 [21740985] J Immunol. 2012 Jan 15;188(2):641-8 [22184721] J Hepatol. 2012 Aug;57(2):430-41 [22504331] J Hepatol. 2012 Sep;57(3):692-4 [22613006] Am J Physiol Gastrointest Liver Physiol. 2013 Feb 1;304(3):G293-9 [23086918] Hepatology. 2013 Apr;57(4):1575-84 [23150232] Hepatology. 2013 May;57(5):1969-79 [22898900] Hepatology. 2013 May;57(5):1688-90 [23390033] Compr Physiol. 2013 Jan;3(1):485-513 [23720294] Proc Natl Acad Sci U S A. 2013 Jun 11;110(24):9914-9 [23716700] Hepatology. 2013 Oct;58(4):1474-85 [23686838] Gastroenterology. 2004 Nov;127(5):1525-39 [15521020] Hepatology. 2000 Apr;31(4):907-15 [10733547] J Exp Med. 2000 Oct 2;192(7):921-30 [11015434] Comment In: Hepatology. 2014 Oct;60(4):1133-5 [24824434] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/hep.27128 ER - TY - JOUR T1 - The effect of the UGT1A1*28 allele on survival after irinotecan-based chemotherapy: a collaborative meta-analysis. AN - 1565502104; 24709690 AB - To date, studies of irinotecan pharmacogenetics have mostly focused on the effect of the UGT1A1*28 allele on irinotecan-related toxicity. However, the clinical utility of routine UGT1A1*28 genotyping to pre-emptively adjust irinotecan dosage is dependent upon whether UGT1A1*28 also affects patient survival following irinotecan therapy. Previous observational studies evaluating the influence of UGT1A1*28 on survival have shown contradictory results. A systematic review and meta-analysis of both published and unpublished data were performed to summarize the available evidence of the relationship between the UGT1A1*28 allele and patient survival related to irinotecan therapy. Overall and progression-free survival meta-analysis data were available for 1524 patients and 1494 patients, respectively. The difference in the survival between patients of different UGT1A1*28 genotypes (homozygous, heterozygous or wild-type) who had received irinotecan was not found to be statistically significant. There was also no evidence of irinotecan dose, regimen or line of therapy having an impact on this association. JF - The pharmacogenomics journal AU - Dias, M M AU - Pignon, J-P AU - Karapetis, C S AU - Boige, V AU - Glimelius, B AU - Kweekel, D M AU - Lara, P N AU - Laurent-Puig, P AU - Martinez-Balibrea, E AU - Páez, D AU - Punt, C J A AU - Redman, M W AU - Toffoli, G AU - Wadelius, M AU - McKinnon, R A AU - Sorich, M J AD - School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia. ; Meta-analysis Unit, Department of Biostatistics and Epidemiology, Gustave-Roussy, Villejuif, France. ; Flinders Centre for Innovation in Cancer, School of Medicine, Flinders University, Adelaide, South Australia, Australia. ; Department of Oncologic Medicine, Gustave-Roussy, Villejuif, France. ; Section of Oncology, Department of Radiology, Oncology and Radiation Science, Uppsala University, Uppsala, Sweden. ; Department of Clinical Pharmacy and Toxicology, Leiden University Medical Centre, Leiden, The Netherlands. ; Davis Comprehensive Cancer Center, University of California, Sacramento, CA, USA. ; Unité Mixte de Recherche S775, Institut National de la Santé et de la Recherche Médicale, Université Paris Descartes, Paris, France. ; Laboratori Biologia Molecular del Càncer, Institut Català d'Oncologia, Fundació Institut IGTP, Badalona, Spain. ; Medical Oncology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain. ; Department of Medical Oncology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. ; Lung and Cancer Control Committees, Fred Hutchinson Cancer Research Center, Statistical Center: SWOG, Seattle, WA, USA. ; Experimental and Clinical Pharmacology Unit, CRO-National Cancer Institute, Aviano, Italy. ; Department of Medical Sciences, Clinical Pharmacology, Uppsala University, Uppsala, Sweden. ; 1] School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, South Australia, Australia [2] Department of Clinical Pharmacology, School of Medicine, Flinders University, Adelaide, South Australia, Australia. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 424 EP - 431 VL - 14 IS - 5 KW - irinotecan KW - 0H43101T0J KW - UGT1A1 enzyme KW - EC 2.4.1.- KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Genotype KW - Humans KW - Disease Progression KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Survival Analysis KW - Neoplasms -- drug therapy KW - Glucuronosyltransferase -- genetics KW - Alleles KW - Camptothecin -- analogs & derivatives KW - Camptothecin -- therapeutic use KW - Neoplasms -- genetics KW - Camptothecin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1565502104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmacogenomics+journal&rft.atitle=The+effect+of+the+UGT1A1*28+allele+on+survival+after+irinotecan-based+chemotherapy%3A+a+collaborative+meta-analysis.&rft.au=Dias%2C+M+M%3BPignon%2C+J-P%3BKarapetis%2C+C+S%3BBoige%2C+V%3BGlimelius%2C+B%3BKweekel%2C+D+M%3BLara%2C+P+N%3BLaurent-Puig%2C+P%3BMartinez-Balibrea%2C+E%3BP%C3%A1ez%2C+D%3BPunt%2C+C+J+A%3BRedman%2C+M+W%3BToffoli%2C+G%3BWadelius%2C+M%3BMcKinnon%2C+R+A%3BSorich%2C+M+J&rft.aulast=Dias&rft.aufirst=M&rft.date=2014-10-01&rft.volume=14&rft.issue=5&rft.spage=424&rft.isbn=&rft.btitle=&rft.title=The+pharmacogenomics+journal&rft.issn=1473-1150&rft_id=info:doi/10.1038%2Ftpj.2014.16 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-12 N1 - Date created - 2014-09-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/tpj.2014.16 ER - TY - JOUR T1 - Effects of deep hypothermic circulatory arrest on the blood brain barrier in a cardiopulmonary bypass model--a pilot study. AN - 1565500341; 24931068 AB - Neurologic injury is common after cardiac surgery and disruption of the blood brain barrier (BBB) has been proposed as a contributing factor. We sought to study BBB characteristics in a rodent model of cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA). Adult rats were subjected to CPB/DHCA or to sham surgery. Analysis included Western blotting of relevant BBB proteins in addition to in vivo brain magnetic resonance imaging (MRI) with a clinically used low-molecular contrast agent. While quantitative analysis of BBB proteins revealed similar expression levels, MRI showed evidence of BBB disruption after CPB/DHCA compared to sham surgery. Combining molecular BBB analysis and MRI technology in a rodent model is a highly translatable approach to study adverse neurologic outcomes following CPB/DHCA. Copyright © 2014 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). All rights reserved. JF - Heart, lung & circulation AU - Bartels, Karsten AU - Ma, Qing AU - Venkatraman, Talaignair N AU - Campos, Christopher R AU - Smith, Lindsay AU - Cannon, Ronald E AU - Podgoreanu, Mihai V AU - Lascola, Christopher D AU - Miller, David S AU - Mathew, Joseph P AD - Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA. ; Department of Radiology, Duke University Medical Center, Durham, NC, USA. ; Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA. ; Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA. Electronic address: joseph.mathew@duke.edu. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 981 EP - 984 VL - 23 IS - 10 KW - Claudin-5 KW - 0 KW - Contrast Media KW - Occludin KW - Organometallic Compounds KW - P-Glycoprotein KW - gadobutrol KW - 1BJ477IO2L KW - Index Medicus KW - Blood brain barrier KW - Cardiac surgery KW - Neurologic injury KW - Deep hypothermic circulatory arrest KW - Cardiopulmonary bypass KW - Rats KW - Models, Animal KW - Animals KW - Rats, Sprague-Dawley KW - P-Glycoprotein -- metabolism KW - Claudin-5 -- metabolism KW - Occludin -- metabolism KW - Pilot Projects KW - Male KW - Magnetic Resonance Imaging KW - Circulatory Arrest, Deep Hypothermia Induced -- adverse effects KW - Cardiopulmonary Bypass -- adverse effects KW - Blood-Brain Barrier -- metabolism KW - Blood-Brain Barrier -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1565500341?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Heart%2C+lung+%26+circulation&rft.atitle=Effects+of+deep+hypothermic+circulatory+arrest+on+the+blood+brain+barrier+in+a+cardiopulmonary+bypass+model--a+pilot+study.&rft.au=Bartels%2C+Karsten%3BMa%2C+Qing%3BVenkatraman%2C+Talaignair+N%3BCampos%2C+Christopher+R%3BSmith%2C+Lindsay%3BCannon%2C+Ronald+E%3BPodgoreanu%2C+Mihai+V%3BLascola%2C+Christopher+D%3BMiller%2C+David+S%3BMathew%2C+Joseph+P&rft.aulast=Bartels&rft.aufirst=Karsten&rft.date=2014-10-01&rft.volume=23&rft.issue=10&rft.spage=981&rft.isbn=&rft.btitle=&rft.title=Heart%2C+lung+%26+circulation&rft.issn=1444-2892&rft_id=info:doi/10.1016%2Fj.hlc.2014.04.131 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-24 N1 - Date created - 2014-09-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Ann Thorac Surg. 2004 Oct;78(4):1418-25 [15464507] Eur J Cardiothorac Surg. 1989;3(6):539-43 [2635941] Mol Pharmacol. 2006 Feb;69(2):462-70 [16278373] J Thorac Cardiovasc Surg. 2006 Apr;131(4):805-12 [16580438] Curr Opin Anaesthesiol. 2013 Feb;26(1):91-7 [23235523] Pharmacol Rev. 2008 Jun;60(2):196-209 [18560012] Neurobiol Dis. 2010 Jan;37(1):13-25 [19664713] Trends Pharmacol Sci. 2010 Jun;31(6):246-54 [20417575] Ann Thorac Surg. 2010 Dec;90(6):2001-8 [21095352] Stroke. 2008 May;39(5):1427-33 [18323490] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.hlc.2014.04.131 ER - TY - JOUR T1 - Role of alpha-1 antitrypsin in human health and disease. AN - 1564602676; 24661570 AB - Alpha-1 antitrypsin (AAT) deficiency is an under-recognized hereditary disorder associated with the premature onset of chronic obstructive pulmonary disease, liver cirrhosis in children and adults, and less frequently, relapsing panniculitis, systemic vasculitis and other inflammatory, autoimmune and neoplastic diseases. Severe AAT deficiency mainly affects Caucasian individuals and has its highest prevalence (1 : 2000-1 : 5000 individuals) in Northern, Western and Central Europe. In the USA and Canada, the prevalence is 1: 5000-10 000. Prevalence is five times lower in Latin American countries and is rare or nonexistent in African and Asian individuals. The key to successful diagnosis is by measuring serum AAT, followed by the determination of the phenotype or genotype if low concentrations are found. Case detection allows implementation of genetic counselling and, in selected cases, the application of augmentation therapy. Over the past decade, it has been demonstrated that AAT is a broad-spectrum anti-inflammatory, immunomodulatory, anti-infective and tissue-repair molecule. These new capacities are promoting an increasing number of clinical studies, new pharmacological formulations, new patent applications and the search for alternative sources of AAT (including transgenic and recombinant AAT) to meet the expected demand for treating a large number of diseases, inside and outside the context of AAT deficiency. © 2014 The Association for the Publication of the Journal of Internal Medicine. JF - Journal of internal medicine AU - de Serres, F AU - Blanco, I AD - Center for the Evaluation of Risks to Human Reproduction, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 311 EP - 335 VL - 276 IS - 4 KW - alpha 1-Antitrypsin KW - 0 KW - Index Medicus KW - hereditary disorder KW - alpha-1 antitrypsin KW - AAT deficiency KW - therapy KW - Genotype KW - Animals KW - Injections, Intravenous KW - Humans KW - Genetic Therapy KW - Prevalence KW - alpha 1-Antitrypsin Deficiency -- drug therapy KW - alpha 1-Antitrypsin Deficiency -- complications KW - alpha 1-Antitrypsin -- blood KW - alpha 1-Antitrypsin Deficiency -- diagnosis KW - alpha 1-Antitrypsin -- therapeutic use KW - alpha 1-Antitrypsin -- physiology KW - alpha 1-Antitrypsin Deficiency -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1564602676?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+internal+medicine&rft.atitle=Role+of+alpha-1+antitrypsin+in+human+health+and+disease.&rft.au=de+Serres%2C+F%3BBlanco%2C+I&rft.aulast=de+Serres&rft.aufirst=F&rft.date=2014-10-01&rft.volume=276&rft.issue=4&rft.spage=311&rft.isbn=&rft.btitle=&rft.title=Journal+of+internal+medicine&rft.issn=1365-2796&rft_id=info:doi/10.1111%2Fjoim.12239 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-19 N1 - Date created - 2014-09-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/joim.12239 ER - TY - JOUR T1 - Crucial role of macrophage selenoproteins in experimental colitis. AN - 1563993583; 25187657 AB - Inflammation is a hallmark of inflammatory bowel disease (IBD) that involves macrophages. Given the inverse link between selenium (Se) status and IBD-induced inflammation, our objective was to demonstrate that selenoproteins in macrophages were essential to suppress proinflammatory mediators, in part, by the modulation of arachidonic acid metabolism. Acute colitis was induced using 4% dextran sodium sulfate in wild-type mice maintained on Se-deficient (<0.01 ppm Se), Se-adequate (0.08 ppm; sodium selenite), and two supraphysiological levels in the form of Se-supplemented (0.4 ppm; sodium selenite) and high Se (1.0 ppm; sodium selenite) diets. Selenocysteinyl transfer RNA knockout mice (Trsp(fl/fl)LysM(Cre)) were used to examine the role of selenoproteins in macrophages on disease progression and severity using histopathological evaluation, expression of proinflammatory and anti-inflammatory genes, and modulation of PG metabolites in urine and plasma. Whereas Se-deficient and Se-adequate mice showed increased colitis and exhibited poor survival, Se supplementation at 0.4 and 1.0 ppm increased survival of mice and decreased colitis-associated inflammation with an upregulation of expression of proinflammatory and anti-inflammatory genes. Metabolomic profiling of urine suggested increased oxidation of PGE2 at supraphysiological levels of Se that also correlated well with Se-dependent upregulation of 15-hydroxy-PG dehydrogenase (15-PGDH) in macrophages. Pharmacological inhibition of 15-PGDH, lack of selenoprotein expression in macrophages, and depletion of infiltrating macrophages indicated that macrophage-specific selenoproteins and upregulation of 15-PGDH expression were key for Se-dependent anti-inflammatory and proresolving effects. Selenoproteins in macrophages protect mice from dextran sodium sulfate-colitis by enhancing 15-PGDH-dependent oxidation of PGE2 to alleviate inflammation, suggesting a therapeutic role for Se in IBD. Copyright © 2014 by The American Association of Immunologists, Inc. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kaushal, Naveen AU - Kudva, Avinash K AU - Patterson, Andrew D AU - Chiaro, Christopher AU - Kennett, Mary J AU - Desai, Dhimant AU - Amin, Shantu AU - Carlson, Bradley A AU - Cantorna, Margherita T AU - Prabhu, K Sandeep AD - Center for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802; ; Department of Pharmacology, Penn State College of Medicine, Hershey, PA 17033; and. ; Molecular Biology of Selenium Section, Mouse Cancer Genetics Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. ; Center for Molecular Immunology and Infectious Disease and Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, PA 16802; ksprabhu@psu.edu. Y1 - 2014/10/01/ PY - 2014 DA - 2014 Oct 01 SP - 3683 EP - 3692 VL - 193 IS - 7 KW - RNA, Transfer, Amino Acyl KW - 0 KW - Selenoproteins KW - selenocysteinyl-tRNA KW - Dextran Sulfate KW - 9042-14-2 KW - Hydroxyprostaglandin Dehydrogenases KW - EC 1.1.1.- KW - 15-hydroxyprostaglandin dehydrogenase KW - EC 1.1.1.141 KW - Selenium KW - H6241UJ22B KW - Dinoprostone KW - K7Q1JQR04M KW - Abridged Index Medicus KW - Index Medicus KW - Dinoprostone -- immunology KW - Animals KW - Selenium -- pharmacology KW - RNA, Transfer, Amino Acyl -- genetics KW - Inflammation -- genetics KW - Mice KW - Dextran Sulfate -- toxicity KW - Mice, Knockout KW - Hydroxyprostaglandin Dehydrogenases -- genetics KW - Hydroxyprostaglandin Dehydrogenases -- immunology KW - RNA, Transfer, Amino Acyl -- immunology KW - Dietary Supplements KW - Inflammation -- immunology KW - Dinoprostone -- genetics KW - Cell Line KW - Macrophages -- pathology KW - Macrophages -- immunology KW - Colitis -- immunology KW - Selenoproteins -- genetics KW - Selenoproteins -- immunology KW - Colitis -- pathology KW - Colitis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1563993583?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Crucial+role+of+macrophage+selenoproteins+in+experimental+colitis.&rft.au=Kaushal%2C+Naveen%3BKudva%2C+Avinash+K%3BPatterson%2C+Andrew+D%3BChiaro%2C+Christopher%3BKennett%2C+Mary+J%3BDesai%2C+Dhimant%3BAmin%2C+Shantu%3BCarlson%2C+Bradley+A%3BCantorna%2C+Margherita+T%3BPrabhu%2C+K+Sandeep&rft.aulast=Kaushal&rft.aufirst=Naveen&rft.date=2014-10-01&rft.volume=193&rft.issue=7&rft.spage=3683&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.1400347 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-14 N1 - Date created - 2014-09-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Metastasis Rev. 2011 Dec;30(3-4):409-17 [22020925] J Leukoc Biol. 2011 Sep;90(3):483-92 [21685246] J Biol Chem. 2013 Jul 5;288(27):19484-502 [23687300] PLoS One. 2013;8(7):e67845 [23861820] Wiad Lek. 2013;66(1):3-9 [23905422] J Clin Invest. 2000 Feb;105(4):469-78 [10683376] Eur J Clin Nutr. 2000 Jun;54(6):514-21 [10878655] Am J Physiol Gastrointest Liver Physiol. 2000 Jul;279(1):G238-44 [10898767] Acta Gastroenterol Belg. 2001 Jan-Mar;64(1):1-5 [11322060] Nat Immunol. 2001 Jul;2(7):612-9 [11429545] Rocz Akad Med Bialymst. 2001;46:60-8 [11780581] Methods. 2001 Dec;25(4):402-8 [11846609] J Clin Invest. 2002 Apr;109(7):883-93 [11927615] Prostaglandins Other Lipid Mediat. 2002 Aug;68-69:483-93 [12432938] Scand J Gastroenterol. 2002 Dec;37(12):1428-36 [12523593] Mol Cell Biol. 2003 Mar;23(5):1477-88 [12588969] FEBS Lett. 1976 Sep 15;68(1):59-62 [964381] Adv Prostaglandin Thromboxane Res. 1976;1:163-9 [826140] Gastroenterology. 1978 Oct;75(4):638-40 [30669] J Invest Dermatol. 1982 Mar;78(3):206-9 [6276474] Biochem Pharmacol. 1983 Oct 1;32(19):2863-71 [6138042] Gut. 1984 Nov;25(11):1271-8 [6149981] Gut. 1987 Aug;28(8):1002-7 [3117625] Gastroenterology. 1990 Mar;98(3):694-702 [1688816] Annu Rev Med. 1992;43:125-33 [1580577] Gastroenterology. 1993 Jun;104(6):1832-47 [8500743] Scand J Gastroenterol. 1993 Jul;28(7):605-8 [8362213] PCR Methods Appl. 1995 Jun;4(6):357-62 [7580930] J Biol Chem. 2005 Feb 4;280(5):3217-23 [15542609] Nutrition. 2005 May;21(5):574-9 [15850963] Prostaglandins Other Lipid Mediat. 2005 Dec;78(1-4):160-8 [16303613] Am J Physiol Gastrointest Liver Physiol. 2006 Feb;290(2):G361-8 [16195422] Curr Pharm Des. 2006;12(8):943-54 [16533161] ScientificWorldJournal. 2006;6:577-88 [16752007] J Leukoc Biol. 2006 Oct;80(4):802-15 [16888083] Br J Pharmacol. 2006 Nov;149(6):611-23 [17016496] BMC Immunol. 2007;8:5 [17397543] J Immunol. 2007 Jun 15;178(12):8138-47 [17548652] Proc Natl Acad Sci U S A. 2007 Dec 26;104(52):20979-84 [18077391] Mol Nutr Food Res. 2008 Nov;52(11):1273-80 [18384097] BMC Immunol. 2009;10:57 [19863805] Inflamm Bowel Dis. 2010 Jan;16(1):87-95 [19572372] Nat Chem Biol. 2010 Jun;6(6):401-2 [20479749] PLoS Pathog. 2010 May;6(5):e1000902 [20485566] Proc Natl Acad Sci U S A. 2010 Jun 29;107(26):12023-7 [20547854] BMC Gastroenterol. 2010;10:82 [20637112] Gastroenterology. 2010 Dec;139(6):1912-7 [20950616] J Biol Chem. 2011 Aug 5;286(31):27471-82 [21669866] J Nutr. 2011 Sep;141(9):1754-61 [21775527] Nature. 2013 Apr 25;496(7446):445-55 [23619691] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4049/jimmunol.1400347 ER - TY - JOUR T1 - A microRNA 221- and 222-mediated feedback loop maintains constitutive activation of NFκB and STAT3 in colorectal cancer cells. AN - 1563991779; 24931456 AB - Constitutive activation of the transcription factors nuclear factor κB (NF-κB) and STAT3 is involved in the development and progression of human colorectal cancer (CRC). Little is known about how these factors become activated in cancer cells. We investigated whether microRNA miR-221 and miR-222 regulate NF-κB and signal transducer and activator of transcription 3 (STAT3) activation in human CRC cell lines. CRC cell lines (HCT116 and RKO) were transfected with miR-221 or miR-222 mimics or inhibitors. The activity levels of NF-κB and STAT3 were measured in dual luciferase reporter assays. We used immunoblot and real-time polymerase chain reaction analyses to measure protein and messenger RNA (mRNA) levels. Cells were analyzed by proliferation, viability, and flow cytometry analyses. Mice were given injections of azoxymethane, followed by dextran sodium sulfate, along with control lentivirus or those expressing mRNAs that bind miR-221 and miR-222 (miR-221/miR-222 sponge). The levels of miR-221 and miR-222 as well as RelA, STAT3, and PDLIM2 mRNAs were measured in 57 paired CRC and adjacent nontumor tissues from patients. In CRC cell lines, mimics of miR-221 and miR-222 activated NF-κB and STAT3, further increasing expression of miR-221 and miR-222. miR-221 and miR-222 bound directly to the coding region of RelA mRNA, increasing its stability. miR-221 and miR-222 also reduced the ubiquitination and degradation of the RelA and STAT3 proteins by binding to the 3' untranslated region of PDLIM2 mRNA (PDLIM2 is a nuclear ubiquitin E3 ligase for RelA and STAT3). Incubation of CRC cells with miR-221 and miR-222 inhibitors reduced their proliferation and colony formation compared with control cells. In mice with colitis, injection of lentiviruses expressing miR-221/miR-222 sponges led to formation of fewer tumors than injection of control lentiviruses. Human CRC tissues had higher levels of miR-221 and miR-222 than nontumor colon tissues; increases correlated with increased levels of RelA and STAT3 mRNAs. Levels of PDLIM2 mRNA were lower in CRC than nontumor tissues. In human CRC cells, miR-221 and miR-222 act in a positive feedback loop to increase expression levels of RelA and STAT3. Antagonism of miR-221 and miR-222 reduces growth of colon tumors in mice with colitis. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved. JF - Gastroenterology AU - Liu, Sanhong AU - Sun, Xiaohua AU - Wang, Mingliang AU - Hou, Yingyong AU - Zhan, Yu AU - Jiang, Yuhang AU - Liu, Zhanjie AU - Cao, Xinwei AU - Chen, Pengfei AU - Liu, Zhi AU - Chen, Xi AU - Tao, Yu AU - Xu, Chen AU - Mao, Jie AU - Cheng, Chunyan AU - Li, Cuifeng AU - Hu, Yiming AU - Wang, Lunshan AU - Chin, Y Eugene AU - Shi, Yufang AU - Siebenlist, Ulrich AU - Zhang, Xiaoren AD - Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai, China. ; General Surgery Department, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. ; Department of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China. ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. ; Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: xrzhang@sibs.ac.cn. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 847 EP - 859.e11 VL - 147 IS - 4 KW - 3' Untranslated Regions KW - 0 KW - LIM Domain Proteins KW - MIRN221 microRNA, human KW - MIRN222 microRNA, human KW - MicroRNAs KW - Microfilament Proteins KW - NF-kappa B KW - PDLIM2 protein, human KW - RELA protein, human KW - RNA, Messenger KW - STAT3 Transcription Factor KW - STAT3 protein, human KW - Transcription Factor RelA KW - Abridged Index Medicus KW - Index Medicus KW - Carcinogenesis KW - microRNA 221 KW - microRNA 222 KW - Colon Cancer KW - Animals KW - Microfilament Proteins -- metabolism KW - LIM Domain Proteins -- genetics KW - Open Reading Frames KW - Humans KW - Tumor Burden KW - Disease Models, Animal KW - Colitis -- pathology KW - Mice, Nude KW - Feedback, Physiological KW - Cell Proliferation KW - Mice, Inbred BALB C KW - Colitis -- metabolism KW - Cell Survival KW - Gene Expression Regulation, Neoplastic KW - Genes, Reporter KW - Xenograft Model Antitumor Assays KW - HT29 Cells KW - RNA Interference KW - Time Factors KW - Signal Transduction KW - Male KW - Transcription Factor RelA -- metabolism KW - LIM Domain Proteins -- metabolism KW - Microfilament Proteins -- genetics KW - Mice KW - HCT116 Cells KW - Colitis -- genetics KW - Binding Sites KW - RNA, Messenger -- metabolism KW - Transfection KW - Colitis -- therapy KW - Mice, Inbred C57BL KW - MicroRNAs -- metabolism KW - Colorectal Neoplasms -- pathology KW - Colorectal Neoplasms -- metabolism KW - STAT3 Transcription Factor -- genetics KW - STAT3 Transcription Factor -- metabolism KW - Colorectal Neoplasms -- genetics KW - Colorectal Neoplasms -- prevention & control KW - NF-kappa B -- genetics KW - NF-kappa B -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1563991779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=A+microRNA+221-+and+222-mediated+feedback+loop+maintains+constitutive+activation+of+NF%CE%BAB+and+STAT3+in+colorectal+cancer+cells.&rft.au=Liu%2C+Sanhong%3BSun%2C+Xiaohua%3BWang%2C+Mingliang%3BHou%2C+Yingyong%3BZhan%2C+Yu%3BJiang%2C+Yuhang%3BLiu%2C+Zhanjie%3BCao%2C+Xinwei%3BChen%2C+Pengfei%3BLiu%2C+Zhi%3BChen%2C+Xi%3BTao%2C+Yu%3BXu%2C+Chen%3BMao%2C+Jie%3BCheng%2C+Chunyan%3BLi%2C+Cuifeng%3BHu%2C+Yiming%3BWang%2C+Lunshan%3BChin%2C+Y+Eugene%3BShi%2C+Yufang%3BSiebenlist%2C+Ulrich%3BZhang%2C+Xiaoren&rft.aulast=Liu&rft.aufirst=Sanhong&rft.date=2014-10-01&rft.volume=147&rft.issue=4&rft.spage=847&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2014.06.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-25 N1 - Date created - 2014-09-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Carcinogenesis. 2006 Jun;27(6):1285-91 [16497702] Oncogene. 2004 Mar 18;23(12):2138-45 [14676835] J Biol Chem. 2007 Aug 10;282(32):23716-24 [17569667] EMBO J. 2007 Aug 8;26(15):3699-708 [17627278] Nat Methods. 2007 Sep;4(9):721-6 [17694064] Cancer Cell. 2008 Jan;13(1):7-9 [18167335] Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1608-13 [18227514] Int J Colorectal Dis. 2004 Jan;19(1):18-22 [12827408] Oncology. 2003;65(1):37-45 [12837981] Anticancer Res. 2004 Mar-Apr;24(2B):675-81 [15161011] Cell. 2004 Aug 6;118(3):285-96 [15294155] Cell. 2005 Jan 14;120(1):15-20 [15652477] Immunity. 2005 Jun;22(6):729-36 [15963787] Cell. 2008 Feb 8;132(3):344-62 [18267068] Cancer Res. 2008 Apr 15;68(8):2745-54 [18417445] Mol Cell. 2008 May 23;30(4):460-71 [18498749] Blood. 2008 Aug 1;112(3):551-9 [18505785] Oncogene. 2008 Aug 7;27(34):4712-23 [18408758] Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):14879-84 [18812516] Nature. 2008 Oct 23;455(7216):1124-8 [18806776] EMBO J. 2008 Dec 17;27(24):3300-10 [19020517] Cell. 2009 Jan 23;136(2):215-33 [19167326] Cancer Cell. 2009 Apr 7;15(4):283-93 [19345327] Gut. 2009 Oct;58(10):1375-81 [19201770] Cancer Cell. 2009 Oct 6;16(4):309-23 [19800576] Nat Rev Cancer. 2009 Nov;9(11):798-809 [19851315] Cancer Cell. 2009 Dec 8;16(6):498-509 [19962668] Cold Spring Harb Perspect Biol. 2009 Nov;1(5):a000141 [20066113] Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):264-9 [20018759] Mol Cell Biochem. 2010 Mar;336(1-2):25-37 [19823771] Cancer Res. 2010 Mar 1;70(5):1766-72 [20145149] Gastroenterology. 2010 Jun;138(6):2101-2114.e5 [20420949] Gut. 2010 Jul;59(7):1002-4; author reply 1004 [20581247] EMBO J. 2011 Jan 5;30(1):57-67 [21113131] FASEB J. 2011 Mar;25(3):863-74 [21084693] Sci Signal. 2011;4(202):ra85 [22155789] Cancer Cell. 2012 Jan 17;21(1):121-35 [22264793] FEBS Lett. 2012 Mar 23;586(6):722-8 [22321642] Mol Cell. 2012 Mar 30;45(6):777-89 [22364742] Proc Natl Acad Sci U S A. 2012 Aug 28;109(35):14007-12 [22893683] Cell. 2002 Apr;109 Suppl:S81-96 [11983155] Nat Immunol. 2007 Jun;8(6):584-91 [17468759] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1053/j.gastro.2014.06.006 ER - TY - JOUR T1 - Docetaxel, oxaliplatin, and capecitabine combination chemotherapy for metastatic gastric cancer. AN - 1563991337; 24318671 AB - The incorporation of docetaxel into the cisplatin and fluorouracil backbone has been demonstrated to be an active combination in metastatic gastric cancer. Nevertheless, this regimen is burdened by nonnegligible toxicity. We hypothesized that replacing cisplatin and fluorouracil with oxaliplatin and capecitabine should be an active and safe option for metastatic gastric cancer patients. In this phase II study, we tested the activity of docetaxel in combination with oxaliplatin and capecitabine (DOC) as a first-line treatment. DOC was administered as follows: docetaxel (60 mg/m(2)) and oxaliplatin (100 mg/m(2)) on day 1, and capecitabine (500 mg/m(2)) was administered orally twice daily given continuously, with cycles repeated every 3 weeks. The primary endpoint was the overall response rate. Forty-eight patients entered the study. All patients had metastatic disease (stage IV). None of the patients had previously received chemotherapy for advanced disease. Performance status was 0, 1, and 2 in 25, 58, and 17 % of patients, respectively; 13 patients (27 %) had adenocarcinoma of the gastroesophageal junction, and 29 patients (60.5 %) had two or more metastatic sites. The overall response rate was 52.1 %. Progression-free survival and overall survival were 6.9 and 12.6 months, respectively. The treatment was well tolerated with no treatment-related deaths. The most common grade 3-4 toxicity was neutropenia (41 %). DOC is an effective and tolerated first-line treatment, and the lower dose of docetaxel and oxaliplatin used in this study compared with other similar regimens does not seem to hamper the antitumor activity. JF - Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association AU - Di Lauro, Luigi AU - Vici, Patrizia AU - Belli, Franca AU - Tomao, Silverio AU - Fattoruso, Silvia Ileana AU - Arena, Maria Grazia AU - Pizzuti, Laura AU - Giannarelli, Diana AU - Paoletti, Giancarlo AU - Barba, Maddalena AU - Sergi, Domenico AU - Maugeri-Saccà, Marcello AD - Division of Medical Oncology B, "Regina Elena" National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy, dilauro@ifo.it. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 718 EP - 724 VL - 17 IS - 4 KW - Organoplatinum Compounds KW - 0 KW - Taxoids KW - oxaliplatin KW - 04ZR38536J KW - Deoxycytidine KW - 0W860991D6 KW - docetaxel KW - 15H5577CQD KW - Capecitabine KW - 6804DJ8Z9U KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Organoplatinum Compounds -- administration & dosage KW - Humans KW - Deoxycytidine -- analogs & derivatives KW - Adenocarcinoma -- mortality KW - Neutropenia -- chemically induced KW - Aged KW - Taxoids -- administration & dosage KW - Adenocarcinoma -- pathology KW - Esophageal Neoplasms -- mortality KW - Esophageal Neoplasms -- pathology KW - Fluorouracil -- administration & dosage KW - Fluorouracil -- analogs & derivatives KW - Adult KW - Treatment Outcome KW - Deoxycytidine -- administration & dosage KW - Middle Aged KW - Adenocarcinoma -- drug therapy KW - Male KW - Female KW - Esophageal Neoplasms -- drug therapy KW - Stomach Neoplasms -- drug therapy KW - Stomach Neoplasms -- pathology KW - Stomach Neoplasms -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1563991337?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastric+cancer+%3A+official+journal+of+the+International+Gastric+Cancer+Association+and+the+Japanese+Gastric+Cancer+Association&rft.atitle=Docetaxel%2C+oxaliplatin%2C+and+capecitabine+combination+chemotherapy+for+metastatic+gastric+cancer.&rft.au=Di+Lauro%2C+Luigi%3BVici%2C+Patrizia%3BBelli%2C+Franca%3BTomao%2C+Silverio%3BFattoruso%2C+Silvia+Ileana%3BArena%2C+Maria+Grazia%3BPizzuti%2C+Laura%3BGiannarelli%2C+Diana%3BPaoletti%2C+Giancarlo%3BBarba%2C+Maddalena%3BSergi%2C+Domenico%3BMaugeri-Sacc%C3%A0%2C+Marcello&rft.aulast=Di+Lauro&rft.aufirst=Luigi&rft.date=2014-10-01&rft.volume=17&rft.issue=4&rft.spage=718&rft.isbn=&rft.btitle=&rft.title=Gastric+cancer+%3A+official+journal+of+the+International+Gastric+Cancer+Association+and+the+Japanese+Gastric+Cancer+Association&rft.issn=1436-3305&rft_id=info:doi/10.1007%2Fs10120-013-0321-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-23 N1 - Date created - 2014-09-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10120-013-0321-3 ER - TY - JOUR T1 - Chemoprevention of head and neck squamous cell carcinoma through inhibition of NF-κB signaling. AN - 1562430931; 24177052 AB - Nuclear factor-kappa B (NF-κB) transcription factors regulate cellular processes such as inflammation and cell survival. The NF-κB pathway is often activated with development and progression of head and neck squamous cell carcinoma (HNSCC). As such, NF-κB represents an attractive target for chemoprevention. HNSCC involves progression of lesions from premalignant to malignant, providing a window of opportunity for intervention with chemopreventive agents. Appropriate chemopreventive agents should be inexpensive, nontoxic, and target important pathways involved in the development of HNSCC. Several such agents that inhibit the NF-κB pathway have been investigated in HNSCC. Retinoids have been studied most extensively but have shown limited potential in human trials. Epidermal growth factor receptor inhibitors and PI3K-mTOR inhibitors may benefit a subset of patients. Other agents such as green tea extract and curcumin are appealing because they are generally regarded as safe. In contrast, there is evidence that Vitamin E supplementation may actually increase mortality of cancer patients. Repurposed drugs such as cyclooxygenase (COX) inhibitors and antidiabetic drugs are an emerging area of interest. Future research to develop agents with lower toxicity and higher specificity for the NF-κB pathway, and to target these therapies to individual patient genetic signatures should help to increase the utility of chemoprevention in HSNCC. Published by Elsevier Ltd. JF - Oral oncology AU - Vander Broek, Robert AU - Snow, Grace E AU - Chen, Zhong AU - Van Waes, Carter AD - Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, United States; Medical Research Scholars Program, NIH, Bethesda, Maryland, United States. ; Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, United States. ; Tumor Biology Section, Head and Neck Surgery Branch, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, United States. Electronic address: vanwaesc@nidcd.nih.gov. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 930 EP - 941 VL - 50 IS - 10 KW - Anticarcinogenic Agents KW - 0 KW - NF-kappa B KW - Index Medicus KW - Cyclooxygenase (COX) inhibitors KW - Green tea extract (GTE) KW - Curcumin KW - Nuclear factor-kappa B (NF-κB) KW - Epidermal growth factor receptor (EGFR) KW - Head and neck cancer KW - Mammalian target of rapamycin (mTOR) KW - Chemoprevention KW - Retinoids KW - Phosphatidylinositol 3-kinase (PI3K) KW - Humans KW - Disease Progression KW - Head and Neck Neoplasms -- prevention & control KW - Head and Neck Neoplasms -- metabolism KW - Anticarcinogenic Agents -- pharmacology KW - Carcinoma, Squamous Cell -- prevention & control KW - Carcinoma, Squamous Cell -- metabolism KW - Signal Transduction KW - NF-kappa B -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562430931?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oral+oncology&rft.atitle=Chemoprevention+of+head+and+neck+squamous+cell+carcinoma+through+inhibition+of+NF-%CE%BAB+signaling.&rft.au=Vander+Broek%2C+Robert%3BSnow%2C+Grace+E%3BChen%2C+Zhong%3BVan+Waes%2C+Carter&rft.aulast=Vander+Broek&rft.aufirst=Robert&rft.date=2014-10-01&rft.volume=50&rft.issue=10&rft.spage=930&rft.isbn=&rft.btitle=&rft.title=Oral+oncology&rft.issn=1879-0593&rft_id=info:doi/10.1016%2Fj.oraloncology.2013.10.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-26 N1 - Date created - 2014-09-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pharmacol Res. 2011 Aug;64(2):113-22 [21397027] Nat Immunol. 2011 Aug;12(8):695-708 [21772278] Cancer Biol Ther. 2011 Aug 15;12(4):288-96 [21613824] Oral Oncol. 2011 Sep;47(9):818-26 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[18829502] J Exp Ther Oncol. 2008;7(3):173-82 [19066126] Clin Cancer Res. 2008 Dec 15;14(24):8094-101 [19073969] Cancer Prev Res (Phila). 2008 Oct;1(5):339-48 [19138978] Cancer Prev Res (Phila). 2009 Jan;2(1):22-6 [19139014] Cancer Prev Res (Phila). 2009 Jan;2(1):27-36 [19139015] J Clin Oncol. 2009 Feb 1;27(4):599-604 [19075276] Int J Cancer. 2009 May 1;124(9):2200-9 [19123475] J Clin Oncol. 2001 Jun 15;19(12):3010-7 [11408495] Clin Cancer Res. 2001 Jun;7(6):1812-20 [11410524] J Eur Acad Dermatol Venereol. 2000 Nov;14(6):473-8 [11444269] Arch Otolaryngol Head Neck Surg. 2001 Jul;127(7):813-20 [11448356] Cancer Res. 2001 Aug 15;61(16):6112-9 [11507061] Mutat Res. 2001 Sep 20;496(1-2):181-90 [11551494] J Biol Chem. 2001 Sep 28;276(39):36530-4 [11479302] Anticancer Res. 2001 Jul-Aug;21(4B):2895-900 [11712783] Annu Rev Pharmacol Toxicol. 2002;42:25-54 [11807163] Nutr Cancer. 2001;40(2):125-33 [11962247] Int J Cancer. 2002 Jun 1;99(4):538-48 [11992543] Virchows Arch. 2002 Jun;440(6):594-7 [12070598] Clin Cancer Res. 2002 Jul;8(7):2369-77 [12114442] Laryngoscope. 2002 Mar;112(3):472-81 [12148857] Laryngoscope. 2002 May;112(5):839-43 [12150615] Carcinogenesis. 2002 Sep;23(9):1511-8 [12189195] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.oraloncology.2013.10.005 ER - TY - JOUR T1 - Chronic treatment with novel brain-penetrating selective NOP receptor agonist MT-7716 reduces alcohol drinking and seeking in the rat. AN - 1562430826; 24863033 AB - Since its discovery, the nociceptin/orphanin FQ (N/OFQ)-NOP receptor system has been extensively investigated as a promising target to treat alcoholism. Encouraging results obtained with the endogenous ligand N/OFQ stimulated research towards the development of novel brain-penetrating NOP receptor agonists with a pharmacological and toxicological profile compatible with clinical development. Here we describe the biochemical and alcohol-related behavioral effects of the novel NOP receptor agonist MT-7716. MT-7716 has high affinity for human NOP receptors expressed in HEK293 cells with a Ki value of 0.21 nM. MT-7716 concentration-dependently stimulated GTPγ(35)S binding with an EC50 value of 0.30 nM and its efficacy was similar to N/OFQ, suggesting that MT7716 is a full agonist at NOP receptors. In the two bottle choice test MT-7716 (0, 0.3, 1, and 3 mg/kg, bid) given orally for 14 days dose-dependently decreased voluntary alcohol intake in Marchigian Sardinian rats. The effect became gradually stronger following repeated administration, and was still significant 1 week after discontinuation of the drug. Oral naltrexone (30 mg/kg, bid) for 14 days also reduced ethanol intake; however, the effect decreased over the treatment period and rapidly disappeared when drug treatment was discontinued. MT-7716 is also effective for preventing reinstatement caused by both ethanol-associated environmental stimuli and stress. Finally, to investigate the effect of MT-7716 on alcohol withdrawal symptoms, Wistar rats were withdrawn from a 7-day alcohol liquid diet. MT-7716 significantly attenuated somatic alcohol withdrawal symptoms. Together these findings indicate that MT-7716 is a promising candidate for alcoholism treatment remaining effective with chronic administration. JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology AU - Ciccocioppo, Roberto AU - Stopponi, Serena AU - Economidou, Daina AU - Kuriyama, Makoto AU - Kinoshita, Hiroshi AU - Heilig, Markus AU - Roberto, Marisa AU - Weiss, Friedbert AU - Teshima, Koji AD - Pharmacology Unit, School of Pharmacy, University of Camerino, Camerino, Italy. ; Department II (CNS), Pharmacology Research Laboratories I, Research Division, Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan. ; Laboratory of Clinical and Translational Studies, National Institute of Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA. ; Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, USA. ; Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, La Jolla, CA, USA. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 2601 EP - 2610 VL - 39 IS - 11 KW - 2-(3-(1-(acenaphthen-1-yl)piperidin-4-yl)-2-oxo-2,3-dihydro-1H-benzimidazol-1-yl)-N-methylacetamide KW - 0 KW - Acenaphthenes KW - Alcohol Deterrents KW - Benzimidazoles KW - Narcotic Antagonists KW - Opioid Peptides KW - Receptors, Opioid KW - nociceptin receptor KW - Naltrexone KW - 5S6W795CQM KW - nociceptin KW - 7AYI9N34FF KW - Index Medicus KW - Animals KW - Substance Withdrawal Syndrome -- physiopathology KW - Dose-Response Relationship, Drug KW - HEK293 Cells KW - Humans KW - Rats KW - Choice Behavior -- drug effects KW - Choice Behavior -- physiology KW - Naltrexone -- pharmacology KW - Rats, Wistar KW - Substance Withdrawal Syndrome -- drug therapy KW - Narcotic Antagonists -- pharmacology KW - Male KW - Opioid Peptides -- metabolism KW - Stress, Psychological -- complications KW - Receptors, Opioid -- agonists KW - Drug-Seeking Behavior -- drug effects KW - Acenaphthenes -- pharmacology KW - Alcohol Drinking -- drug therapy KW - Receptors, Opioid -- metabolism KW - Benzimidazoles -- pharmacology KW - Alcohol Drinking -- physiopathology KW - Alcohol Deterrents -- pharmacology KW - Drug-Seeking Behavior -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562430826?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.atitle=Chronic+treatment+with+novel+brain-penetrating+selective+NOP+receptor+agonist+MT-7716+reduces+alcohol+drinking+and+seeking+in+the+rat.&rft.au=Ciccocioppo%2C+Roberto%3BStopponi%2C+Serena%3BEconomidou%2C+Daina%3BKuriyama%2C+Makoto%3BKinoshita%2C+Hiroshi%3BHeilig%2C+Markus%3BRoberto%2C+Marisa%3BWeiss%2C+Friedbert%3BTeshima%2C+Koji&rft.aulast=Ciccocioppo&rft.aufirst=Roberto&rft.date=2014-10-01&rft.volume=39&rft.issue=11&rft.spage=2601&rft.isbn=&rft.btitle=&rft.title=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.issn=1740-634X&rft_id=info:doi/10.1038%2Fnpp.2014.113 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-15 N1 - Date created - 2014-09-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4321-6 [10760299] Addict Biol. 2014 Mar;19(2):225-32 [24589296] Neuroreport. 2000 Jun 26;11(9):1939-43 [10884047] Eur J Pharmacol. 2000 Sep 15;404(1-2):153-9 [10980274] Peptides. 2000 Jul;21(7):1071-80 [10998542] Peptides. 2000 Jul;21(7):1125-30 [10998547] J Abnorm Psychol. 2000 Nov;109(4):738-42 [11195999] Alcohol Clin Exp Res. 2001 Oct;25(10):1414-9 [11696659] Peptides. 2002 Jan;23(1):117-25 [11814626] Psychopharmacology (Berl). 2002 May;161(2):113-9 [11981590] Behav Pharmacol. 2002 May;13(3):229-35 [12122313] Neuropsychopharmacology. 2002 Sep;27(3):391-9 [12225696] J Neurosci. 2003 Oct 15;23(28):9445-51 [14561874] J Neurosci. 2003 Nov 12;23(32):10331-7 [14614092] Neuroreport. 2003 Dec 19;14(18):2383-5 [14663196] J Neurosci. 2004 Feb 18;24(7):1551-60 [14973230] Psychopharmacology (Berl). 2004 Mar;172(2):170-8 [14624331] Neuropsychopharmacology. 2004 Apr;29(4):686-93 [14872205] Physiol Behav. 2004 Aug;82(1):63-8 [15234592] Br J Pharmacol. 1977 Aug;60(4):537-45 [409448] Science. 1982 Mar 12;215(4538):1394-6 [6278591] J Pharmacol Exp Ther. 1982 Oct;223(1):157-62 [6288917] Life Sci. 1983 Jul 4;33(1):19-29 [6865647] J Pharmacol Exp Ther. 1985 Jun;233(3):735-40 [2989495] Neuroscience. 1988 Dec;27(3):897-904 [3252176] Nature. 1995 Oct 12;377(6549):532-5 [7566152] Science. 1995 Nov 3;270(5237):792-4 [7481766] J Pharmacol Exp Ther. 1996 Feb;276(2):532-44 [8632319] Alcohol. 1996 Mar-Apr;13(2):163-70 [8814651] Neuroscience. 1996 Nov;75(2):333-7 [8930999] Trends Neurosci. 1998 May;21(5):215-21 [9610886] Brain Res. 1999 Jun 19;832(1-2):168-70 [10375664] J Comp Neurol. 1999 Oct 4;412(4):563-605 [10464356] Alcohol Clin Exp Res. 1999 Aug;23(8):1386-94 [10470982] Proc Natl Acad Sci U S A. 1999 Aug 31;96(18):10444-9 [10468628] Nature. 1962 Mar 31;193:1313-4 [13908500] Psychopharmacology (Berl). 2005 May;179(2):366-73 [15551068] Br J Pharmacol. 2005 Sep;146(1):33-40 [15980870] Proc Natl Acad Sci U S A. 2006 Oct 10;103(41):15236-41 [17015825] Peptides. 2006 Dec;27(12):3299-306 [17097763] Biol Psychiatry. 2007 Jan 1;61(1):4-12 [16533497] Neuropsychopharmacology. 2007 Apr;32(4):902-10 [16880770] Psychopharmacology (Berl). 2007 Dec;195(3):345-55 [17705061] Addict Biol. 2008 Mar;13(1):80-7 [17910740] Addict Biol. 2008 Mar;13(1):88-94 [18269382] Psychopharmacology (Berl). 2008 Mar;196(4):523-31 [17989958] Biol Psychiatry. 2008 Aug 1;64(3):211-8 [18367152] Neuropharmacology. 2009 Apr;56(5):896-904 [19371589] Neuropsychopharmacology. 2009 Aug;34(9):2125-34 [19322167] Alcohol Clin Exp Res. 2011 Apr;35(4):747-55 [21223310] Neuropsychopharmacology. 2011 May;36(6):1178-86 [21289601] Curr Top Med Chem. 2011;11(9):1151-6 [21050175] J Med Chem. 2011 Apr 28;54(8):2687-700 [21438532] J Nucl Med. 2011 Oct;52(10):1638-45 [21880575] Curr Drug Abuse Rev. 2011 Dec;4(4):270-85 [21834753] J Nucl Med. 2012 Mar;53(3):385-92 [22312136] Biol Psychiatry. 2012 Apr 15;71(8):666-76 [22153590] Neuron. 2012 Oct 4;76(1):192-208 [23040815] Addict Biol. 2013 May;18(3):467-79 [22804785] Eur J Pharmacol. 2013 May 5;707(1-3):41-5 [23524092] PLoS One. 2013;8(6):e65648 [23799031] Curr Opin Neurobiol. 2013 Aug;23(4):684-91 [23648086] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4938-43 [10758169] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/npp.2014.113 ER - TY - JOUR T1 - PPARγ in head and neck cancer prevention. AN - 1562430628; 24434068 AB - Head and neck cancer is a major source of morbidity and mortality worldwide. Intervention during the early phases of carcinogenesis represents a promising new strategy for curbing the devastating effects of this disease and its primary treatment modalities, surgery and radiation with or without concomitant chemotherapy. This review focuses on the peroxisome proliferator-activated receptor gamma (PPARγ) as a target for chemoprevention of oral cancer. Accumulating data suggest that ligands of PPARγ, which include the thiazolidinedione class of agents approved for the treatment of diabetes, inhibit cancer cell growth in vitro and in animal carcinogenesis models, providing the rationale for testing this approach in populations at risk for head and neck cancer. Published by Elsevier Ltd. JF - Oral oncology AU - Burotto, Mauricio AU - Szabo, Eva AD - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, United States. ; Lung and Upper Aerodigestive Cancer Research Group, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, United States. Electronic address: szaboe@mail.nih.gov. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 924 EP - 929 VL - 50 IS - 10 KW - PPAR gamma KW - 0 KW - Thiazolidinediones KW - pioglitazone KW - X4OV71U42S KW - Index Medicus KW - Pioglitazone KW - Head and neck cancer KW - PPARγ (peroxisome proliferator-activated receptor γ) KW - Oral carcinoma KW - Evidence-Based Medicine KW - Humans KW - Thiazolidinediones -- pharmacology KW - Disease Progression KW - Clinical Trials as Topic KW - Head and Neck Neoplasms -- prevention & control KW - PPAR gamma -- drug effects KW - Head and Neck Neoplasms -- pathology KW - PPAR gamma -- physiology KW - Precancerous Conditions -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562430628?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oral+oncology&rft.atitle=PPAR%CE%B3+in+head+and+neck+cancer+prevention.&rft.au=Burotto%2C+Mauricio%3BSzabo%2C+Eva&rft.aulast=Burotto&rft.aufirst=Mauricio&rft.date=2014-10-01&rft.volume=50&rft.issue=10&rft.spage=924&rft.isbn=&rft.btitle=&rft.title=Oral+oncology&rft.issn=1879-0593&rft_id=info:doi/10.1016%2Fj.oraloncology.2013.12.020 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-26 N1 - Date created - 2014-09-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Cancer Res Clin Oncol. 2011 Feb;137(2):251-9 [20390425] Ann Oncol. 2011 May;22(5):1088-93 [21127011] J Clin Oncol. 2011 Nov 10;29(32):4294-301 [21969503] JAMA. 2012 Feb 15;307(7):693-703 [22282321] Cell. 2000 Jan 7;100(1):57-70 [10647931] Cancer Res. 2000 Feb 15;60(4):1129-38 [10706135] Clin Cancer Res. 2000 May;6(5):1702-10 [10815888] J Natl Cancer Inst. 2000 Jun 21;92(12):977-86 [10861309] J Neurochem. 2002 Jun;81(5):1052-60 [12065618] J Lab Clin Med. 2002 Jul;140(1):17-26 [12080324] Crit Rev Oral Biol Med. 2002;13(5):390-6 [12393758] Cancer Res. 2002 Nov 15;62(22):6447-50 [12438233] Clin Cancer Res. 2003 Jan;9(1):1-9 [12538445] Curr Oncol Rep. 2003 Mar;5(2):152-7 [12583833] J Eur Acad Dermatol Venereol. 2003 Mar;17(2):216-8 [12705757] Cancer Sci. 2003 Apr;94(4):365-71 [12824906] J Clin Endocrinol Metab. 2004 Jan;89(1):200-6 [14715850] Lancet Oncol. 2004 Jul;5(7):419-29 [15231248] N Engl J Med. 2004 Sep 9;351(11):1106-18 [15356308] Nutr Cancer. 2004;49(1):1-6 [15454352] Nat Rev Cancer. 2012 Mar;12(3):181-95 [22318237] Biochim Biophys Acta. 2012 Jul;1822(7):1090-5 [22504298] Diabetologia. 2012 Jul;55(7):1953-62 [22460763] Cancer Prev Res (Phila). 2012 Sep;5(9):1081-9 [22911111] Oral Oncol. 2013 Jan;49(1):1-8 [22841678] Oral Oncol. 2013 Dec;49(12):1136-40 [24084407] Cancer. 1974 Jan;33(1):256-70 [4810100] Oral Surg Oral Med Oral Pathol. 1985 Jul;60(1):50-5 [3862013] N Engl J Med. 1986 Dec 11;315(24):1501-5 [3537787] Arzneimittelforschung. 1990 Mar;40(3):263-7 [2189419] N Engl J Med. 1990 Sep 20;323(12):795-801 [2202902] Chem Biol Interact. 1992 Dec;85(2-3):141-50 [1493606] J Clin Oncol. 1994 Apr;12(4):851-73 [8151328] Nat Med. 1996 Jun;2(6):682-5 [8640560] J Natl Cancer Inst. 1997 Jun 18;89(12):857-62 [9196251] Oral Oncol. 1997 Jul;33(4):231-6 [9307711] Cancer. 1998 Apr 1;82(7):1367-75 [9529030] N Engl J Med. 1961 Aug 10;265:253-67 [13685078] Oncogene. 2005 Feb 17;24(8):1412-22 [15608671] Cancer Epidemiol Biomarkers Prev. 2005 Feb;14(2):467-75 [15734974] J Natl Cancer Inst. 2005 Apr 6;97(7):481-8 [15812073] Am J Physiol Endocrinol Metab. 2005 May;288(5):E930-4 [15632102] Oral Oncol. 2005 Jul;41(6):551-61 [15975518] J Natl Cancer Inst. 2006 Apr 5;98(7):441-50 [16595780] Am J Cardiol. 2007 Feb 19;99(4A):51B-67B [17307058] J Clin Endocrinol Metab. 2007 Apr;92(4):1256-62 [17244785] J Clin Oncol. 2007 Apr 20;25(12):1476-81 [17442990] J Am Coll Cardiol. 2007 May 1;49(17):1772-80 [17466227] JAMA. 2007 Sep 12;298(10):1180-8 [17848652] J Otolaryngol. 2007 Oct;36(5):282-90 [17963667] Mol Pharmacol. 2008 Mar;73(3):709-17 [18055759] Oral Dis. 2008 Apr;14(3):229-43 [18298420] Haematologica. 2008 Apr;93(4):511-7 [18322251] Clin Cancer Res. 2008 Apr 1;14(7):2095-101 [18381950] JAMA. 2008 Apr 2;299(13):1561-73 [18378631] Lancet. 2008 May 17;371(9625):1695-709 [18486742] Clin Cancer Res. 2009 Jan 1;15(1):2-8 [19118026] Cancer Epidemiol Biomarkers Prev. 2009 Feb;18(2):541-50 [19190158] Diabetologia. 2009 Apr;52(4):723-32 [19169664] Head Neck. 2009 Dec;31(12):1600-9 [19455705] Carcinogenesis. 2009 Dec;30(12):2095-9 [19861651] Nat Rev Immunol. 2010 May;10(5):365-76 [20414208] Mol Cancer Ther. 2010 Nov;9(11):3074-82 [21045137] Cell. 2011 Mar 4;144(5):646-74 [21376230] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] N Engl J Med. 2011 Mar 24;364(12):1104-15 [21428766] Diabetes Care. 2011 Apr;34(4):916-22 [21447663] Diabetes Care. 2011 Apr;34(4):923-9 [21447664] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.oraloncology.2013.12.020 ER - TY - JOUR T1 - 2-[5-Selenocyanato-pentyl]-6-amino-benzo[de]isoquinoline-1,3-dione inhibits angiogenesis, induces p53 dependent mitochondrial apoptosis and enhances therapeutic efficacy of cyclophosphamide. AN - 1562426638; 25038569 AB - The present study embodies a detailed investigation of the chemoenhancement property of a synthetic organoselenium compound, 2-[5-selenocyanato-pentyl]-7-amino benzo[de]isoquinoline-1,3-dione (ANOS) in tumor bearing Swiss albino mice. The results accumulated from this study illustrated that the administration of ANOS significantly potentiated the therapeutic efficacy of cyclophosphamide by reducing the tumor burden and chemotherapy induced toxicity in the host. Ability of ANOS in inducing apoptosis and inhibiting angiogenesis was thought to be the crucial effecter for enhancing the therapeutic efficacy of cyclophosphamide. Fluorescence microscopic study revealed that ANOS was capable of penetrating tumor cells and distributed in the subcellular compartments. We showed that ANOS-induced apoptosis, as evidenced by the TUNEL assay and cleavage of poly(ADP-ribose) polymerase (PARP), involved ROS production and DNA damage in tumor cells. ROS production subsequently activated p53 phosphorylation at Ser-15. This in turn activated cytochrome c (cyt c) release from mitochondria via Bcl-2 and Bax. Finally activation of caspase 3 led to PARP cleavage and apoptosis. These results suggested that p53 dependent mitochondrial pathway was playing an important role in ANOS induced apoptosis of tumor cells. Administration of ANOS also resulted in significant improvement of tumor vasculature and sprouting of the peritoneal cavity along with the normalization of MMP-9 level in serum and ascites fluid of tumor bearing mice. This potential antiangiogenic activity of ANOS also facilitated the therapeutic efficacy of the combination therapy. Furthermore, ANOS significantly suppressed cyclophosphamide-induced liver, hematopoietic and genetic damages. A concomitant decrease in drug-induced toxicity by ANOS might also have enhanced the efficacy of cyclophosphamide by improving the intrinsic defense machineries of the host. Copyright © 2014 Elsevier Masson SAS. All rights reserved. JF - Biochimie AU - Roy, Somnath Singha AU - Chakraborty, Pramita AU - Biswas, Jaydip AU - Bhattacharya, Sudin AD - Chittaranjan National Cancer Institute, Department of Cancer Chemoprevention, 37, S.P. Mukherjee Road, Kolkata 700 026, West Bengal, India. ; Chittaranjan National Cancer Institute, Department of Translational Research, 37, S.P. Mukherjee Road, Kolkata 700 026, West Bengal, India. ; Chittaranjan National Cancer Institute, Department of Cancer Chemoprevention, 37, S.P. Mukherjee Road, Kolkata 700 026, West Bengal, India. Electronic address: sudinb19572004@yahoo.co.in. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 137 EP - 148 VL - 105 KW - 2-(5-selenocyanato-pentyl)-6-amino-benzo(de)isoquinoline-1,3-dione KW - 0 KW - Isoquinolines KW - Organoselenium Compounds KW - Proto-Oncogene Proteins c-bcl-2 KW - Reactive Oxygen Species KW - Tumor Suppressor Protein p53 KW - Cyclophosphamide KW - 8N3DW7272P KW - isoquinoline KW - JGX76Y85M6 KW - Index Medicus KW - Apoptosis KW - Mitochondrial pathway KW - Angiogenesis KW - Organoselenocyanate KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Humans KW - Mitochondria -- drug effects KW - Apoptosis -- drug effects KW - Mice KW - Drug Synergism KW - DNA Damage -- drug effects KW - Cyclophosphamide -- administration & dosage KW - Cyclophosphamide -- chemistry KW - Organoselenium Compounds -- administration & dosage KW - Neovascularization, Pathologic -- metabolism KW - Neoplasms, Experimental -- metabolism KW - Neoplasms, Experimental -- pathology KW - Tumor Suppressor Protein p53 -- metabolism KW - Neovascularization, Pathologic -- pathology KW - Isoquinolines -- chemistry KW - Neovascularization, Pathologic -- drug therapy KW - Neoplasms, Experimental -- drug therapy KW - Isoquinolines -- administration & dosage KW - Organoselenium Compounds -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562426638?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=2-%5B5-Selenocyanato-pentyl%5D-6-amino-benzo%5Bde%5Disoquinoline-1%2C3-dione+inhibits+angiogenesis%2C+induces+p53+dependent+mitochondrial+apoptosis+and+enhances+therapeutic+efficacy+of+cyclophosphamide.&rft.au=Roy%2C+Somnath+Singha%3BChakraborty%2C+Pramita%3BBiswas%2C+Jaydip%3BBhattacharya%2C+Sudin&rft.aulast=Roy&rft.aufirst=Somnath&rft.date=2014-10-01&rft.volume=105&rft.issue=&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=Biochimie&rft.issn=1638-6183&rft_id=info:doi/10.1016%2Fj.biochi.2014.07.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-29 N1 - Date created - 2014-09-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.biochi.2014.07.010 ER - TY - JOUR T1 - Methamphetamine and amphetamine isomer concentrations in human urine following controlled Vicks VapoInhaler administration. AN - 1561978911; 25217541 AB - Legitimate use of legal intranasal decongestants containing l-methamphetamine may complicate interpretation of urine drug tests positive for amphetamines. Our study hypotheses were that commonly used immunoassays would produce no false-positive results and a recently developed enantiomer-specific gas chromatography-mass spectrometry (GC-MS) procedure would find no d-amphetamine or d-methamphetamine in urine following controlled Vicks VapoInhaler administration at manufacturer's recommended doses. To evaluate these hypotheses, 22 healthy adults were each administered one dose (two inhalations in each nostril) of a Vicks VapoInhaler every 2 h for 10 h on Day 1 (six doses), followed by a single dose on Day 2. Every urine specimen was collected as an individual void for 32 h after the first dose and assayed for d- and l-amphetamines specific isomers with a GC-MS method with >99% purity of R-(-)-α-methoxy-α-(trifluoromethyl)phenylacetyl derivatives and 10 µg/L lower limits of quantification. No d-methamphetamine or d-amphetamine was detected in any urine specimen by GC-MS. The median l-methamphetamine maximum concentration was 62.8 µg/L (range: 11.0-1,440). Only two subjects had detectable l-amphetamine, with maximum concentrations coinciding with l-methamphetamine peak levels, and always ≤ 4% of the parent's maximum. Three commercial immunoassays for amphetamines EMIT(®) II Plus, KIMS(®) II and DRI(®) had sensitivities, specificities and efficiencies of 100, 97.8, 97.8; 100, 99.6, 99.6 and 100, 100, 100%, respectively. The immunoassays had high efficiencies, but our first hypothesis was not affirmed. The EMIT(®) II Plus assay produced 2.2% false-positive results, requiring an enantiomer-specific confirmation. Published by Oxford University Press 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Journal of analytical toxicology AU - Smith, Michael L AU - Nichols, Daniel C AU - Underwood, Paula AU - Fuller, Zachary AU - Moser, Matthew A AU - Flegel, Ron AU - Gorelick, David A AU - Newmeyer, Matthew N AU - Concheiro, Marta AU - Huestis, Marilyn A AD - U.S. Army Forensic Toxicology Drug Testing Laboratory, Fort Meade, MD, USA. ; Division of Workplace Programs, Department of Health and Human Services, Substance Abuse Mental Health Services Administration, Rockville, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Suite 200 Room 05A-721, Baltimore, MD 21224, USA Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Suite 200 Room 05A-721, Baltimore, MD 21224, USA Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Suite 200 Room 05A-721, Baltimore, MD 21224, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Suite 200 Room 05A-721, Baltimore, MD 21224, USA mhuestis@intra.nida.nih.gov. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 524 EP - 527 VL - 38 IS - 8 KW - Methamphetamine KW - 44RAL3456C KW - Creatinine KW - AYI8EX34EU KW - Amphetamine KW - CK833KGX7E KW - Index Medicus KW - Sensitivity and Specificity KW - Young Adult KW - Stereoisomerism KW - Creatinine -- urine KW - Dose-Response Relationship, Drug KW - Humans KW - Specimen Handling KW - Aged KW - Substance Abuse Detection -- methods KW - False Positive Reactions KW - Immunoassay -- methods KW - Adult KW - Gas Chromatography-Mass Spectrometry KW - Middle Aged KW - Healthy Volunteers KW - Administration, Inhalation KW - Adolescent KW - Male KW - Female KW - Methamphetamine -- urine KW - Amphetamine -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561978911?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+analytical+toxicology&rft.atitle=Methamphetamine+and+amphetamine+isomer+concentrations+in+human+urine+following+controlled+Vicks+VapoInhaler+administration.&rft.au=Smith%2C+Michael+L%3BNichols%2C+Daniel+C%3BUnderwood%2C+Paula%3BFuller%2C+Zachary%3BMoser%2C+Matthew+A%3BFlegel%2C+Ron%3BGorelick%2C+David+A%3BNewmeyer%2C+Matthew+N%3BConcheiro%2C+Marta%3BHuestis%2C+Marilyn+A&rft.aulast=Smith&rft.aufirst=Michael&rft.date=2014-10-01&rft.volume=38&rft.issue=8&rft.spage=524&rft.isbn=&rft.btitle=&rft.title=Journal+of+analytical+toxicology&rft.issn=1945-2403&rft_id=info:doi/10.1093%2Fjat%2Fbku077 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-05 N1 - Date created - 2014-09-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Chem. 1977 Aug;23(8):1504 [872410] BMC Clin Pharmacol. 2008;8:4 [18644153] J Anal Toxicol. 2004 Sep;28(6):449-55 [15516295] J Anal Toxicol. 1988 Sep-Oct;12(5):255-9 [3226121] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jat/bku077 ER - TY - JOUR T1 - A case-control study of occupational exposure to metalworking fluids and bladder cancer risk among men. AN - 1561130152; 25201311 AB - Metalworking has been associated with an excess risk of bladder cancer in over 20 studies. Metalworking fluids (MWFs) are suspected as the responsible exposure, but epidemiological data are limited. We investigated this association among men in the New England Bladder Cancer Study using state-of-the-art, quantitative exposure assessment methods. Cases (n=895) and population controls (n=1031) provided occupational histories during personal interviews. For selected jobs, exposure-oriented modules were administered to collect information on use of three MWF types: (1) straight (mineral oil, additives), (2) soluble (mineral oil, water, additives) and (3) synthetic (water, organics, additives) or semisynthetic (hybrid of soluble and synthetic). We computed ORs and 95% CIs relating bladder cancer risk to a variety of exposure metrics, adjusting for smoking and other factors. Non-metalworkers who had held jobs with possible exposure to mineral oil were analysed separately. Bladder cancer risk was elevated among men who reported using straight MWFs (OR=1.7, 95% CI 1.1 to 2.8); risk increased monotonically with increasing cumulative exposure (p=0.041). Use of soluble MWFs was associated with a 50% increased risk (95% CI 0.96 to 2.5). ORs were non-significantly elevated for synthetic/semisynthetic MWFs based on a small number of exposed men. Non-metalworkers holding jobs with possible exposure to mineral oil had a 40% increased risk (95% CI 1.1 to 1.8). Exposure to straight MWFs was associated with a significantly increased bladder cancer risk, as was employment in non-metalworking jobs with possible exposure to mineral oil. These findings strengthen prior evidence for mineral oil as a bladder carcinogen. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions. JF - Occupational and environmental medicine AU - Colt, Joanne S AU - Friesen, Melissa C AU - Stewart, Patricia A AU - Donguk, Park AU - Johnson, Alison AU - Schwenn, Molly AU - Karagas, Margaret R AU - Armenti, Karla AU - Waddell, Richard AU - Verrill, Castine AU - Ward, Mary H AU - Freeman, Laura E Beane AU - Moore, Lee E AU - Koutros, Stella AU - Baris, Dalsu AU - Silverman, Debra T AD - Department of Health and Human Services, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Department of Health and Human Services, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA Stewart Exposure Assessments, LLC, Arlington, Virginia, USA. ; Korea National Open University, Seoul, Korea. ; Vermont Cancer Registry, Burlington, Vermont, USA. ; Maine Cancer Registry, Augusta, Maine, USA. ; Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, USA. ; New Hampshire Department of Health and Human Services, Concord, New Hampshire, USA. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 667 EP - 674 VL - 71 IS - 10 KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Aged KW - Middle Aged KW - New England -- epidemiology KW - Male KW - Occupational Exposure KW - Urinary Bladder Neoplasms -- epidemiology KW - Metallurgy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561130152?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+environmental+medicine&rft.atitle=A+case-control+study+of+occupational+exposure+to+metalworking+fluids+and+bladder+cancer+risk+among+men.&rft.au=Colt%2C+Joanne+S%3BFriesen%2C+Melissa+C%3BStewart%2C+Patricia+A%3BDonguk%2C+Park%3BJohnson%2C+Alison%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BArmenti%2C+Karla%3BWaddell%2C+Richard%3BVerrill%2C+Castine%3BWard%2C+Mary+H%3BFreeman%2C+Laura+E+Beane%3BMoore%2C+Lee+E%3BKoutros%2C+Stella%3BBaris%2C+Dalsu%3BSilverman%2C+Debra+T&rft.aulast=Colt&rft.aufirst=Joanne&rft.date=2014-10-01&rft.volume=71&rft.issue=10&rft.spage=667&rft.isbn=&rft.btitle=&rft.title=Occupational+and+environmental+medicine&rft.issn=1470-7926&rft_id=info:doi/10.1136%2Foemed-2013-102056 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-29 N1 - Date created - 2014-09-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 1983 Feb;70(2):237-45 [6571931] Scand J Work Environ Health. 1983 Oct;9(5):449-50 [6673102] IARC Monogr Eval Carcinog Risk Chem Hum. 1984 Apr;33:1-222 [6590450] Cancer. 1986 Jan 15;57(2):362-7 [3942969] Int J Cancer. 1987 Mar 15;39(3):287-92 [3818120] Am J Epidemiol. 1987 Aug;126(2):247-57 [3605053] Am J Public Health. 1987 Oct;77(10):1298-300 [3631363] Cancer Res. 1987 Dec 15;47(24 Pt 1):6763-6 [3677105] Int J Cancer. 1987 Dec 15;40(6):734-40 [3692621] Scand J Work Environ Health. 1987 Dec;13(6):493-504 [3433051] Arch Environ Health. 1987 Nov-Dec;42(6):361-6 [3439814] Int J Cancer. 1988 Mar 15;41(3):371-9 [3346100] J Natl Cancer Inst. 1989 Oct 4;81(19):1472-80 [2778834] Br J Cancer. 1992 Sep;66(3):568-78 [1520596] Am J Ind Med. 2000 Jul;38(1):90-8 [10861770] Am J Ind Med. 2000 Oct;38(4):410-6 [10982981] J Occup Environ Med. 2002 Jul;44(7):685-91 [12134533] Scand J Work Environ Health. 2002 Dec;28(6):371-85 [12539797] Appl Occup Environ Hyg. 2003 Nov;18(11):855-64 [14555438] Appl Occup Environ Hyg. 2003 Nov;18(11):902-12 [14555443] Appl Occup Environ Hyg. 2003 Nov;18(11):913-20 [14555444] Cancer Causes Control. 2003 Dec;14(10):907-14 [14750529] Cancer Causes Control. 2004 Oct;15(8):759-69 [15456989] J Natl Cancer Inst. 1980 Apr;64(4):701-13 [6928984] Scand J Work Environ Health. 1992 Dec;18(6):351-60 [1485160] Int J Epidemiol. 1993 Jun;22(3):403-11 [8359955] Occup Environ Med. 1995 Aug;52(8):557-8 [7663646] Occup Environ Med. 1996 Jan;53(1):6-10 [8563860] Am J Ind Med. 1996 Dec;30(6):664-73 [8914713] Occup Environ Med. 1997 Jun;54(6):443-51 [9245952] Am J Ind Med. 1998 Mar;33(3):282-92 [9481427] J Occup Environ Med. 2005 Aug;47(8):854-8 [16093936] Am J Ind Med. 2005 Oct;48(4):249-58 [16167347] Lancet Oncol. 2005 Dec;6(12):931-2 [16353404] Occup Environ Med. 2007 Aug;64(8):520-6 [17332134] Ann Occup Hyg. 2009 Apr;53(3):271-88 [19329796] Am J Epidemiol. 2009 Jun 15;169(12):1471-8 [19414495] J Occup Environ Hyg. 2009 Sep;6(9):530-41 [19544177] Occup Environ Med. 2011 Apr;68(4):239-49 [20864470] Am J Ind Med. 2011 Jun;54(6):450-60 [21328414] IARC Monogr Eval Carcinog Risks Hum. 2013;101:9-549 [24772663] Am J Ind Med. 2014 Aug;57(8):915-27 [25060071] J Occup Environ Hyg. 2014;11(11):757-70 [25256317] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1136/oemed-2013-102056 ER - TY - JOUR T1 - Functional selectivity of allosteric interactions within G protein-coupled receptor oligomers: the dopamine D1-D3 receptor heterotetramer. AN - 1561035527; 25097189 AB - The dopamine D1 receptor-D3 receptor (D1R-D3R) heteromer is being considered as a potential therapeutic target for neuropsychiatric disorders. Previous studies suggested that this heteromer could be involved in the ability of D3R agonists to potentiate locomotor activation induced by D1R agonists. It has also been postulated that its overexpression plays a role in L-dopa-induced dyskinesia and in drug addiction. However, little is known about its biochemical properties. By combining bioluminescence resonance energy transfer, bimolecular complementation techniques, and cell-signaling experiments in transfected cells, evidence was obtained for a tetrameric stoichiometry of the D1R-D3R heteromer, constituted by two interacting D1R and D3R homodimers coupled to Gs and Gi proteins, respectively. Coactivation of both receptors led to the canonical negative interaction at the level of adenylyl cyclase signaling, to a strong recruitment of β-arrestin-1, and to a positive cross talk of D1R and D3R agonists at the level of mitogen-activated protein kinase (MAPK) signaling. Furthermore, D1R or D3R antagonists counteracted β-arrestin-1 recruitment and MAPK activation induced by D3R and D1R agonists, respectively (cross-antagonism). Positive cross talk and cross-antagonism at the MAPK level were counteracted by specific synthetic peptides with amino acid sequences corresponding to D1R transmembrane (TM) domains TM5 and TM6, which also selectively modified the quaternary structure of the D1R-D3R heteromer, as demonstrated by complementation of hemiproteins of yellow fluorescence protein fused to D1R and D3R. These results demonstrate functional selectivity of allosteric modulations within the D1R-D3R heteromer, which can be involved with the reported behavioral synergism of D1R and D3R agonists. U.S. Government work not protected by U.S. copyright. JF - Molecular pharmacology AU - Guitart, Xavier AU - Navarro, Gemma AU - Moreno, Estefania AU - Yano, Hideaki AU - Cai, Ning-Sheng AU - Sánchez-Soto, Marta AU - Kumar-Barodia, Sandeep AU - Naidu, Yamini T AU - Mallol, Josefa AU - Cortés, Antoni AU - Lluís, Carme AU - Canela, Enric I AU - Casadó, Vicent AU - McCormick, Peter J AU - Ferré, Sergi AD - National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Department of Health and Human Services, Baltimore, Maryland (X.G., H.Y., N.-S.C., M.S.-S., S.K.-B., Y.T.N., S.F.); Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas and Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain (G.N., E.M., J.M., A.C., C.L., E.I.C., V.C., P.J.M.); and School of Pharmacy, University of East Anglia, Norwich, United Kingdom (P.J.M.). ; National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Department of Health and Human Services, Baltimore, Maryland (X.G., H.Y., N.-S.C., M.S.-S., S.K.-B., Y.T.N., S.F.); Centro de Investigación Biomédica en Red Sobre Enfermedades Neurodegenerativas and Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain (G.N., E.M., J.M., A.C., C.L., E.I.C., V.C., P.J.M.); and School of Pharmacy, University of East Anglia, Norwich, United Kingdom (P.J.M.) sferre@intra.nida.nih.gov. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 417 EP - 429 VL - 86 IS - 4 KW - ARRB1 protein, human KW - 0 KW - Arrestins KW - DRD1 protein, human KW - DRD3 protein, human KW - Dopamine Agonists KW - Receptors, Dopamine D1 KW - Receptors, Dopamine D3 KW - beta-Arrestin 1 KW - beta-Arrestins KW - GTP-Binding Protein alpha Subunits, Gi-Go KW - EC 3.6.5.1 KW - GTP-Binding Protein alpha Subunits, Gs KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - GTP-Binding Protein alpha Subunits, Gi-Go -- metabolism KW - MAP Kinase Signaling System KW - Dopamine Agonists -- pharmacology KW - Humans KW - HEK293 Cells KW - Adenylyl Cyclases -- metabolism KW - Allosteric Regulation KW - GTP-Binding Protein alpha Subunits, Gs -- metabolism KW - Protein Multimerization KW - Protein Binding KW - Arrestins -- metabolism KW - Receptors, Dopamine D3 -- agonists KW - Receptors, Dopamine D3 -- metabolism KW - Receptors, Dopamine D1 -- agonists KW - Receptors, Dopamine D1 -- chemistry KW - Receptors, Dopamine D3 -- chemistry KW - Allosteric Site KW - Receptors, Dopamine D1 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561035527?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Functional+selectivity+of+allosteric+interactions+within+G+protein-coupled+receptor+oligomers%3A+the+dopamine+D1-D3+receptor+heterotetramer.&rft.au=Guitart%2C+Xavier%3BNavarro%2C+Gemma%3BMoreno%2C+Estefania%3BYano%2C+Hideaki%3BCai%2C+Ning-Sheng%3BS%C3%A1nchez-Soto%2C+Marta%3BKumar-Barodia%2C+Sandeep%3BNaidu%2C+Yamini+T%3BMallol%2C+Josefa%3BCort%C3%A9s%2C+Antoni%3BLlu%C3%ADs%2C+Carme%3BCanela%2C+Enric+I%3BCasad%C3%B3%2C+Vicent%3BMcCormick%2C+Peter+J%3BFerr%C3%A9%2C+Sergi&rft.aulast=Guitart&rft.aufirst=Xavier&rft.date=2014-10-01&rft.volume=86&rft.issue=4&rft.spage=417&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.114.093096 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-07 N1 - Date created - 2014-09-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Neurosci. 2002 Sep 15;22(18):7931-40 [12223546] J Neurosci. 2014 Mar 5;34(10):3545-58 [24599455] J Mol Biol. 2003 Jun 13;329(4):815-29 [12787680] J Biol Chem. 1996 Jul 5;271(27):16384-92 [8663163] J Neurosci. 1996 Oct 1;16(19):6100-6 [8815892] Mol Pharmacol. 1997 Sep;52(3):508-14 [9281614] Nat Rev Mol Cell Biol. 2006 Jun;7(6):449-56 [16625152] Pharmacol Ther. 2007 Dec;116(3):343-54 [17935788] Mol Pharmacol. 2008 Jul;74(1):59-69 [18424554] Nat Methods. 2008 Aug;5(8):727-33 [18587404] J Biol Chem. 2008 Sep 19;283(38):26016-25 [18644790] EMBO J. 2008 Sep 3;27(17):2293-304 [18668123] Neuropsychopharmacology. 2009 Mar;34(4):972-86 [18800071] Nat Chem Biol. 2009 Mar;5(3):131-4 [19219011] Br J Pharmacol. 2009 May;157(1):64-75 [19413572] Methods Mol Biol. 2009;574:215-34 [19685312] Dev Cell. 2009 Oct;17(4):443-58 [19853559] Curr Opin Pharmacol. 2010 Feb;10(1):87-92 [19837631] CNS Neurol Disord Drug Targets. 2010 Nov;9(5):596-600 [20632968] Biochem Biophys Res Commun. 2010 Nov 26;402(4):801-7 [21040702] Nat Med. 2010 Dec;16(12):1393-5 [21113156] Neuron. 2011 Jan 13;69(1):120-31 [21220103] PLoS One. 2011;6(1):e16088 [21264319] Nat Chem Biol. 2011 Sep;7(9):624-30 [21785426] Trends Pharmacol Sci. 2011 Sep;32(9):514-20 [21715028] Annu Rev Pharmacol Toxicol. 2012;52:179-97 [21942629] Mol Psychiatry. 2012 Jun;17(6):650-62 [21844870] Mol Pharmacol. 2013 Jul;84(1):158-69 [23632086] Pharmacol Rev. 2014;66(2):413-34 [24515647] J Biol Chem. 2003 Feb 14;278(7):4385-8 [12496294] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/mol.114.093096 ER - TY - JOUR T1 - Promiscuous and specific recognition among ephrins and Eph receptors. AN - 1561032653; 25017878 AB - Eph-ephrin interactions control the signal transduction between cells and play an important role in carcinogenesis and other diseases. The interactions between Eph receptors and ephrins of the same subclass are promiscuous; there are cross-interactions between some subclasses, but not all. To understand how Eph-ephrin interactions can be both promiscuous and specific, we investigated sixteen energy landscapes of four Eph receptors (A2, A4, B2, and B4) interacting with four ephrin ligands (A1, A2, A5, and B2). We generated conformational ensembles and recognition energy landscapes starting from separated Eph and ephrin molecules and proceeding up to the formation of Eph-ephrin complexes. Analysis of the Eph-ephrin recognition trajectories and the co-evolution entropy of 400 ligand binding domains of Eph receptor and 241 ephrin ligands identified conserved residues during the recognition process. Our study correctly predicted the promiscuity and specificity of the interactions and provided insights into their recognition. The dynamic conformational changes during Eph-ephrin recognition can be described by progressive conformational selection and population shift events, with two dynamic salt bridges between EphB4 and ephrin-B2 contributing to the specific recognition. EphA3 cancer-related mutations lowered the binding energies. The specificity is not only controlled by the final stage of the interaction across the protein-protein interface, but also has large contributions from binding kinetics with the help of dynamic intermediates along the pathway from the separated Eph and ephrin to the Eph-ephrin complex. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biochimica et biophysica acta AU - Dai, Dandan AU - Huang, Qiang AU - Nussinov, Ruth AU - Ma, Buyong AD - State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai 200433, China. ; State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai 200433, China. Electronic address: huangqiang@fudan.edu.cn. ; Basic Science Program, Leidos Biomedical Research, Inc., Cancer and Inflammation Program, National Cancer Institute, Frederick, MD 21702, USA; Sackler Inst. of Molecular Medicine, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. ; Basic Science Program, Leidos Biomedical Research, Inc., Cancer and Inflammation Program, National Cancer Institute, Frederick, MD 21702, USA. Electronic address: mabuyong@mail.nih.gov. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 1729 EP - 1740 VL - 1844 IS - 10 SN - 0006-3002, 0006-3002 KW - Index Medicus KW - Energy landscape KW - Protein–protein interaction KW - Induced fit KW - Conformational selection KW - Eph receptor tyrosine kinase KW - Conformational dynamics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561032653?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Promiscuous+and+specific+recognition+among+ephrins+and+Eph+receptors.&rft.au=Dai%2C+Dandan%3BHuang%2C+Qiang%3BNussinov%2C+Ruth%3BMa%2C+Buyong&rft.aulast=Dai&rft.aufirst=Dandan&rft.date=2014-10-01&rft.volume=1844&rft.issue=10&rft.spage=1729&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbapap.2014.07.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2014-09-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nucleic Acids Res. 2010 Jul;38(Web Server issue):W657-61 [20525782] Proc Natl Acad Sci U S A. 2010 Aug 10;107(32):14087-92 [20660315] Biochem Biophys Res Commun. 2010 Sep 3;399(4):555-9 [20678482] J Biol Chem. 2010 Sep 10;285(37):28651-8 [20639195] Curr Opin Cell Biol. 2010 Oct;22(5):611-6 [20810264] Trends Biochem Sci. 2010 Oct;35(10):539-46 [20541943] Curr Opin Chem Biol. 2010 Oct;14(5):652-9 [20822947] Genes Dev. 2010 Nov 15;24(22):2480-92 [21078817] J Natl Cancer Inst. 2010 Nov 17;102(22):1692-4 [21060063] Bioessays. 2011 Jan;33(1):30-4 [21053308] Nat Rev Genet. 2011 Jan;12(1):43-55 [21164524] J Mol Biol. 2011 Jan 14;405(2):479-96 [21075117] J Mol Biol. 2011 Jan 21;405(3):819-30 [21087615] J Chem Inf Model. 2011 Jan 24;51(1):69-82 [21117705] Proc Natl Acad Sci U S A. 2011 Jun 14;108(24):9981-6 [21628570] PLoS One. 2011;6(7):e22644 [21818358] PLoS One. 2011;6(9):e24712 [21961043] J Mol Biol. 2011 Dec 2;414(3):385-400 [22019736] PLoS One. 2011;6(12):e28611 [22194865] Front Biosci (Landmark Ed). 2012;17:473-97 [22201756] Semin Cell Dev Biol. 2012 Feb;23(1):109-15 [22040911] Cancer Metastasis Rev. 2012 Jun;31(1-2):353-73 [22549394] Adv Cancer Res. 2012;114:21-57 [22588055] Eur J Immunol. 2012 Jun;42(6):1562-72 [22622783] Curr Opin Virol. 2012 Jun;2(3):242-7 [22483665] J Mol Biol. 2012 Aug 10;421(2-3):172-84 [22119878] Cell Adh Migr. 2012 Mar-Apr;6(2):148-56 [22660185] J Phys Chem B. 2012 Jul 26;116(29):8692-702 [22536820] J Natl Cancer Inst. 2012 Aug 8;104(15):1182-97 [22829656] Curr Opin Struct Biol. 2012 Aug;22(4):421-31 [22664096] J Cell Mol Med. 2012 Dec;16(12):2894-909 [22862837] Pharmacol Res. 2013 Jan;67(1):42-52 [23098817] J Mol Biol. 2013 Feb 8;425(3):466-74 [23207294] Nat Commun. 2013;4:1438 [23385583] PLoS Comput Biol. 2013 Apr;9(4):e1003007 [23637583] Nat Struct Mol Biol. 2013 May;20(5):628-33 [23584454] Annu Rev Biophys. 2013;42:169-89 [23451894] Nat Struct Mol Biol. 2013 Aug;20(8):958-64 [23812375] Biochem J. 2013 Sep 15;454(3):361-9 [23988124] Cold Spring Harb Perspect Biol. 2013 Sep;5(9). pii: a009159. doi: 10.1101/cshperspect.a009159 [24003208] PLoS One. 2013;8(9):e74040 [24086308] Stem Cells Dev. 2013 Oct 15;22(20):2751-64 [23711177] Comput Biol Chem. 2013 Dec;47:126-41 [24076743] PLoS One. 2013;8(11):e81445 [24348920] Biophys Chem. 2014 Feb;186:22-30 [24239303] Proteins. 2014 Apr;82(4):546-55 [24085488] Protein Sci. 2000 Jan;9(1):10-9 [10739242] Neuron. 2000 Mar;25(3):563-74 [10774725] J Mol Biol. 2000 May 19;298(5):937-53 [10801360] Protein Sci. 2002 Feb;11(2):184-97 [11790828] Neuron. 2003 Jul 31;39(3):453-65 [12895420] Proteins. 2004 Aug 1;56(2):211-21 [15211506] FEBS Lett. 1980 Oct 20;120(1):107-9 [6777193] Science. 1987 Dec 18;238(4834):1717-20 [2825356] Trends Pharmacol Sci. 1996 May;17(5):189; 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AN - 1560584330; 25071153 AB - The acetyltransferase Gcn5 is critical for embryogenesis and shows partial functional redundancy with its homolog PCAF. However, the tissue- and cell lineage-specific functions of Gcn5 and PCAF are still not well defined. Here we probe the functions of Gcn5 and PCAF in adipogenesis. We found that the double knockout (DKO) of Gcn5/PCAF inhibits expression of the master adipogenic transcription factor gene PPARγ, thereby preventing adipocyte differentiation. The adipogenesis defects in Gcn5/PCAF DKO cells are rescued by ectopic expression of peroxisome proliferator-activated receptor γ (PPARγ), suggesting Gcn5/PCAF act upstream of PPARγ to facilitate adipogenesis. The requirement of Gcn5/PCAF for PPARγ expression was unexpectedly bypassed by prolonged treatment with an adipogenic inducer, 3-isobutyl-1-methylxanthine (IBMX). However, neither PPARγ ectopic expression nor prolonged IBMX treatment rescued defects in Prdm16 expression in DKO cells, indicating that Gcn5/PCAF are essential for normal Prdm16 expression. Gcn5/PCAF regulate PPARγ and Prdm16 expression at different steps in the transcription process, facilitating RNA polymerase II recruitment to Prdm16 and elongation of PPARγ transcripts. Overall, our study reveals that Gcn5/PCAF facilitate adipogenesis through regulation of PPARγ expression and regulate brown adipogenesis by influencing Prdm16 expression. Copyright © 2014, American Society for Microbiology. All Rights Reserved. JF - Molecular and cellular biology AU - Jin, Qihuang AU - Wang, Chaochen AU - Kuang, Xianghong AU - Feng, Xuesong AU - Sartorelli, Vittorio AU - Ying, Hao AU - Ge, Kai AU - Dent, Sharon Y R AD - Department of Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas M. D. Anderson Cancer Center, Smithville, Texas, USA Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA. ; Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA. ; Department of Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas M. D. Anderson Cancer Center, Smithville, Texas, USA. ; Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis, Musculoskeletal, and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA. ; Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. ; Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA kaig@niddk.nih.gov sroth@mdanderson.org. ; Department of Molecular Carcinogenesis, Center for Cancer Epigenetics, The University of Texas M. D. Anderson Cancer Center, Smithville, Texas, USA kaig@niddk.nih.gov sroth@mdanderson.org. Y1 - 2014/10/01/ PY - 2014 DA - 2014 Oct 01 SP - 3746 EP - 3753 VL - 34 IS - 19 KW - DNA-Binding Proteins KW - 0 KW - PPAR gamma KW - Phosphodiesterase Inhibitors KW - Prdm16 protein, mouse KW - Transcription Factors KW - p300-CBP Transcription Factors KW - EC 2.3.1.48 KW - RNA Polymerase III KW - EC 2.7.7.6 KW - 1-Methyl-3-isobutylxanthine KW - TBT296U68M KW - Index Medicus KW - Phosphodiesterase Inhibitors -- pharmacology KW - Animals KW - RNA Polymerase III -- physiology KW - Catalytic Domain KW - Mice KW - Gene Expression Regulation KW - 1-Methyl-3-isobutylxanthine -- pharmacology KW - Models, Biological KW - Adipocytes, Brown -- drug effects KW - Transcription Factors -- metabolism KW - p300-CBP Transcription Factors -- metabolism KW - DNA-Binding Proteins -- genetics KW - p300-CBP Transcription Factors -- genetics KW - PPAR gamma -- metabolism KW - Transcription Factors -- genetics KW - Adipogenesis -- drug effects KW - PPAR gamma -- genetics KW - DNA-Binding Proteins -- metabolism KW - Adipocytes, Brown -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560584330?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Gcn5+and+PCAF+regulate+PPAR%CE%B3+and+Prdm16+expression+to+facilitate+brown+adipogenesis.&rft.au=Jin%2C+Qihuang%3BWang%2C+Chaochen%3BKuang%2C+Xianghong%3BFeng%2C+Xuesong%3BSartorelli%2C+Vittorio%3BYing%2C+Hao%3BGe%2C+Kai%3BDent%2C+Sharon+Y+R&rft.aulast=Jin&rft.aufirst=Qihuang&rft.date=2014-10-01&rft.volume=34&rft.issue=19&rft.spage=3746&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=1098-5549&rft_id=info:doi/10.1128%2FMCB.00622-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-11 N1 - Date created - 2014-09-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: EMBO Rep. 2009 Sep;10(9):1009-14 [19633696] Cell. 2009 Sep 4;138(5):1019-31 [19698979] Cell Metab. 2010 Apr 7;11(4):257-62 [20374957] Genes Dev. 2010 May 15;24(10):1035-44 [20478996] Cell. 2010 Oct 1;143(1):156-69 [20887899] EMBO J. 2011 Jan 19;30(2):249-62 [21131905] EMBO J. 2011 Apr 20;30(8):1459-72 [21427703] Nat Rev Mol Cell Biol. 2011 Nov;12(11):722-34 [21952300] Mol Cell. 2012 Jan 27;45(2):255-62 [22196887] Cell Metab. 2012 Mar 7;15(3):395-404 [22405074] Biochim Biophys Acta. 2012 Jul;1819(7):727-32 [22240386] EMBO J. 2013 Jan 9;32(1):45-59 [23178591] Nat Cell Biol. 2012 Dec;14(12):1330-5 [23143398] Elife. 2013;2:e01503 [24368734] Cell. 2014 Jan 16;156(1-2):304-16 [24439384] Mol Cell Biol. 2000 Jan;20(2):556-62 [10611234] Nat Genet. 2000 Oct;26(2):229-32 [11017084] J Biol Chem. 2001 Aug 31;276(35):32627-34 [11418595] Mol Cell. 2001 Dec;8(6):1243-54 [11779500] Annu Rev Biochem. 2001;70:81-120 [11395403] J Biol Chem. 2002 May 10;277(19):16906-12 [11884404] EMBO J. 2004 Oct 27;23(21):4243-52 [15457216] Genes Dev. 1991 Oct;5(10):1754-66 [1655570] Proc Natl Acad Sci U S A. 2005 Jul 12;102(28):9766-71 [15985551] J Mol Endocrinol. 2006 Feb;36(1):139-51 [16461934] Cell Metab. 2006 Jun;3(6):429-38 [16753578] Cell Metab. 2006 Oct;4(4):263-73 [17011499] Nat Rev Mol Cell Biol. 2006 Dec;7(12):885-96 [17139329] Mol Cell. 2007 Jan 12;25(1):31-42 [17218269] Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2703-8 [17301242] Cell Metab. 2007 Jul;6(1):38-54 [17618855] Mol Cell Biol. 2008 Apr;28(7):2201-12 [18250157] Genes Dev. 2008 May 15;22(10):1269-75 [18483216] Nat Genet. 2008 Jul;40(7):897-903 [18552846] Nature. 2008 Aug 21;454(7207):961-7 [18719582] Genes Dev. 2009 Apr 1;23(7):849-61 [19339690] Trends Cell Biol. 2009 Apr;19(4):141-6 [19285866] Cell Metab. 2009 Jul;10(1):27-39 [19583951] Mol Cell. 2009 Aug 14;35(3):352-64 [19683498] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/MCB.00622-14 ER - TY - JOUR T1 - Cholinergic immunotoxin 192 IgG-SAPORIN alters subicular theta-gamma activity and impairs spatial learning in rats. AN - 1556290320; 24907423 AB - Subiculum is an important structure of hippocampal formation and is a part of intra hippocampal network involved in spatial information processing. However, relatively very few studies are available in literature demonstrating the explicit role of subiculum in spatial information processing. The present study investigated the cholinergic modulation of subicular theta-gamma activity on spatial learning and memory functions in rats. The cholinergic projections to ventral subiculum were selectively eliminated using 192 IgG-SAPORIN. Eliminations of cholinergic inputs to ventral subiculum significantly reduced the subicular theta and enhanced the gamma activity during active wake and REM sleep states. In addition, the spatial learning was severely impaired following cholinergic elimination of ventral subiculum. The ChAT immunocytochemical studies showed sparse distribution of cholinergic fibers in the ventral subiculum confirming the cholinergic elimination to ventral subiculum. Cholinotoxic infusions to ventral subiculum did not alter the hippocampal cholinergic innervations and retained the hippocampal theta and gamma activities. The present findings support that cholinergic modulation of subicular theta-gamma oscillations is crucial for spatial information processing. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Neurobiology of learning and memory AU - Rastogi, Shweta AU - Unni, Sumithra AU - Sharma, Sumit AU - Laxmi, T Rao AU - Kutty, Bindu M AD - Department of Neurophysiology, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India. ; Forensic and Medical Systems, Axxonet Systems Technologies Pvt. Ltd., Bangalore, India. ; Department of Neurophysiology, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India. Electronic address: bindu.nimhans@gmail.com. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 117 EP - 126 VL - 114 KW - 192 IgG-saporin KW - 0 KW - Antibodies, Monoclonal KW - Immunotoxins KW - Ribosome Inactivating Proteins, Type 1 KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Index Medicus KW - Cholinotoxin KW - Theta–gamma oscillations KW - Cholinergic projections KW - Spatial memory KW - Ventral subiculum KW - REM sleep KW - Rats KW - Animals KW - Rats, Wistar KW - Cholinergic Fibers -- drug effects KW - Choline O-Acetyltransferase -- metabolism KW - Male KW - Cholinergic Fibers -- metabolism KW - Spatial Learning -- drug effects KW - Hippocampus -- metabolism KW - Ribosome Inactivating Proteins, Type 1 -- pharmacology KW - Antibodies, Monoclonal -- pharmacology KW - Immunotoxins -- pharmacology KW - Theta Rhythm -- drug effects KW - Hippocampus -- drug effects KW - Gamma Rhythm -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556290320?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+learning+and+memory&rft.atitle=Cholinergic+immunotoxin+192+IgG-SAPORIN+alters+subicular+theta-gamma+activity+and+impairs+spatial+learning+in+rats.&rft.au=Rastogi%2C+Shweta%3BUnni%2C+Sumithra%3BSharma%2C+Sumit%3BLaxmi%2C+T+Rao%3BKutty%2C+Bindu+M&rft.aulast=Rastogi&rft.aufirst=Shweta&rft.date=2014-10-01&rft.volume=114&rft.issue=&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+learning+and+memory&rft.issn=1095-9564&rft_id=info:doi/10.1016%2Fj.nlm.2014.05.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-22 N1 - Date created - 2014-08-25 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.nlm.2014.05.008 ER - TY - JOUR T1 - The risk of amyotrophic lateral sclerosis after cancer in U.S. elderly adults: A population-based prospective study AN - 1551622049; 20290577 AB - Although epidemiologic studies have examined the risk of amyotrophic lateral sclerosis (ALS) in relation to cancer, none have been large population-based studies using incident ALS and adjusting for medical surveillance. Addressing those limitations, all first primary cancer cases from the Surveillance, Epidemiology and End Results (SEER) Program (1992-2005), linked to Medicare claims data were used. Cases were followed from cancer diagnosis until the earliest date of ALS diagnosis, a break in Medicare claims data, death, age 85 or December 31, 2005. A comparison group from a 5% random Medicare sample in the SEER areas who were cancer-free and censored as above, or until a cancer diagnosis were selected. ALS outcomes were derived from medical claims. The proportional hazards models to estimate ALS hazard ratios (HRs), using age as the time scale, adjusting for sex, race and physician visits, and stratifying the baseline hazard on birth year and SEER registry were used. A total of 303 ALS cases were ascertained in cancer patients (2,154,062 person-years) compared with 246 ALS cases (2,467,634 person-years) in the reference population. There was no overall relationship between cancer and ALS (HR = 0.99; 95% CI = 0.81-1.22), nor by gender or race. Except for an elevated ALS risk in the first year after a leukemia diagnosis, the relationship between site-specific cancers and ALS was null after correcting for multiple comparisons. Having a cancer diagnosis was not associated with an overall risk of incident ALS. The short-term ALS risk after leukemia may reflect screening or reporting errors. What's new? Studies suggest that incident Parkinson's disease and Alzheimer's disease are inversely associated with cancer, but whether the same is true for amyotrophic lateral sclerosis (ALS), another neurodegenerative disease, remains unclear. Here, following examination of incident ALS risk after cancer in a large population-based study that controlled for medical surveillance, no overall association was found to exist between cancer and ALS risk. Heightened screening or reporting errors may be responsible for the detection of elevated ALS risk in the first year following leukemia diagnosis. JF - International Journal of Cancer AU - Freedman, DMichal AU - Wu, Jincao AU - Daugherty, Sarah E AU - Kuncl, Ralph W AU - Enewold, Lindsey R AU - Pfeiffer, Ruth M AD - U.S. Department of Health and Human Services, National Institutes of Health, National Cancer Institute, Division of Cancer Epidemiology and Genetics, 9609 Medical Center Drive, Rockville, MD. Y1 - 2014/10// PY - 2014 DA - Oct 2014 SP - 1745 EP - 1750 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 135 IS - 7 SN - 0020-7136, 0020-7136 KW - Risk Abstracts KW - Health risks KW - Leukemia KW - Mortality KW - Age KW - Parkinson's disease KW - Alzheimer's disease KW - Gender KW - Elderly KW - Cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551622049?accountid=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=The+risk+of+amyotrophic+lateral+sclerosis+after+cancer+in+U.S.+elderly+adults%3A+A+population-based+prospective+study&rft.au=Freedman%2C+DMichal%3BWu%2C+Jincao%3BDaugherty%2C+Sarah+E%3BKuncl%2C+Ralph+W%3BEnewold%2C+Lindsey+R%3BPfeiffer%2C+Ruth+M&rft.aulast=Freedman&rft.aufirst=DMichal&rft.date=2014-10-01&rft.volume=135&rft.issue=7&rft.spage=1745&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28795 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-08-21 N1 - SubjectsTermNotLitGenreText - Mortality; Leukemia; Health risks; Age; Parkinson's disease; Gender; Alzheimer's disease; Elderly; Cancer DO - http://dx.doi.org/10.1002/ijc.28795 ER - TY - JOUR T1 - Maternal smoking during pregnancy and infant stress response: test of a prenatal programming hypothesis. AN - 1551025049; 24999830 AB - Maternal smoking during pregnancy (MSDP) is associated with early and long-term neurobehavioral deficits; however mechanisms remain unknown. We tested the hypothesis that MSDP programs the hypothalamic pituitary adrenocortical (HPA) axis of the offspring leading to adverse outcomes. In an intensive, prospective study, we investigated associations between MSDP and infant cortisol stress response and explored whether alterations in cortisol response were mediated by epigenetic modulation of the placental glucocorticoid receptor gene (NR3C1). Participants were 100 healthy mother-infant pairs (53% MSDP-exposed; 42% female) from a low income, racially/ethnically diverse sample (55% minorities). MSDP was assessed by timeline followback interview verified by saliva and meconium cotinine. Infant cortisol responses to a neurobehavioral exam were assessed seven times over the first postnatal month. Methylation of placental NR3C1 promoter exon 1F was assessed using bisulfite pyrosequencing in a subsample (n=45). MSDP-exposed infants showed significantly and persistently attenuated basal and reactive cortisol levels over the first postnatal month vs. unexposed infants. Exploratory analyses revealed that MSDP was associated with altered methylation of the placental NR3C1 promoter; degree of methylation of the placental NR3C1 was associated with infant basal and reactive cortisol over the first postnatal month and mediated effects of MSDP on infant basal cortisol. Results provide initial support for our hypothesis that MSDP programs offspring HPA (dys)regulation. Epigenetic regulation of placental GR may serve as a novel underlying mechanism. Results may have implications for delineating pathways to adverse outcomes from MSDP. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - Psychoneuroendocrinology AU - Stroud, Laura R AU - Papandonatos, George D AU - Rodriguez, Daniel AU - McCallum, Meaghan AU - Salisbury, Amy L AU - Phipps, Maureen G AU - Lester, Barry AU - Huestis, Marilyn A AU - Niaura, Raymond AU - Padbury, James F AU - Marsit, Carmen J AD - Department of Psychiatry and Human Behavior, Warren Alpert Medical School, Brown University, Providence, RI 02906, United States; Centers for Behavioral and Preventive Medicine, The Miriam Hospital, Providence, RI 02906, United States. Electronic address: Laura_Stroud@brown.edu. ; Department of Biostatistics, School of Public Health, Brown University, Providence, RI 02903, United States. ; Department of Public Health and Nutrition, School of Nursing and Health Sciences, La Salle University, Philadelphia, PA 19141, United States. ; Department of Psychology, Emory University, Atlanta, GA 30322, United States. ; Department of Psychiatry and Human Behavior, Warren Alpert Medical School, Brown University, Providence, RI 02906, United States; Department of Pediatrics, Warren Alpert Medical School, Brown University, Providence, RI 02903, United States; Women & Infants' Hospital of Rhode Island, Providence, RI 02905, United States. ; Women & Infants' Hospital of Rhode Island, Providence, RI 02905, United States; Department of Obstetrics and Gynecology, Warren Alpert Medical School, Brown University, Providence, RI 02905, United States. ; Chemistry and Drug Metabolism, Intramural Research Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, United States. ; Schroeder Institute for Tobacco Research and Policy Studies, American Legacy Foundation, Washington, DC 20036, United States. ; Department of Pediatrics, Warren Alpert Medical School, Brown University, Providence, RI 02903, United States; Women & Infants' Hospital of Rhode Island, Providence, RI 02905, United States. ; Department of Pharmacology and Toxicology, Dartmouth University, Hanover, NH 03755, United States. Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 29 EP - 40 VL - 48 KW - NR3C1 protein, human KW - 0 KW - Receptors, Glucocorticoid KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Infant KW - Smoking KW - Programming KW - Placenta KW - Cortisol KW - Tobacco KW - Stress KW - NR3C1 KW - Epigenetic KW - Pregnancy KW - Young Adult KW - Epigenesis, Genetic -- physiology KW - DNA Methylation KW - Humans KW - Adult KW - Infant, Newborn KW - Case-Control Studies KW - Hydrocortisone -- metabolism KW - Placenta -- metabolism KW - Adolescent KW - Receptors, Glucocorticoid -- metabolism KW - Receptors, Glucocorticoid -- genetics KW - Female KW - Smoking -- physiopathology KW - Prenatal Exposure Delayed Effects -- metabolism KW - Pregnancy Complications -- metabolism KW - Prenatal Exposure Delayed Effects -- psychology KW - Pregnancy Complications -- psychology KW - Smoking -- metabolism KW - Stress, Physiological -- genetics KW - Smoking -- adverse effects KW - Prenatal Exposure Delayed Effects -- physiopathology KW - Pregnancy Complications -- physiopathology KW - Embryonic Development -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551025049?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychoneuroendocrinology&rft.atitle=Maternal+smoking+during+pregnancy+and+infant+stress+response%3A+test+of+a+prenatal+programming+hypothesis.&rft.au=Stroud%2C+Laura+R%3BPapandonatos%2C+George+D%3BRodriguez%2C+Daniel%3BMcCallum%2C+Meaghan%3BSalisbury%2C+Amy+L%3BPhipps%2C+Maureen+G%3BLester%2C+Barry%3BHuestis%2C+Marilyn+A%3BNiaura%2C+Raymond%3BPadbury%2C+James+F%3BMarsit%2C+Carmen+J&rft.aulast=Stroud&rft.aufirst=Laura&rft.date=2014-10-01&rft.volume=48&rft.issue=&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=Psychoneuroendocrinology&rft.issn=1873-3360&rft_id=info:doi/10.1016%2Fj.psyneuen.2014.05.017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-16 N1 - Date created - 2014-08-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Neurotoxicology. 1996 Summer;17(2):351-8 [8856731] Epigenetics. 2008 Mar-Apr;3(2):97-106 [18536531] J Chromatogr B Biomed Sci Appl. 1998 Aug 21;713(1):137-46 [9700556] Curr Probl Pediatr. 1999 Feb;29(2):37-56 [10021686] J Neurol Neurosurg Psychiatry. 1960 Feb;23:56-62 [14399272] Neurosci Biobehav Rev. 2005 Apr;29(2):209-26 [15811494] Minerva Pediatr. 2005 Dec;57(6):359-71 [16402008] Child Dev. 2006 Jul-Aug;77(4):893-906 [16942496] Horm Behav. 2006 Nov;50(4):632-9 [16876168] BJOG. 2006 Nov;113(11):1289-95 [17014678] J Perinat Med. 2006;34(6):466-70 [17140296] Trends Mol Med. 2007 Jul;13(7):269-77 [17544850] N Engl J Med. 2008 Jul 3;359(1):61-73 [18596274] Dev Psychobiol. 2008 Dec;50(8):819-34 [18690653] J Pediatr. 2009 Jan;154(1):10-6 [18990408] Anal Bioanal Chem. 2009 Apr;393(8):1977-90 [19241063] J Perinat Med. 2009;37(4):364-9 [19290844] Psychoneuroendocrinology. 2009 Aug;34(7):953-67 [19321267] Curr Opin Neurol. 2009 Apr;22(2):121-5 [19532034] Am J Reprod Immunol. 2009 Aug;62(2):78-89 [19614624] Semin Reprod Med. 2009 Sep;27(5):358-68 [19711246] Neurotoxicol Teratol. 2009 Nov-Dec;31(6):356-63 [19619640] Ther Drug Monit. 2009 Dec;31(6):769-75 [19935364] Brain Res Bull. 2010 Apr 5;81(6):552-60 [19913076] Neurosci Biobehav Rev. 2010 May;34(6):853-66 [19631685] Am J Prev Med. 2010 Jul;39(1):45-52 [20547278] Metabolism. 2010 Oct;59(10):1481-90 [20462615] Epigenetics. 2011 May;6(5):566-72 [21521940] Nicotine Tob Res. 2011 Aug;13(8):627-37 [21778148] Am J Obstet Gynecol. 2000 Feb;182(2):465-72 [10694353] Annu Rev Neurosci. 2001;24:1161-92 [11520931] Pediatrics. 2003 Jun;111(6 Pt 1):1318-23 [12777547] Psychoneuroendocrinology. 2003 Oct;28(7):916-31 [12892658] Am J Psychiatry. 2003 Nov;160(11):1978-84 [14594744] Pediatrics. 2004 Mar;113(3 Pt 2):641-67 [14993524] Nat Neurosci. 2004 Aug;7(8):847-54 [15220929] Anal Biochem. 2004 Oct 1;333(1):119-27 [15351288] J Pers Soc Psychol. 1986 Dec;51(6):1173-82 [3806354] Am J Public Health. 1987 Nov;77(11):1435-8 [3661797] Life Sci. 1994;55(20):1567-75 [7968228] Brain Res Dev Brain Res. 1994 Dec 16;83(2):278-84 [7697884] Proc Natl Acad Sci U S A. 2011 Sep 20;108(38):15667-8 [21890794] Neuroscience. 2011 Dec 1;197:1-7 [22001683] PLoS One. 2012;7(1):e30148 [22295073] Epigenomics. 2012 Apr;4(2):115-8 [22449181] Transl Psychiatry. 2011;1:e21 [22832523] Epigenetics. 2012 Aug;7(8):853-7 [22810058] Front Neuroendocrinol. 2013 Jan;34(1):27-46 [23200813] Dev Psychobiol. 2013 Nov;55(7):673-83 [22714792] MMWR Surveill Summ. 2013 Nov 8;62(6):1-19 [24196750] Epigenomics. 2013 Dec;5(6):619-30 [24283877] Epigenetics. 2013 Dec;8(12):1321-9 [24135662] Psychol Addict Behav. 2014 Mar;28(1):154-62 [23276315] Natl Vital Stat Rep. 2012 Oct 3;61(5):1-18 [24979973] J Child Adolesc Psychiatr Nurs. 2013 Aug;26(3):193-203 [23909942] Reprod Toxicol. 2007 Jul;24(1):9-19 [17561370] J Pediatr Psychol. 1996 Dec;21(6):833-40 [8990727] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.psyneuen.2014.05.017 ER - TY - JOUR T1 - International Union of Basic and Clinical Pharmacology. XC. multisite pharmacology: recommendations for the nomenclature of receptor allosterism and allosteric ligands. AN - 1545776692; 25026896 AB - Allosteric interactions play vital roles in metabolic processes and signal transduction and, more recently, have become the focus of numerous pharmacological studies because of the potential for discovering more target-selective chemical probes and therapeutic agents. In addition to classic early studies on enzymes, there are now examples of small molecule allosteric modulators for all superfamilies of receptors encoded by the genome, including ligand- and voltage-gated ion channels, G protein-coupled receptors, nuclear hormone receptors, and receptor tyrosine kinases. As a consequence, a vast array of pharmacologic behaviors has been ascribed to allosteric ligands that can vary in a target-, ligand-, and cell-/tissue-dependent manner. The current article presents an overview of allostery as applied to receptor families and approaches for detecting and validating allosteric interactions and gives recommendations for the nomenclature of allosteric ligands and their properties. U.S. Government work not protected by U.S. copyright. JF - Pharmacological reviews AU - Christopoulos, Arthur AU - Changeux, Jean-Pierre AU - Catterall, William A AU - Fabbro, Doriano AU - Burris, Thomas P AU - Cidlowski, John A AU - Olsen, Richard W AU - Peters, John A AU - Neubig, Richard R AU - Pin, Jean-Philippe AU - Sexton, Patrick M AU - Kenakin, Terry P AU - Ehlert, Frederick J AU - Spedding, Michael AU - Langmead, Christopher J AD - Drug Discovery Biology and Department of Pharmacology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia (A.C., P.M.S., C.J.L.); Collège de France and CNRS URA 2182, Institut Pasteur, Paris, France (J.-P.C.); Department of Pharmacology, School of Medicine, University of Washington, Seattle, Washington (W.A.C.); PIQUR Therapeutics AG, Basel, Switzerland (D.F.); Department of Pharmacological & Physiological Science, Saint Louis University School of Medicine, St. Louis, Louisiana (T.P.B.); Signal Transduction Laboratory, Molecular Endocrinology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina (J.A.C.); Department of Molecular and Medical Pharmacology, University of California, Los Angeles, California (R.W.O.); Division of Neuroscience, School of Medicine, University of Dundee, Scotland, United Kingdom (J.A.P.); Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan (R.R.N.); Institut de Genomique Fonctionelle, CNRS, Montpellier, France (J.-P.P.); Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina (T.P.K.); Department of Pharmacology, University of California, Irvine, California (F.J.E.); and Research Solutions SARL, Paris, France (M.S.) arthur.christopoulos@monash.edu. ; Drug Discovery Biology and Department of Pharmacology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia (A.C., P.M.S., C.J.L.); Collège de France and CNRS URA 2182, Institut Pasteur, Paris, France (J.-P.C.); Department of Pharmacology, School of Medicine, University of Washington, Seattle, Washington (W.A.C.); PIQUR Therapeutics AG, Basel, Switzerland (D.F.); Department of Pharmacological & Physiological Science, Saint Louis University School of Medicine, St. Louis, Louisiana (T.P.B.); Signal Transduction Laboratory, Molecular Endocrinology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina (J.A.C.); Department of Molecular and Medical Pharmacology, University of California, Los Angeles, California (R.W.O.); Division of Neuroscience, School of Medicine, University of Dundee, Scotland, United Kingdom (J.A.P.); Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan (R.R.N.); Institut de Genomique Fonctionelle, CNRS, Montpellier, France (J.-P.P.); Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina (T.P.K.); Department of Pharmacology, University of California, Irvine, California (F.J.E.); and Research Solutions SARL, Paris, France (M.S.). Y1 - 2014/10// PY - 2014 DA - October 2014 SP - 918 EP - 947 VL - 66 IS - 4 KW - Ion Channels KW - 0 KW - Ligands KW - Receptors, Cytoplasmic and Nuclear KW - Receptors, G-Protein-Coupled KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Receptors, G-Protein-Coupled -- chemistry KW - Receptors, Cytoplasmic and Nuclear -- metabolism KW - Receptors, Cytoplasmic and Nuclear -- chemistry KW - Humans KW - Receptors, G-Protein-Coupled -- metabolism KW - Models, Chemical KW - Protein-Tyrosine Kinases -- metabolism KW - Protein-Tyrosine Kinases -- chemistry KW - Ion Channels -- metabolism KW - Allosteric Regulation -- drug effects KW - Terminology as Topic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1545776692?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacological+reviews&rft.atitle=International+Union+of+Basic+and+Clinical+Pharmacology.+XC.+multisite+pharmacology%3A+recommendations+for+the+nomenclature+of+receptor+allosterism+and+allosteric+ligands.&rft.au=Christopoulos%2C+Arthur%3BChangeux%2C+Jean-Pierre%3BCatterall%2C+William+A%3BFabbro%2C+Doriano%3BBurris%2C+Thomas+P%3BCidlowski%2C+John+A%3BOlsen%2C+Richard+W%3BPeters%2C+John+A%3BNeubig%2C+Richard+R%3BPin%2C+Jean-Philippe%3BSexton%2C+Patrick+M%3BKenakin%2C+Terry+P%3BEhlert%2C+Frederick+J%3BSpedding%2C+Michael%3BLangmead%2C+Christopher+J&rft.aulast=Christopoulos&rft.aufirst=Arthur&rft.date=2014-10-01&rft.volume=66&rft.issue=4&rft.spage=918&rft.isbn=&rft.btitle=&rft.title=Pharmacological+reviews&rft.issn=1521-0081&rft_id=info:doi/10.1124%2Fpr.114.008862 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-30 N1 - Date created - 2014-07-16 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/pr.114.008862 ER - TY - JOUR T1 - Quantitative high-throughput profiling of environmental chemicals and drugs that modulate farnesoid X receptor. AN - 1566408416; 25257666 AB - The farnesoid X receptor (FXR) regulates the homeostasis of bile acids, lipids, and glucose. Because endogenous chemicals bind and activate FXR, it is important to examine which xenobiotic compounds would disrupt normal receptor function. We used a cell-based human FXR β-lactamase (Bla) reporter gene assay to profile the Tox21 10K compound collection of environmental chemicals and drugs. Structure-activity relationships of FXR-active compounds revealed by this screening were then compared against the androgen receptor, estrogen receptor α, peroxisome proliferator-activated receptors δ and γ, and the vitamin D receptor. We identified several FXR-active structural classes including anthracyclines, benzimidazoles, dihydropyridines, pyrethroids, retinoic acids, and vinca alkaloids. Microtubule inhibitors potently decreased FXR reporter gene activity. Pyrethroids specifically antagonized FXR transactivation. Anthracyclines affected reporter activity in all tested assays, suggesting non-specific activity. These results provide important information to prioritize chemicals for further investigation, and suggest possible modes of action of compounds in FXR signaling. JF - Scientific reports AU - Hsu, Chia-Wen AU - Zhao, Jinghua AU - Huang, Ruili AU - Hsieh, Jui-Hua AU - Hamm, Jon AU - Chang, Xiaoqing AU - Houck, Keith AU - Xia, Menghang AD - National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC. ; Integrated Laboratory Systems, Inc., Morrisville, NC. ; U.S. Environmental Protection Agency, Research Triangle Park, NC. Y1 - 2014/09/26/ PY - 2014 DA - 2014 Sep 26 SP - 6437 VL - 4 KW - Bile Acids and Salts KW - 0 KW - DNA-Binding Proteins KW - Receptors, Cytoplasmic and Nuclear KW - Xenobiotics KW - farnesoid X-activated receptor KW - beta-Lactamases KW - EC 3.5.2.6 KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Lipid Metabolism -- drug effects KW - Promoter Regions, Genetic -- drug effects KW - Humans KW - HEK293 Cells KW - Glucose -- metabolism KW - Genes, Reporter KW - DNA-Binding Proteins -- genetics KW - Bile Acids and Salts -- metabolism KW - Signal Transduction KW - Binding Sites KW - beta-Lactamases -- biosynthesis KW - Xenobiotics -- pharmacology KW - Receptors, Cytoplasmic and Nuclear -- genetics KW - Xenobiotics -- toxicity KW - Receptors, Cytoplasmic and Nuclear -- biosynthesis KW - beta-Lactamases -- genetics KW - Structure-Activity Relationship UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566408416?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Quantitative+high-throughput+profiling+of+environmental+chemicals+and+drugs+that+modulate+farnesoid+X+receptor.&rft.au=Hsu%2C+Chia-Wen%3BZhao%2C+Jinghua%3BHuang%2C+Ruili%3BHsieh%2C+Jui-Hua%3BHamm%2C+Jon%3BChang%2C+Xiaoqing%3BHouck%2C+Keith%3BXia%2C+Menghang&rft.aulast=Hsu&rft.aufirst=Chia-Wen&rft.date=2014-09-26&rft.volume=4&rft.issue=&rft.spage=6437&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep06437 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-21 N1 - Date created - 2014-09-26 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep06437 ER - TY - JOUR T1 - Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis. AN - 1564354749; 25242624 AB - Di-(2-ethylhexyl)-phthalate (DEHP) is a ubiquitously used endocrine disruptor.There is widespread exposure to DEHP in the general population which has raised substantial public concern due to its potential detrimental health effects. It is particularly pertinent to investigate the molecular mechanisms of its testicular toxicity which are largely unknown. By feeding male rats DEHP for 2 weeks, rat spermatogenesis became disrupted, resulting in a decreased number of spermatocytes and spermatids. Since rapidly dividing tissues appeared to be particularly vulnerable to DEHP toxicity we investigated the effect of DEHP on DNA replication. Intriguingly, DEHP appeared to inhibit DNA replication as evidenced by results of fiber tract analysis. This led to induction of the mitochondrial apoptotic pathways and increased ROS production. Furthermore, the toxicity of DEHP led to respiratory chain defects and attenuation of ATP level probably brought about by hyperPARylation and undermined SIRT1 activity. Our findings reveal a previously unknown mitochondrial dysfunction in DEHP-induced testicular toxicity and highlight the importance of SIRT1 in male reproduction. JF - Scientific reports AU - Li, Xiaolin AU - Fang, Evandro Fei AU - Scheibye-Knudsen, Morten AU - Cui, Honghua AU - Qiu, Lu AU - Li, Jian AU - He, Yuping AU - Huang, Jing AU - Bohr, Vilhelm A AU - Ng, Tzi Bun AU - Guo, Hongwei AD - 1] School of Public Health, Fudan University, Shanghai, 200032, China [2] Shanghai Entry-Exit Inspection and Quarantine Bureau, Shanghai, 200135, China [3]. ; 1] Laboratory of Molecular Gerontology, National Institute on Ageing, National Institutes of Health, Baltimore, MD USA [2] School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, Shatin, New Territories, Hong Kong [3]. ; Laboratory of Molecular Gerontology, National Institute on Ageing, National Institutes of Health, Baltimore, MD USA. ; Shanghai Stomatological Disease Centre. Shanghai, 200001, PR China. ; Shanghai Entry-Exit Inspection and Quarantine Bureau, Shanghai, 200135, China. ; School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, Shatin, New Territories, Hong Kong. ; School of Public Health, Fudan University, Shanghai, 200032, China. Y1 - 2014/09/22/ PY - 2014 DA - 2014 Sep 22 SP - 6434 VL - 4 KW - Sirt1 protein, rat KW - EC 3.5.1.- KW - Sirtuin 1 KW - Index Medicus KW - Rats KW - Animals KW - Testis -- drug effects KW - Reproduction -- drug effects KW - Reproduction -- genetics KW - Humans KW - Male KW - Spermatogenesis -- genetics KW - Sirtuin 1 -- biosynthesis KW - DNA Replication -- genetics KW - Mitochondria -- pathology KW - Mitochondria -- drug effects KW - Spermatogenesis -- drug effects KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1564354749?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Di-%282-ethylhexyl%29+phthalate+inhibits+DNA+replication+leading+to+hyperPARylation%2C+SIRT1+attenuation%2C+and+mitochondrial+dysfunction+in+the+testis.&rft.au=Li%2C+Xiaolin%3BFang%2C+Evandro+Fei%3BScheibye-Knudsen%2C+Morten%3BCui%2C+Honghua%3BQiu%2C+Lu%3BLi%2C+Jian%3BHe%2C+Yuping%3BHuang%2C+Jing%3BBohr%2C+Vilhelm+A%3BNg%2C+Tzi+Bun%3BGuo%2C+Hongwei&rft.aulast=Li&rft.aufirst=Xiaolin&rft.date=2014-09-22&rft.volume=4&rft.issue=&rft.spage=6434&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep06434 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-06 N1 - Date created - 2014-09-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Occup Health. 2008;50(2):169-80 [18403868] Int J Hyg Environ Health. 2007 Oct;210(5):623-34 [17889607] Nat Rev Cancer. 2009 Feb;9(2):123-8 [19132007] NTP CERHR MON. 2006 Nov;(18):v, vii-7, II-iii-xiii passim [19407857] Diabetes. 2010 Apr;59(4):829-35 [20107110] Nucleic Acids Res. 2010 Nov;38(21):7458-71 [20660480] Environ Res. 2011 Apr;111(3):329-36 [21315328] Cancer Prev Res (Phila). 2012 Jan;5(1):109-21 [21933914] FASEB J. 2012 Feb;26(2):555-66 [22006156] Endocr Regul. 2012 Jan;46(1):37-46 [22329821] Arch Environ Contam Toxicol. 2012 Apr;62(3):539-47 [22002783] J Exp Med. 2012 Apr 9;209(4):855-69 [22473955] Biol Res. 2012;45(1):5-14 [22688978] Food Chem Toxicol. 2012 Jul;50(7):2424-31 [22542555] PLoS One. 2012;7(11):e50465 [23226291] Annu Rev Public Health. 2013;34:139-58 [23514318] Arch Toxicol. 2013 Apr;87(4):735-51 [23192238] Int J Hyg Environ Health. 2013 Jul;216(4):472-80 [23394848] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2013;30(4):735-42 [23641808] Food Chem Toxicol. 2013 Aug;58:362-8 [23684997] Mol Cell. 2013 Nov 7;52(3):434-46 [24207054] Cell. 2014 May 8;157(4):882-96 [24813611] Int Arch Occup Environ Health. 2014 Aug;87(6):635-46 [23995610] Autophagy. 2014 Aug;10(8):1468-9 [24991831] Toxicol Sci. 2001 Aug;62(2):236-49 [11452136] Toxicology. 2002 Feb 28;171(2-3):105-15 [11836017] Environ Health Perspect. 2003 Jul;111(9):1164-9 [12842768] Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):775-80 [14715905] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6570-5 [15100410] Toxicol Appl Pharmacol. 1975 Feb;31(2):283-9 [1129799] Hepatology. 1995 May;21(5):1465-8 [7737654] J Cell Sci. 1995 Feb;108 ( Pt 2):747-53 [7769016] Cell. 1995 Jun 2;81(5):801-9 [7774019] Environ Health Perspect. 1996 Aug;104 Suppl 4:715-40 [8880000] Hum Reprod. 1999 Mar;14(3):694-7 [10221697] Clin Chim Acta. 2005 Nov;361(1-2):20-9 [16004980] Occup Environ Med. 2005 Nov;62(11):806-18 [16234408] Int J Androl. 2006 Feb;29(1):134-9; discussion 181-5 [16466533] Int J Androl. 2006 Feb;29(1):155-65; discussion 181-5 [16466535] Risk Anal. 2006 Jun;26(3):803-24 [16834635] Proc Natl Acad Sci U S A. 2006 Oct 10;103(41):15148-53 [17005726] Toxicology. 2006 Nov 10;228(1):85-97 [16996189] Hum Reprod. 2007 Mar;22(3):688-95 [17090632] Environ Res. 2008 Oct;108(2):177-84 [18949837] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep06434 ER - TY - JOUR T1 - Single-molecule sequencing to track plasmid diversity of hospital-associated carbapenemase-producing Enterobacteriaceae AN - 1727695220; PQ0002040669 AB - Public health officials have raised concerns that plasmid transfer between Enterobacteriaceae species may spread resistance to carbapenems, an antibiotic class of last resort, thereby rendering common health care-associated infections nearly impossible to treat. To determine the diversity of carbapenemase-encoding plasmids and assess their mobility among bacterial species, we performed comprehensive surveillance and genomic sequencing of carbapenem-resistant Enterobacteriaceae in the National Institutes of Health (NIH) Clinical Center patient population and hospital environment. We isolated a repertoire of carbapenemase-encoding Enterobacteriaceae, including multiple strains of Klebsiella pneumoniae, Klebsiella oxytoca, Escherichia coli, Enterobacter cloacae, Citrobacter freundii, and Pantoea species. Long-read genome sequencing with full end-to-end assembly revealed that these organisms carry the carbapenem resistance genes on a wide array of plasmids. K. pneumoniae and E. cloacae isolated simultaneously from a single patient harbored two different carbapenemase-encoding plasmids, indicating that plasmid transfer between organisms was unlikely within this patient. We did, however, find evidence of horizontal transfer of carbapenemase-encoding plasmids between K. pneumoniae, E. cloacae, and C. freundii in the hospital environment. Our data, including full plasmid identification, challenge assumptions about horizontal gene transfer events within patients and identify possible connections between patients and the hospital environment. In addition, we identified a new carbapenemase-encoding plasmid of potentially high clinical impact carried by K. pneumoniae, E. coli, E. cloacae, and Pantoea species, in unrelated patients and in the hospital environment. JF - Science Translational Medicine AU - Conlan, Sean AU - Thomas, Pamela J AU - Deming, Clayton AU - Park, Morgan AU - Lau, Anna F AU - Dekker, John P AU - Snitkin, Evan S AU - Clark, Tyson A AU - Luong, Khai AU - Song, Yi AD - National Human Genome Research Institute, Bethesda, MD 20892, USA Y1 - 2014/09/17/ PY - 2014 DA - 2014 Sep 17 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 6 IS - 254 SN - 1946-6234, 1946-6234 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - Genomes KW - Translation KW - Data processing KW - Mobility KW - Citrobacter freundii KW - Carbapenems KW - Antibiotics KW - Plasmids KW - Infection KW - Horizontal transfer KW - Public health KW - Enterobacter cloacae KW - Escherichia coli KW - Klebsiella oxytoca KW - genomics KW - Enterobacteriaceae KW - Klebsiella pneumoniae KW - Hospitals KW - J 02400:Human Diseases KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727695220?accountid=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=Science+Translational+Medicine&rft.atitle=Single-molecule+sequencing+to+track+plasmid+diversity+of+hospital-associated+carbapenemase-producing+Enterobacteriaceae&rft.au=Conlan%2C+Sean%3BThomas%2C+Pamela+J%3BDeming%2C+Clayton%3BPark%2C+Morgan%3BLau%2C+Anna+F%3BDekker%2C+John+P%3BSnitkin%2C+Evan+S%3BClark%2C+Tyson+A%3BLuong%2C+Khai%3BSong%2C+Yi&rft.aulast=Conlan&rft.aufirst=Sean&rft.date=2014-09-17&rft.volume=6&rft.issue=254&rft.spage=254ra126&rft.isbn=&rft.btitle=&rft.title=Science+Translational+Medicine&rft.issn=19466234&rft_id=info:doi/10.1126%2Fscitranslmed.3009845 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Genomes; Translation; Data processing; Mobility; Carbapenems; Antibiotics; genomics; Infection; Plasmids; Horizontal transfer; Public health; Hospitals; Enterobacter cloacae; Citrobacter freundii; Escherichia coli; Klebsiella oxytoca; Enterobacteriaceae; Klebsiella pneumoniae DO - http://dx.doi.org/10.1126/scitranslmed.3009845 ER - TY - JOUR T1 - The Role of Age on Dose-Limiting Toxicities in Phase I Dose-Escalation Trials AN - 1808635150; PQ0003448822 AB - Purpose: Elderly oncology patients are not enrolled in early-phase trials in proportion to the numbers of geriatric patients with cancer. There may be concern that elderly patients will not tolerate investigational agents as well as younger patients, resulting in a disproportionate number of dose-limiting toxicities (DLT). Recent single-institution studies provide conflicting data on the relationship between age and DLT.Experimental Design: We retrospectively reviewed data about patients treated on single-agent, dose-escalation, phase I clinical trials sponsored by the Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute. Patients' dose levels were described as a percentage of maximum tolerated dose, the highest dose level at which <33% of patients had a DLT, or recommended phase II dose (RP2D). Mixed-effect logistic regression models were used to analyze relationships between the probability of a DLT and age and other explanatory variables.Results: Increasing dose, increasing age, and worsening performance status (PS) were significantly related to an increased probability of a DLT in this model (P < 0.05). There was no association between dose level administered and age (P = 0.57).Conclusions: This analysis of phase I dose-escalation trials, involving more than 500 patients older than 70 years of age, is the largest reported. As age and dose level increased and PS worsened, the probability of a DLT increased. Although increasing age was associated with occurrence of DLT, this risk remained within accepted thresholds of risk for phase I trials. There was no evidence of age bias on enrollment of patients on low or high dose levels. Clin Cancer Res; 20(18); 4768-75. copyright 2014 AACR. JF - Clinical Cancer Research AU - Schwandt, A AU - Harris, P J AU - Hunsberger, S AU - Deleporte, A AU - Smith, G L AU - Vulih, D AU - Anderson, B D AU - Ivy, S P AD - Case Western Reserve School of Medicine, Cleveland, Ohio, ivyp@ctep.nci.nih.gov Y1 - 2014/09/15/ PY - 2014 DA - 2014 Sep 15 SP - 4768 EP - 4775 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 20 IS - 18 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Age KW - Data processing KW - Geriatrics KW - Regression analysis KW - Oncology KW - Toxicity KW - Clinical trials KW - Cancer KW - Models KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808635150?accountid=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=The+Role+of+Age+on+Dose-Limiting+Toxicities+in+Phase+I+Dose-Escalation+Trials&rft.au=Schwandt%2C+A%3BHarris%2C+P+J%3BHunsberger%2C+S%3BDeleporte%2C+A%3BSmith%2C+G+L%3BVulih%2C+D%3BAnderson%2C+B+D%3BIvy%2C+S+P&rft.aulast=Schwandt&rft.aufirst=A&rft.date=2014-09-15&rft.volume=20&rft.issue=18&rft.spage=4768&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-0866 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Age; Data processing; Regression analysis; Geriatrics; Oncology; Toxicity; Clinical trials; Cancer; Models DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-0866 ER - TY - JOUR T1 - Is the "3+3" dose-escalation phase I clinical trial design suitable for therapeutic cancer vaccine development? A recommendation for alternative design. AN - 1562663788; 25037736 AB - Phase I clinical trials are generally conducted to identify the maximum tolerated dose (MTD) or the biologically active dose (BAD) using a traditional dose-escalation design. This design may not be applied to cancer vaccines, given their unique mechanism of action. The FDA recently published "Guidance for Industry: Clinical Considerations for Therapeutic Cancer Vaccines." However, many questions about the design of cancer vaccine studies remain unanswered. We analyzed the toxicity profile in 239 phase I therapeutic cancer vaccine trials. We addressed the ability of dose escalation to determine the MTD or the BAD in trials that used a dose-escalation design. The rate of grade 3/4 vaccine-related systemic toxicities was 1.25 adverse events per 100 patients and 2 per 1,000 vaccines. Only two of the 127 dose-escalation trials reported vaccine-related dose limiting toxicities, both of which used bacterial vector vaccines. Out of the 116 trials analyzed for the dose-immune response relationship, we found a statistically significant dose-immune response correlation only when the immune response was measured by antibodies (P < 0.001) or delayed type hypersensitivity (P < 0.05). However, the increase in cellular immune response did not appear further sustainable with the continued increase in dose. Our analysis suggests that the risks of serious toxicities with therapeutic cancer vaccines are extremely low and that toxicities do not correlate with dose levels. Accordingly, the conventional dose-escalation design is not suitable for cancer vaccines with few exceptions. Here, we propose an alternative design for therapeutic cancer vaccine development. ©2014 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Rahma, Osama E AU - Gammoh, Emily AU - Simon, Richard M AU - Khleif, Samir N AD - Vaccine Branch, National Cancer Institute, Bethesda, Maryland. Division of Hematology/Oncology, University of Virginia, Charlottesville, Virginia. ; Vaccine Branch, National Cancer Institute, Bethesda, Maryland. ; Biometric Research Branch, National Cancer Institute, Rockville, Maryland. ; Vaccine Branch, National Cancer Institute, Bethesda, Maryland. Georgia Health Sciences Cancer Center, Augusta, Georgia. skhleif@gru.edu. Y1 - 2014/09/15/ PY - 2014 DA - 2014 Sep 15 SP - 4758 EP - 4767 VL - 20 IS - 18 SN - 1078-0432, 1078-0432 KW - Cancer Vaccines KW - 0 KW - Index Medicus KW - Humans KW - Clinical Trials, Phase I as Topic -- methods KW - Neoplasms -- drug therapy KW - Cancer Vaccines -- administration & dosage KW - Clinical Trials, Phase I as Topic -- standards KW - Research Design -- standards UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562663788?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Is+the+%223%2B3%22+dose-escalation+phase+I+clinical+trial+design+suitable+for+therapeutic+cancer+vaccine+development%3F+A+recommendation+for+alternative+design.&rft.au=Rahma%2C+Osama+E%3BGammoh%2C+Emily%3BSimon%2C+Richard+M%3BKhleif%2C+Samir+N&rft.aulast=Rahma&rft.aufirst=Osama&rft.date=2014-09-15&rft.volume=20&rft.issue=18&rft.spage=4758&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-13-2671 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-31 N1 - Date created - 2014-09-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Immunother. 2007 Feb-Mar;30(2):227-33 [17471169] J Immunother. 2007 Jan;30(1):1-15 [17198079] Cancer Biol Ther. 2008 Apr;7(4):488-95 [18285705] Cancer. 2008 Sep 1;113(5):975-84 [18646045] J Clin Oncol. 2008 Oct 20;26(30):4973-80 [18809608] Clin Cancer Res. 2009 Feb 15;15(4):1443-51 [19228745] Vaccine. 2009 Jun 19;27(30):3975-83 [19389451] J Clin Oncol. 2009 Nov 1;27(31):5270-7 [19752336] Cancer Res. 2010 Feb 1;70(3):875-82 [20103634] Clin Cancer Res. 2010 Feb 15;16(4):1289-97 [20145187] Stat Med. 2010 Mar 30;29(7-8):712-20 [20213706] Cancer Immunol Immunother. 2010 Jun;59(6):863-73 [20043222] J Clin Oncol. 2011 Feb 20;29(6):601-3 [21245434] Cancer Immunol Immunother. 2011 Mar;60(3):433-42 [21221967] Expert Rev Vaccines. 2011 Mar;10(3):299-306 [21434798] OMICS. 2011 Sep;15(9):579-88 [21732821] Cancer Immunol Immunother. 2012 Mar;61(3):373-84 [21927947] Semin Oncol. 2012 Jun;39(3):323-39 [22595055] J Clin Oncol. 2000 Feb;18(3):684-92 [10653884] Blood. 2000 Mar 1;95(5):1781-7 [10688838] Clin Cancer Res. 2000 Jun;6(6):2219-28 [10873071] Clin Cancer Res. 2000 Dec;6(12):4719-24 [11156225] J Clin Oncol. 2001 Jan 1;19(1):265-72 [11134222] J Immunother. 2002 Mar-Apr;25(2):97-138 [12074049] J Clin Oncol. 2002 Oct 15;20(20):4225-31 [12377966] Oncologist. 2002;7(5):401-9 [12401902] Hum Gene Ther. 2003 Jul 20;14(11):1117-23 [12885350] J Natl Cancer Inst. 2004 Feb 18;96(4):326-31 [14970281] Proc Natl Acad Sci U S A. 2004 Sep 21;101(38):13885-90 [15365188] Ann Oncol. 1996 Aug;7(6):567-73 [8879369] J Immunother. 2004 Nov-Dec;27(6):442-51 [15534488] N Engl J Med. 2005 Mar 3;352(9):895-904 [15745980] Stat Med. 2005 Jul 30;24(14):2171-81 [15909289] Cancer Immunol Immunother. 2005 Sep;54(9):848-57 [15754205] Cancer Treat Res. 2005;123:339-50 [16211877] Cancer Res. 2006 Apr 15;66(8):4496-502 [16618777] Br J Clin Pharmacol. 2006 Jul;62(1):15-26 [16842375] J Immunother. 2008 Feb-Mar;31(2):215-23 [18481391] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-2671 ER - TY - JOUR T1 - Mitochondrial topoisomerase I (top1mt) is a novel limiting factor of doxorubicin cardiotoxicity. AN - 1562663778; 24714774 AB - Doxorubicin is one of the most effective chemotherapeutic agents. However, up to 30% of the patients treated with doxorubicin suffer from congestive heart failure. The mechanism of doxorubicin cardiotoxicity is likely multifactorial and most importantly, the genetic factors predisposing to doxorubicin cardiotoxicity are unknown. On the basis of the fact that mtDNA lesions and mitochondrial dysfunctions have been found in human hearts exposed to doxorubicin and that mitochondrial topoisomerase 1 (Top1mt) specifically controls mtDNA homeostasis, we hypothesized that Top1mt knockout (KO) mice might exhibit hypersensitivity to doxorubicin. Wild-type (WT) and KO Top1mt mice were treated once a week with 4 mg/kg doxorubicin for 8 weeks. Heart tissues were analyzed one week after the last treatment. Genetic inactivation of Top1mt in mice accentuates mtDNA copy number loss and mtDNA damage in heart tissue following doxorubicin treatment. Top1mt KO mice also fail to maintain respiratory chain protein production and mitochondrial cristae ultrastructure organization. These mitochondrial defects result in decreased O2 consumption, increased reactive oxygen species production, and enhanced heart muscle damage in animals treated with doxorubicin. Accordingly, Top1mt KO mice die within 45 days after the last doxorubicin injection, whereas the WT mice survive. Our results provide evidence that Top1mt, which is conserved across vertebrates, is critical for cardiac tolerance to doxorubicin and adaptive response to doxorubicin cardiotoxicity. They also suggest the potential of Top1mt single-nucleotide polymorphisms testing to investigate patient susceptibility to doxorubicin-induced cardiotoxicity. ©2014 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Khiati, Salim AU - Dalla Rosa, Ilaria AU - Sourbier, Carole AU - Ma, Xuefei AU - Rao, V Ashutosh AU - Neckers, Leonard M AU - Zhang, Hongliang AU - Pommier, Yves AD - Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology; ; Urologic Oncology Branch, Center for Cancer Research, National Cancer Institute; ; Laboratory of Molecular Cardiology, National Heart, Lung, and Blood Institute, NIH; and. ; Center for Drug Evaluation and Research, Food and Drug Administration, Bethesda, Maryland. ; Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology; pommier@nih.gov. Y1 - 2014/09/15/ PY - 2014 DA - 2014 Sep 15 SP - 4873 EP - 4881 VL - 20 IS - 18 SN - 1078-0432, 1078-0432 KW - Antibiotics, Antineoplastic KW - 0 KW - DNA, Mitochondrial KW - Doxorubicin KW - 80168379AG KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - Index Medicus KW - Animals KW - DNA, Mitochondrial -- drug effects KW - Blotting, Western KW - DNA, Mitochondrial -- metabolism KW - Mice KW - Fluorescent Antibody Technique KW - Mice, Knockout KW - Mitochondria, Heart -- enzymology KW - Mitochondria, Heart -- drug effects KW - Doxorubicin -- toxicity KW - Cardiotoxicity -- enzymology KW - DNA Topoisomerases, Type I -- metabolism KW - Antibiotics, Antineoplastic -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562663778?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mitochondrial+topoisomerase+I+%28top1mt%29+is+a+novel+limiting+factor+of+doxorubicin+cardiotoxicity.&rft.au=Khiati%2C+Salim%3BDalla+Rosa%2C+Ilaria%3BSourbier%2C+Carole%3BMa%2C+Xuefei%3BRao%2C+V+Ashutosh%3BNeckers%2C+Leonard+M%3BZhang%2C+Hongliang%3BPommier%2C+Yves&rft.aulast=Khiati&rft.aufirst=Salim&rft.date=2014-09-15&rft.volume=20&rft.issue=18&rft.spage=4873&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-13-3373 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-31 N1 - Date created - 2014-09-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cell Biol Toxicol. 2007 Jan;23(1):15-25 [17009097] Curr Cancer Drug Targets. 2006 Nov;6(7):579-602 [17100565] Mutat Res. 2007 Oct 1;623(1-2):83-97 [17681352] Biochemistry. 2008 Oct 28;47(43):11196-203 [18826252] Biochem Biophys Res Commun. 2009 Jan 16;378(3):450-5 [19032935] Biophys J. 2009 Feb 18;96(4):1388-98 [19217856] Nat Rev Cancer. 2009 May;9(5):338-50 [19377506] Antioxid Redox Signal. 2009 Nov;11(11):2685-700 [19558212] Methods. 2010 Aug;51(4):444-51 [20123023] Proc Natl Acad Sci U S A. 2010 Nov 16;107(46):19790-5 [21041670] Cold Spring Harb Protoc. 2011 May;2011(5):pdb.prot5623 [21536757] PLoS One. 2011;6(7):e21746 [21799747] Am J Physiol Heart Circ Physiol. 2011 Dec;301(6):H2181-90 [21949114] Nat Rev Drug Discov. 2012 Jan;11(1):25-36 [22173432] J Clin Oncol. 2012 May 1;30(13):1415-21 [22124095] Tex Heart Inst J. 2012;39(3):424-7 [22719160] PLoS One. 2012;7(7):e41094 [22911747] Nat Med. 2012 Nov;18(11):1639-42 [23104132] J Biol Chem. 2013 Jan 11;288(2):915-26 [23152496] ACS Chem Biol. 2013 Jan 18;8(1):82-95 [23259582] Biochemistry (Mosc). 2012 Dec;77(13):1424-35 [23379519] PLoS One. 2013;8(8):e70575 [23940596] Life Sci. 2001 Jan 12;68(8):889-901 [11213359] Adv Drug Deliv Rev. 2001 Jul 2;49(1-2):87-105 [11377805] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10608-13 [11526219] Cardiovasc Toxicol. 2001;1(4):267-83 [12213966] Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12114-9 [12209014] Eur J Biochem. 2003 Oct;270(20):4173-86 [14519130] Circulation. 2003 Nov 11;108(19):2423-9 [14568902] N Engl J Med. 2004 Jul 8;351(2):120-1 [15247351] J Biol Chem. 2004 Sep 3;279(36):37575-87 [15220329] Biochim Biophys Acta. 1978 Jun 22;519(1):23-30 [566561] J Clin Invest. 1980 Jan;65(1):128-35 [7350193] Am J Pathol. 1980 Apr;99(1):13-42 [7361854] Biochem Biophys Res Commun. 1982 Jan 15;104(1):314-20 [6280691] Science. 1984 Oct 26;226(4673):466-8 [6093249] Am J Cardiol. 1985 Jul 1;56(1):157-61 [4014022] Biochemistry. 1987 Feb 24;26(4):1152-63 [3567161] Biochim Biophys Acta. 1987 Jul 22;892(3):320-30 [3036220] Biochem J. 1987 Jul 1;245(1):309-12 [3663157] Virchows Arch A Pathol Anat Histopathol. 1987;412(1):47-52 [3120403] Nucleic Acids Res. 1990 Nov 25;18(22):6611-9 [2174543] Biochim Biophys Acta. 1992 Aug 17;1132(1):43-8 [1380833] Semin Oncol. 1992 Dec;19(6):670-86 [1462166] Biochem Biophys Res Commun. 1993 Sep 15;195(2):945-51 [8373427] Semin Oncol. 1996 Aug;23(4 Suppl 8):23-34 [8783663] Biochim Biophys Acta. 1997 Aug 22;1321(2):101-6 [9332499] J Pathol. 2005 Dec;207(4):436-44 [16278810] Cardiovasc Toxicol. 2007;7(2):108-13 [17652814] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-3373 ER - TY - CPAPER T1 - Mitigation of Radiation Induced Pulmonary Injury with Systemic Delivery of Mesenchymal Stem Cells T2 - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014) AN - 1645181593; 6319308 JF - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014) AU - Scroggins, Bradley Y1 - 2014/09/14/ PY - 2014 DA - 2014 Sep 14 KW - Stem cells KW - Mitigation KW - Injuries KW - Radiation KW - Lung KW - Mesenchyme UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645181593?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.atitle=Mitigation+of+Radiation+Induced+Pulmonary+Injury+with+Systemic+Delivery+of+Mesenchymal+Stem+Cells&rft.au=Scroggins%2C+Bradley&rft.aulast=Scroggins&rft.aufirst=Bradley&rft.date=2014-09-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://online.myiwf.com/astro2014/Abstract.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Radiation Enhancement of Head and Neck Squamous Cell Carcinoma by the Dual PI3K/mTOR Inhibitor PF-05212384 T2 - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014) AN - 1645181412; 6319419 JF - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014) AU - Leiker, Andrew Y1 - 2014/09/14/ PY - 2014 DA - 2014 Sep 14 KW - 1-Phosphatidylinositol 3-kinase KW - Radiation KW - Head and neck cancer KW - Inhibitors KW - squamous cell carcinoma KW - Tumors KW - TOR protein UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645181412?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.atitle=Radiation+Enhancement+of+Head+and+Neck+Squamous+Cell+Carcinoma+by+the+Dual+PI3K%2FmTOR+Inhibitor+PF-05212384&rft.au=Leiker%2C+Andrew&rft.aulast=Leiker&rft.aufirst=Andrew&rft.date=2014-09-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://online.myiwf.com/astro2014/Abstract.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Il-13 is a Critical Mediator of Radiation-Induced Pulmonary Fibrosis T2 - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014) AN - 1645179122; 6319310 JF - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014) AU - Citrin, Deborah Y1 - 2014/09/14/ PY - 2014 DA - 2014 Sep 14 KW - Interleukin 13 KW - Fibrosis KW - Lung diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645179122?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.atitle=Il-13+is+a+Critical+Mediator+of+Radiation-Induced+Pulmonary+Fibrosis&rft.au=Citrin%2C+Deborah&rft.aulast=Citrin&rft.aufirst=Deborah&rft.date=2014-09-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://online.myiwf.com/astro2014/Abstract.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - CPAPER T1 - Interim Analysis Results Of A Phase II Trial Of Low Dose Radiotherapy For Palliation Of Diffuse Large B Cell Lymphoma T2 - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014) AN - 1645168132; 6319148 JF - 56th Annual Meeting of the American Society for Therapeutic Radiology and Oncology (ASTRO 2014) AU - Furlan, Carlo Y1 - 2014/09/14/ PY - 2014 DA - 2014 Sep 14 KW - B-cell lymphoma KW - Radiotherapy KW - Lymphoma KW - Palliation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645168132?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.atitle=Interim+Analysis+Results+Of+A+Phase+II+Trial+Of+Low+Dose+Radiotherapy+For+Palliation+Of+Diffuse+Large+B+Cell+Lymphoma&rft.au=Furlan%2C+Carlo&rft.aulast=Furlan&rft.aufirst=Carlo&rft.date=2014-09-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=56th+Annual+Meeting+of+the+American+Society+for+Therapeutic+Radiology+and+Oncology+%28ASTRO+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://online.myiwf.com/astro2014/Abstract.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-30 N1 - Last updated - 2015-01-14 ER - TY - JOUR T1 - Rates of HIV-1 superinfection and primary HIV-1 infection are similar in female sex workers in Uganda AN - 1765969978; PQ0002559486 AB - Objective: To determine and compare the rates of HIV superinfection and primary HIV infection in high-risk female sex workers (FSWs) in Kampala, Uganda. Design: A retrospective analysis of individuals who participated in a clinical cohort study among high-risk FSWs in Kampala, Uganda. Methods: Plasma samples from HIV-infected FSWs in Kampala, Uganda were examined with next-generation sequencing of the p24 and gp41HIV genomic regions for the occurrence of superinfection. Primary HIV incidence was determined from initially HIV-uninfected FSWs from the same cohort, and incidence rate ratios were compared. Results: The rate of superinfection in these women (7/85; 3.4/100 person-years) was not significantly different from the rate of primary infection in the same population (3.7/ 100 person-years; incidence rate ratio = 0.91, P = 0.42). Seven women also entered the study dual-infected (16.5% either dual or superinfected). The women with any presence of dual infection were more likely to report sex work as their only source of income (P = 0.05), and trended to be older and more likely to be widowed (P = 0.07). Conclusions: In this cohort of FSWs, HIV superinfection occurred at a high rate and was similar to that of primary HIV infection. These results differ from a similar study of high-risk female bar workers in Kenya that found the rate of superinfection to be significantly lower than the rate of primary HIV infection. JF - AIDS AU - Redd, Andrew D AU - Ssemwanga, Deogratius AU - Vandepitte, Judith AU - Wendel, Sarah K AU - Ndembi, Nicaise AU - Bukenya, Justine AU - Nakubulwa, Susan AU - Grosskurth, Heiner AU - Parry, Chris M AU - Martens, Craig AU - Bruno, Daniel AU - Porcella, Stephen F AU - Quinn, Thomas C AU - Kaleebu, Pontiano AD - Laboratory of Immunoregulation, Division of Intramural Research, NIAID, NIH, Bethesda, aredd2@jhmi.edu Y1 - 2014/09/10/ PY - 2014 DA - 2014 Sep 10 SP - 2147 EP - 2152 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 IS - 14 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - Africa KW - female sex workers KW - HIV KW - superinfection KW - Uganda KW - Acquired immune deficiency syndrome KW - Uganda, Kampala KW - Prostitution KW - Infection KW - Superinfection KW - Income KW - Workers KW - Kenya KW - Human immunodeficiency virus KW - Human immunodeficiency virus 1 KW - Risk groups KW - Females KW - genomics KW - Sex KW - V 22360:AIDS and HIV KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765969978?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Rates+of+HIV-1+superinfection+and+primary+HIV-1+infection+are+similar+in+female+sex+workers+in+Uganda&rft.au=Redd%2C+Andrew+D%3BSsemwanga%2C+Deogratius%3BVandepitte%2C+Judith%3BWendel%2C+Sarah+K%3BNdembi%2C+Nicaise%3BBukenya%2C+Justine%3BNakubulwa%2C+Susan%3BGrosskurth%2C+Heiner%3BParry%2C+Chris+M%3BMartens%2C+Craig%3BBruno%2C+Daniel%3BPorcella%2C+Stephen+F%3BQuinn%2C+Thomas+C%3BKaleebu%2C+Pontiano&rft.aulast=Redd&rft.aufirst=Andrew&rft.date=2014-09-10&rft.volume=28&rft.issue=14&rft.spage=2147&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000365 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Workers; Risk groups; Prostitution; genomics; Superinfection; Sex; Acquired immune deficiency syndrome; Human immunodeficiency virus; Females; Infection; Income; Human immunodeficiency virus 1; Kenya; Uganda, Kampala; Uganda DO - http://dx.doi.org/10.1097/QAD.0000000000000365 ER - TY - JOUR T1 - Substance P exacerbates dopaminergic neurodegeneration through neurokinin-1 receptor-independent activation of microglial NADPH oxidase. AN - 1561974409; 25209287 AB - Although dysregulated substance P (SP) has been implicated in the pathophysiology of Parkinson's disease (PD), how SP affects the survival of dopaminergic neurons remains unclear. Here, we found that mice lacking endogenous SP (TAC1(-/-)), but not those deficient in the SP receptor (neurokinin-1 receptor, NK1R), were more resistant to lipopolysaccharide (LPS)- and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced nigral dopaminergic neurodegeneration than wild-type controls, suggesting a NK1R-independent toxic action of SP. In vitro dose-response studies revealed that exogenous SP enhanced LPS- and 1-methyl-4-phenylpyridinium (MPP(+))-induced dopaminergic neurodegeneration in a bimodal manner, peaking at submicromolar and subpicomolar concentrations, but was substantially less effective at intermediate concentrations. Mechanistically, the actions of submicromolar levels of SP were NK1R-dependent, whereas subpicomolar SP-elicited actions required microglial NADPH oxidase (NOX2), the key superoxide-producing enzyme, but not NK1R. Subpicomolar concentrations of SP activated NOX2 by binding to the catalytic subunit gp91(phox) and inducing membrane translocation of the cytosolic subunits p47(phox) and p67(phox). The importance of NOX2 was further corroborated by showing that inhibition or disruption of NOX2 blocked subpicomolar SP-exacerbated neurotoxicity. Together, our findings revealed a critical role of microglial NOX2 in mediating the neuroinflammatory and dopaminergic neurodegenerative effects of SP, which may provide new insights into the pathogenesis of PD. Copyright © 2014 the authors 0270-6474/14/3412490-14$15.00/0. JF - The Journal of neuroscience : the official journal of the Society for Neuroscience AU - Wang, Qingshan AU - Chu, Chun-Hsien AU - Qian, Li AU - Chen, Shih-Heng AU - Wilson, Belinda AU - Oyarzabal, Esteban AU - Jiang, Lulu AU - Ali, Syed AU - Robinson, Bonnie AU - Kim, Hyoung-Chun AU - Hong, Jau-Shyong AD - Neuropharmacology Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, wangq4@niehs.nih.gov hong3@niehs.nih.gov. ; Neuropharmacology Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. ; Neurochemistry Laboratory, Division of Neurotoxicology, National Center for Toxicological Research/Food and Drug Administration, Jefferson, Arkansas 72079, and. ; Neuropsychopharmacology and Toxicology Program, College of Pharmacy, Kangwon National University, Chunchon 200-701, Korea. Y1 - 2014/09/10/ PY - 2014 DA - 2014 Sep 10 SP - 12490 EP - 12503 VL - 34 IS - 37 KW - Lipopolysaccharides KW - 0 KW - Receptors, Neurokinin-1 KW - Substance P KW - 33507-63-0 KW - NADPH Oxidase KW - EC 1.6.3.1 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Parkinson's disease KW - substance P KW - GPCR independence KW - neuroinflammation KW - NADPH oxidase KW - Animals KW - Enzyme Activation KW - Mice, Inbred C57BL KW - Mice KW - Male KW - Mice, Knockout KW - NADPH Oxidase -- metabolism KW - Parkinsonian Disorders -- chemically induced KW - Substance P -- metabolism KW - Receptors, Neurokinin-1 -- metabolism KW - Dopaminergic Neurons -- metabolism KW - Dopamine -- metabolism KW - Parkinsonian Disorders -- pathology KW - Parkinsonian Disorders -- metabolism KW - Microglia -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561974409?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.atitle=Substance+P+exacerbates+dopaminergic+neurodegeneration+through+neurokinin-1+receptor-independent+activation+of+microglial+NADPH+oxidase.&rft.au=Wang%2C+Qingshan%3BChu%2C+Chun-Hsien%3BQian%2C+Li%3BChen%2C+Shih-Heng%3BWilson%2C+Belinda%3BOyarzabal%2C+Esteban%3BJiang%2C+Lulu%3BAli%2C+Syed%3BRobinson%2C+Bonnie%3BKim%2C+Hyoung-Chun%3BHong%2C+Jau-Shyong&rft.aulast=Wang&rft.aufirst=Qingshan&rft.date=2014-09-10&rft.volume=34&rft.issue=37&rft.spage=12490&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.issn=1529-2401&rft_id=info:doi/10.1523%2FJNEUROSCI.2238-14.2014 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-07 N1 - Date created - 2014-09-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: FASEB J. 2006 Feb;20(2):251-8 [16449797] Brain. 2012 Nov;135(Pt 11):3355-70 [23087045] Nat Rev Neurosci. 2007 Jan;8(1):57-69 [17180163] Glia. 2007 Apr 1;55(5):453-62 [17203472] Int Rev Neurobiol. 2007;82:297-325 [17678968] Trends Neurosci. 2007 Nov;30(11):596-602 [17950926] Naunyn Schmiedebergs Arch Pharmacol. 2007 Oct;376(1-2):73-82 [17879086] Environ Health Perspect. 2008 May;116(5):593-8 [18470306] J Immunol. 2008 Jun 15;180(12):8241-9 [18523290] J Immunol. 2008 Jul 1;181(1):660-8 [18566433] Semin Immunopathol. 2008 Jul;30(3):339-63 [18509646] J Immunol. 2008 Nov 15;181(10):7194-204 [18981141] Antioxid Redox Signal. 2009 Oct;11(10):2481-504 [19309263] Antioxid Redox Signal. 2009 Sep;11(9):2151-66 [19243239] J Vis Exp. 2010;(35). pii: 1488. doi: 10.3791/1488 [20110936] Brain. 2010 Mar;133(Pt 3):808-21 [20123724] Neuropeptides. 2010 Oct;44(5):399-406 [20579732] J Neurosci. 2011 Jan 19;31(3):1081-92 [21248133] Environ Health Perspect. 2011 Jun;119(6):807-14 [21245015] J Immunol. 2011 Jun 15;186(12):7255-63 [21562162] Neurosci Lett. 2011 Sep 15;502(2):107-11 [21820035] Neuropharmacology. 2011 Dec;61(8):1389-98 [21907219] J Neuroinflammation. 2012;9:32 [22340895] Methods Mol Biol. 2013;1041:231-40 [23813383] J Neurosci. 2000 Aug 15;20(16):6309-16 [10934283] Occup Environ Med. 2003 May;60(5):378 [12709528] Brain. 2003 Jul;126(Pt 7):1683-90 [12805119] J Biol Chem. 2004 Jan 9;279(2):1415-21 [14578353] FASEB J. 2004 Mar;18(3):589-91 [14734632] J Immunol. 2004 May 1;172(9):5707-13 [15100316] Neurosci Lett. 2004 Sep 23;368(2):226-30 [15351454] Front Biosci. 2004 Sep 1;9:2153-65 [15353277] Brain Res. 1976 Nov 5;116(2):299-305 [974776] Res Publ Assoc Res Nerv Ment Dis. 1986;64:135-61 [2425403] Neurology. 1988 Aug;38(8):1285-91 [3399080] Exp Brain Res. 1990;82(2):293-303 [1704847] Mol Pharmacol. 1992 Jan;41(1):24-30 [1310144] Proc Natl Acad Sci U S A. 1992 May 1;89(9):3859-63 [1570304] Proc Natl Acad Sci U S A. 1996 May 14;93(10):4565-71 [8643444] Adv Exp Med Biol. 1996;387:97-106 [8794199] J Neural Transm Suppl. 1997;49:103-10 [9266419] J Biol Chem. 1997 Oct 24;272(43):27288-94 [9341176] FASEB J. 2005 Apr;19(6):550-7 [15791005] PLoS One. 2012;7(4):e34138 [22485158] J Neuroinflammation. 2012;9:124 [22695044] Brain. 2012 Sep;135(Pt 9):2750-65 [22915735] J Pharmacol Exp Ther. 2006 Nov;319(2):595-603 [16891616] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1523/JNEUROSCI.2238-14.2014 ER - TY - JOUR T1 - Synthesis and Structure-Activity Relationship Studies of N-Benzyl-2-phenylpyrimidin-4-amine Derivatives as Potent USP1/UAF1 Deubiquitinase Inhibitors with Anticancer Activity against Nonsmall Cell Lung Cancer AN - 1753465124; PQ0002067543 AB - Deregulation of ubiquitin conjugation or deconjugation has been implicated in the pathogenesis of many human diseases including cancer. The deubiquitinating enzyme USP1 (ubiquitin-specific protease 1), in association with UAF1 (USP1-associated factor 1), is a known regulator of DNA damage response and has been shown as a promising anticancer target. To further evaluate USP1/UAF1 as a therapeutic target, we conducted a quantitative high throughput screen of >400000 compounds and subsequent medicinal chemistry optimization of small molecules that inhibit the deubiquitinating activity of USP1/UAF1. Ultimately, these efforts led to the identification of ML323 (70) and related N-benzyl-2-phenylpyrimidin-4-amine derivatives, which possess nanomolar USP1/UAF1 inhibitory potency. Moreover, we demonstrate a strong correlation between compound IC50 values for USP1/UAF1 inhibition and activity in nonsmall cell lung cancer cells, specifically increased monoubiquitinated PCNA (Ub-PCNA) levels and decreased cell survival. Our results establish the druggability of the USP1/UAF1 deubiquitinase complex and its potential as a molecular target for anticancer therapies. JF - Journal of Medicinal Chemistry AU - Dexheimer, Thomas S AU - Rosenthal, Andrew S AU - Luci, Diane K AU - Liang, Qin AU - Villamil, Mark A AU - Chen, Junjun AU - Sun, Hongmao AU - Kerns, Edward H AU - Simeonov, Anton AU - Jadhav, Ajit AU - Zhuang, Zhihao AU - Maloney, David J AD - National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, Maryland 20850, United States PY - 2014 SP - 8099 EP - 8110 PB - American Chemical Society, P.O. Box 182426 Columbus OH 43218-2426 United States VL - 57 IS - 19 SN - 0022-2623, 0022-2623 KW - Biotechnology and Bioengineering Abstracts KW - Cell survival KW - DNA damage KW - Enzymes KW - ubiquitin-specific proteinase KW - Proliferating cell nuclear antigen KW - Structure-activity relationships KW - Lung cancer KW - Ubiquitin KW - Antitumor activity KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753465124?accountid=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+Medicinal+Chemistry&rft.atitle=Synthesis+and+Structure-Activity+Relationship+Studies+of+N-Benzyl-2-phenylpyrimidin-4-amine+Derivatives+as+Potent+USP1%2FUAF1+Deubiquitinase+Inhibitors+with+Anticancer+Activity+against+Nonsmall+Cell+Lung+Cancer&rft.au=Dexheimer%2C+Thomas+S%3BRosenthal%2C+Andrew+S%3BLuci%2C+Diane+K%3BLiang%2C+Qin%3BVillamil%2C+Mark+A%3BChen%2C+Junjun%3BSun%2C+Hongmao%3BKerns%2C+Edward+H%3BSimeonov%2C+Anton%3BJadhav%2C+Ajit%3BZhuang%2C+Zhihao%3BMaloney%2C+David+J&rft.aulast=Dexheimer&rft.aufirst=Thomas&rft.date=2014-09-07&rft.volume=57&rft.issue=19&rft.spage=8099&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medicinal+Chemistry&rft.issn=00222623&rft_id=info:doi/10.1021%2Fjm5010495 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Cell survival; DNA damage; Enzymes; ubiquitin-specific proteinase; Proliferating cell nuclear antigen; Structure-activity relationships; Antitumor activity; Ubiquitin; Lung cancer DO - http://dx.doi.org/10.1021/jm5010495 ER - TY - JOUR T1 - Evaluation of the Murine Immune Response to Xenopsylla cheopis Flea Saliva and Its Effect on Transmission of Yersinia pestis AN - 1618149286; 20801535 AB - The saliva of blood-feeding arthropods contains a variety of components that prevent blood clotting and interfere with the immune system of the vertebrate host. These properties have been shown to enhance or inhibit the transmission of different pathogens transmitted by arthropods. Yersinia pestis, the bacterial agent of plague, is maintained in nature by flea to rodent transmission cycles. Most rodents live in close association with fleas and are constantly being bitten by them, but the influence this has on plague transmission is unknown - previous studies used laboratory animals which have never experienced a flea bite. We found that flea bites caused a mild inflammatory response in mice, and eventually an antibody response to components of flea saliva, but did not significantly affect pathogenesis. The transmission of Y. pestis by infected fleas and the incidence rate of bubonic plague mortality were the same in mice that had been exposed to frequent uninfected flea bites and mice with no prior exposure to fleas. Therefore, in contrast to what has been shown for many other arthropod-borne disease systems, vector saliva did not enhance or inhibit Y. pestis infection in mice, regardless of the immune status of the host to flea saliva. JF - PLoS Neglected Tropical Diseases AU - Bosio, Christopher F AU - Viall, Austin K AU - Jarrett, Clayton O AU - Gardner, Donald AU - Rood, Michael P AU - Hinnebusch, BJoseph AD - Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana PY - 2014 PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States VL - 8 IS - 9 SN - 1935-2727, 1935-2727 KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - Immune status KW - Mortality KW - Bites KW - Laboratory animals KW - Yersinia pestis KW - Vectors KW - Pathogens KW - Antibody response KW - Infection KW - Inflammation KW - Disease transmission KW - Xenopsylla cheopis KW - Blood coagulation KW - Arthropoda KW - Immune response KW - Plague KW - Saliva KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618149286?accountid=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+Neglected+Tropical+Diseases&rft.atitle=Evaluation+of+the+Murine+Immune+Response+to+Xenopsylla+cheopis+Flea+Saliva+and+Its+Effect+on+Transmission+of+Yersinia+pestis&rft.au=Bosio%2C+Christopher+F%3BViall%2C+Austin+K%3BJarrett%2C+Clayton+O%3BGardner%2C+Donald%3BRood%2C+Michael+P%3BHinnebusch%2C+BJoseph&rft.aulast=Bosio&rft.aufirst=Christopher&rft.date=2014-09-05&rft.volume=8&rft.issue=9&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0003196 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-10-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Immune status; Mortality; Bites; Laboratory animals; Vectors; Antibody response; Pathogens; Infection; Disease transmission; Inflammation; Blood coagulation; Saliva; Plague; Immune response; Xenopsylla cheopis; Arthropoda; Yersinia pestis DO - http://dx.doi.org/10.1371/journal.pntd.0003196 ER - TY - CPAPER T1 - Southern Tick Associated Rash Illness (STARI) T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AN - 1611579609; 6306169 JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AU - Marques, Adriana Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 KW - Exanthema KW - Ixodidae UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611579609?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.atitle=Southern+Tick+Associated+Rash+Illness+%28STARI%29&rft.au=Marques%2C+Adriana&rft.aulast=Marques&rft.aufirst=Adriana&rft.date=2014-09-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/index.php/scientific-program/course-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-30 N1 - Last updated - 2014-10-15 ER - TY - CPAPER T1 - The HOPE Act: Criteria for Transplanting Kidneys or Livers from HIV+ donors to HIV+ recipients T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AN - 1611579213; 6306325 JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AU - Odim Odim, Jonah Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 KW - Donors KW - Transplantation KW - Liver KW - Kidneys KW - Human immunodeficiency virus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611579213?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.atitle=The+HOPE+Act%3A+Criteria+for+Transplanting+Kidneys+or+Livers+from+HIV%2B+donors+to+HIV%2B+recipients&rft.au=Odim+Odim%2C+Jonah&rft.aulast=Odim+Odim&rft.aufirst=Jonah&rft.date=2014-09-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/index.php/scientific-program/course-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-30 N1 - Last updated - 2014-10-15 ER - TY - CPAPER T1 - Chemokine Receptor Cxcr1 Promotes Candida Killing by Neutrophils and Host Survival After Systemic Candidiasis T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AN - 1611578620; 6306383 JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AU - Swamydas, M AU - Gao, J-L AU - Break, T AU - Green, N AU - Murphy, P AU - Lionakis, M Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 KW - Cell survival KW - Candidiasis KW - Leukocytes (neutrophilic) KW - Chemokine receptors KW - Survival KW - Candida UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611578620?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.atitle=Chemokine+Receptor+Cxcr1+Promotes+Candida+Killing+by+Neutrophils+and+Host+Survival+After+Systemic+Candidiasis&rft.au=Swamydas%2C+M%3BGao%2C+J-L%3BBreak%2C+T%3BGreen%2C+N%3BMurphy%2C+P%3BLionakis%2C+M&rft.aulast=Swamydas&rft.aufirst=M&rft.date=2014-09-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/index.php/scientific-program/course-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-30 N1 - Last updated - 2014-10-15 ER - TY - CPAPER T1 - Effects of Recombinant Human Interleukin 7 on T-Cell Recovery in Patients with Idiopathic CD4 Lymphocytopenia: Results of a Phase I/IIa Study T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AN - 1611578504; 6306205 JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AU - Sheikh, V AU - Porter, B AU - DerSimonian, R AU - Kovacs, S AU - Freeman, A AU - Roby, G AU - Mican, J AU - Pau, A AU - Adelsberger, J AU - Higgins, J AU - Croughs, T AU - Estes, J AU - Yao, M AU - Sereti, I Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 KW - Recombinants KW - Interleukin 7 KW - CD4 antigen KW - Lymphocytes T UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611578504?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.atitle=Effects+of+Recombinant+Human+Interleukin+7+on+T-Cell+Recovery+in+Patients+with+Idiopathic+CD4+Lymphocytopenia%3A+Results+of+a+Phase+I%2FIIa+Study&rft.au=Sheikh%2C+V%3BPorter%2C+B%3BDerSimonian%2C+R%3BKovacs%2C+S%3BFreeman%2C+A%3BRoby%2C+G%3BMican%2C+J%3BPau%2C+A%3BAdelsberger%2C+J%3BHiggins%2C+J%3BCroughs%2C+T%3BEstes%2C+J%3BYao%2C+M%3BSereti%2C+I&rft.aulast=Sheikh&rft.aufirst=V&rft.date=2014-09-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/index.php/scientific-program/course-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-30 N1 - Last updated - 2014-10-15 ER - TY - CPAPER T1 - Development of Animal Models for Pathogenicity and Drug/Vaccine Studies T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AN - 1611578317; 6306359 JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AU - Hensley, Lisa Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 KW - Pathogenicity KW - Disease control KW - Animal models KW - Drug development KW - Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611578317?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.atitle=Development+of+Animal+Models+for+Pathogenicity+and+Drug%2FVaccine+Studies&rft.au=Hensley%2C+Lisa&rft.aulast=Hensley&rft.aufirst=Lisa&rft.date=2014-09-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/index.php/scientific-program/course-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-30 N1 - Last updated - 2014-10-15 ER - TY - CPAPER T1 - Pathogenesis of ICL T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AN - 1611577841; 6306432 JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AU - Sereti, Irini Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 KW - Chemotherapy KW - Oncology KW - Antimicrobial agents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611577841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.atitle=Pathogenesis+of+ICL&rft.au=Sereti%2C+Irini&rft.aulast=Sereti&rft.aufirst=Irini&rft.date=2014-09-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/index.php/scientific-program/course-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-30 N1 - Last updated - 2014-10-15 ER - TY - CPAPER T1 - The Role of HIV Reservoirs in HIV Pathogenesis T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AN - 1611577730; 6306548 JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AU - Douek, Daniel Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 KW - Human immunodeficiency virus KW - Reservoirs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611577730?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.atitle=The+Role+of+HIV+Reservoirs+in+HIV+Pathogenesis&rft.au=Douek%2C+Daniel&rft.aulast=Douek&rft.aufirst=Daniel&rft.date=2014-09-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/index.php/scientific-program/course-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-30 N1 - Last updated - 2014-10-15 ER - TY - CPAPER T1 - Phase I/IIA Clinical Trial of IL-7 for ICL T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AN - 1611576558; 6306433 JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AU - Sheikh, Virginia Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 KW - Interleukin 7 KW - Clinical trials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611576558?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.atitle=Phase+I%2FIIA+Clinical+Trial+of+IL-7+for+ICL&rft.au=Sheikh%2C+Virginia&rft.aulast=Sheikh&rft.aufirst=Virginia&rft.date=2014-09-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/index.php/scientific-program/course-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-30 N1 - Last updated - 2014-10-15 ER - TY - CPAPER T1 - Clinical Consequences of ICL/NIH ICL Cohort T2 - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AN - 1611576357; 6306430 JF - 54th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2014) AU - Freeman, Alexandra Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 KW - Chemotherapy KW - Oncology KW - Antimicrobial agents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611576357?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.atitle=Clinical+Consequences+of+ICL%2FNIH+ICL+Cohort&rft.au=Freeman%2C+Alexandra&rft.aulast=Freeman&rft.aufirst=Alexandra&rft.date=2014-09-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/index.php/scientific-program/course-program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-30 N1 - Last updated - 2014-10-15 ER - TY - JOUR T1 - Rapid quantitative chiral amphetamines liquid chromatography-tandem mass spectrometry: method in plasma and oral fluid with a cost-effective chiral derivatizing reagent. AN - 1553104982; 25065924 AB - Methamphetamine is a widely abused psychostimulant containing a chiral center. Consumption of over-the-counter and prescription medications may yield positive amphetamines results, but chiral separation of l- and d-methamphetamine and its metabolite amphetamine can help determine whether the source was licit or illicit. We present the first LC-MS/MS method with precolumn derivatization for methamphetamine and amphetamine chiral resolution in plasma and oral fluid collected with the Oral-Eze(®) and Quantisal™ devices. To 0.5mL plasma, 0.75mL Oral-Eze, or 1mL Quantisal specimen racemic d11-methamphetamine and amphetamine internal standards were added, followed by protein precipitation. Samples were centrifuged and supernatants loaded onto pre-conditioned Phenomenex(®) Strata™-XC Polymeric Strong Cation solid phase extraction columns. After washing, analytes were eluted with 5% ammonium hydroxide in methanol. The eluate was evaporated to dryness and reconstituted in water. Derivatization was performed with 1-fluoro-2,4-dinitrophenyl-5-l-alanineamide (Marfey's reagent) and heating at 45°C for 1h. Derivatized enantiomer separations were performed under isocratic conditions (methanol:water, 60:40) with a Phenomenex(®) Kinetex(®) 2.6μm C18 column. Analytes were identified and quantified by two MRM transitions and their ratio on a 3200 QTrap (AB Sciex) mass spectrometer in ESI negative mode. In all three matrices, the method was linear for all enantiomers from 1 to 500μg/L, with imprecision and accuracy of ≤11.3% and 85.3-108%, respectively. Extraction efficiencies ranged from 67.4 to 117% and matrix effects from -17.0 to 468%, with variation always ≤19.1%. Authentic plasma and OF specimens were collected from an IRB-approved study that included controlled Vicks(®) VapoInhaler™ administration. The present method is sensitive, selective, economic and rapid (separations accomplished in <10min), and improves methamphetamine result interpretation. Published by Elsevier B.V. JF - Journal of chromatography. A AU - Newmeyer, Matthew N AU - Concheiro, Marta AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism Section, IRP, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Chemistry and Drug Metabolism Section, IRP, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. ; Chemistry and Drug Metabolism Section, IRP, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. Electronic address: mhuestis@intra.nida.nih.gov. Y1 - 2014/09/05/ PY - 2014 DA - 2014 Sep 05 SP - 68 EP - 74 VL - 1358 KW - Central Nervous System Stimulants KW - 0 KW - Dinitrobenzenes KW - Methamphetamine KW - 44RAL3456C KW - Marfey's reagent KW - 95713-52-3 KW - Alanine KW - OF5P57N2ZX KW - Index Medicus KW - Amphetamines KW - Plasma KW - Oral fluid KW - Chiral analysis KW - Chromatography, High Pressure Liquid -- standards KW - Stereoisomerism KW - Tandem Mass Spectrometry -- standards KW - Saliva -- chemistry KW - Humans KW - Reference Standards KW - Adult KW - Limit of Detection KW - Spectrometry, Mass, Electrospray Ionization -- standards KW - Male KW - Methamphetamine -- isolation & purification KW - Alanine -- analogs & derivatives KW - Methamphetamine -- blood KW - Dinitrobenzenes -- chemistry KW - Central Nervous System Stimulants -- isolation & purification KW - Central Nervous System Stimulants -- blood KW - Methamphetamine -- chemistry KW - Alanine -- chemistry KW - Central Nervous System Stimulants -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1553104982?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chromatography.+A&rft.atitle=Rapid+quantitative+chiral+amphetamines+liquid+chromatography-tandem+mass+spectrometry%3A+method+in+plasma+and+oral+fluid+with+a+cost-effective+chiral+derivatizing+reagent.&rft.au=Newmeyer%2C+Matthew+N%3BConcheiro%2C+Marta%3BHuestis%2C+Marilyn+A&rft.aulast=Newmeyer&rft.aufirst=Matthew&rft.date=2014-09-05&rft.volume=1358&rft.issue=&rft.spage=68&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography.+A&rft.issn=1873-3778&rft_id=info:doi/10.1016%2Fj.chroma.2014.06.096 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-10 N1 - Date created - 2014-08-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Chromatogr A. 2012 Dec 21;1269:122-35 [22858363] J Anal Toxicol. 2013 Sep;37(7):452-74 [23934984] Anal Bioanal Chem. 2012 Nov;404(8):2427-35 [23010844] J Mass Spectrom. 2011 Jul;46(7):603-14 [21656610] Br J Clin Pharmacol. 2010 Feb;69(2):187-92 [20233182] Chirality. 2010 Mar;22(3):320-30 [19544347] Clin Chem. 2009 Nov;55(11):1910-31 [19745062] Drug Metab Dispos. 2009 Nov;37(11):2212-20 [19666989] Anal Bioanal Chem. 2009 Jan;393(2):709-18 [18982317] Clin Chem. 2007 Apr;53(4):702-10 [17332148] Clin Pharmacol Ther. 2006 Oct;80(4):403-20 [17015058] J Anal Toxicol. 1998 Jul-Aug;22(4):265-9 [9681327] Electrophoresis. 2005 Oct;26(20):3910-20 [16167308] J Anal Toxicol. 2006 May;30(4):232-7 [16803660] Drug Metab Rev. 2000 Feb;32(1):15-44 [10711406] Ther Drug Monit. 2002 Apr;24(2):277-89 [11897973] Clin Chem. 2002 Sep;48(9):1472-85 [12194924] Rapid Commun Mass Spectrom. 2003;17(6):569-75 [12621619] J Anal Toxicol. 2003 Nov-Dec;27(8):552-9 [14670133] Drug Metab Dispos. 1997 Sep;25(9):1059-64 [9311621] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.chroma.2014.06.096 ER - TY - JOUR T1 - Mutant IDH inhibits HNF-4α to block hepatocyte differentiation and promote biliary cancer. AN - 1560581844; 25043045 AB - Mutations in isocitrate dehydrogenase 1 (IDH1) and IDH2 are among the most common genetic alterations in intrahepatic cholangiocarcinoma (IHCC), a deadly liver cancer. Mutant IDH proteins in IHCC and other malignancies acquire an abnormal enzymatic activity allowing them to convert α-ketoglutarate (αKG) to 2-hydroxyglutarate (2HG), which inhibits the activity of multiple αKG-dependent dioxygenases, and results in alterations in cell differentiation, survival, and extracellular matrix maturation. However, the molecular pathways by which IDH mutations lead to tumour formation remain unclear. Here we show that mutant IDH blocks liver progenitor cells from undergoing hepatocyte differentiation through the production of 2HG and suppression of HNF-4α, a master regulator of hepatocyte identity and quiescence. Correspondingly, genetically engineered mouse models expressing mutant IDH in the adult liver show an aberrant response to hepatic injury, characterized by HNF-4α silencing, impaired hepatocyte differentiation, and markedly elevated levels of cell proliferation. Moreover, IDH and Kras mutations, genetic alterations that co-exist in a subset of human IHCCs, cooperate to drive the expansion of liver progenitor cells, development of premalignant biliary lesions, and progression to metastatic IHCC. These studies provide a functional link between IDH mutations, hepatic cell fate, and IHCC pathogenesis, and present a novel genetically engineered mouse model of IDH-driven malignancy. JF - Nature AU - Saha, Supriya K AU - Parachoniak, Christine A AU - Ghanta, Krishna S AU - Fitamant, Julien AU - Ross, Kenneth N AU - Najem, Mortada S AU - Gurumurthy, Sushma AU - Akbay, Esra A AU - Sia, Daniela AU - Cornella, Helena AU - Miltiadous, Oriana AU - Walesky, Chad AU - Deshpande, Vikram AU - Zhu, Andrew X AU - Hezel, Aram F AU - Yen, Katharine E AU - Straley, Kimberly S AU - Travins, Jeremy AU - Popovici-Muller, Janeta AU - Gliser, Camelia AU - Ferrone, Cristina R AU - Apte, Udayan AU - Llovet, Josep M AU - Wong, Kwok-Kin AU - Ramaswamy, Sridhar AU - Bardeesy, Nabeel AD - 1] Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA [2]. ; Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA. ; Department of Medical Oncology, Dana-Farber Cancer Institute, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA. ; 1] HCC Translational Research Laboratory, Barcelona-Clínic Liver Cancer Group, Liver Unit, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic, University of Barcelona, Catalonia 08036, Spain [2] Mount Sinai Liver Cancer Program, Division of Liver Diseases, Dept of Medicine. Icahn School of Medicine at Mount Sinai, New York 10029, USA [3] Gastrointestinal Surgery and Liver Transplantation Unit, National Cancer Institute, and Department of Experimental Oncology, Milan 20133, Italy. ; HCC Translational Research Laboratory, Barcelona-Clínic Liver Cancer Group, Liver Unit, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic, University of Barcelona, Catalonia 08036, Spain. ; Mount Sinai Liver Cancer Program, Division of Liver Diseases, Dept of Medicine. Icahn School of Medicine at Mount Sinai, New York 10029, USA. ; Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, Kansas 66160, USA. ; University of Rochester Medical Center, Rochester, New York 14642, USA. ; Agios Pharmaceuticals, Cambridge, Massachusetts 02139, USA. ; 1] HCC Translational Research Laboratory, Barcelona-Clínic Liver Cancer Group, Liver Unit, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Hospital Clínic, University of Barcelona, Catalonia 08036, Spain [2] Mount Sinai Liver Cancer Program, Division of Liver Diseases, Dept of Medicine. Icahn School of Medicine at Mount Sinai, New York 10029, USA [3] Institució Catalana de Recerca i Estudis Avançats, Barcelona, Catalonia 08010, Spain [4] University of Barcelona, Catalonia 08036, Spain. ; 1] Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts 02114, USA [2] Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA. Y1 - 2014/09/04/ PY - 2014 DA - 2014 Sep 04 SP - 110 EP - 114 VL - 513 IS - 7516 KW - Glutarates KW - 0 KW - HNF4A protein, human KW - Hepatocyte Nuclear Factor 4 KW - KRAS protein, human KW - Mutant Proteins KW - Proto-Oncogene Proteins KW - alpha-hydroxyglutarate KW - 2889-31-8 KW - Isocitrate Dehydrogenase KW - EC 1.1.1.41 KW - isocitrate dehydrogenase 2, human KW - IDH1 protein, human KW - EC 1.1.1.42. KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - ras Proteins KW - Index Medicus KW - ras Proteins -- genetics KW - Animals KW - Glutarates -- metabolism KW - Humans KW - Proto-Oncogene Proteins -- metabolism KW - Stem Cells -- pathology KW - Disease Models, Animal KW - Mice KW - Cell Lineage -- genetics KW - Mice, Transgenic KW - Bile Ducts, Intrahepatic -- enzymology KW - Bile Ducts, Intrahepatic -- pathology KW - Neoplasm Metastasis KW - Mutation -- genetics KW - ras Proteins -- metabolism KW - Proto-Oncogene Proteins -- genetics KW - Cell Division -- genetics KW - Female KW - Male KW - Bile Duct Neoplasms -- genetics KW - Hepatocyte Nuclear Factor 4 -- antagonists & inhibitors KW - Mutant Proteins -- metabolism KW - Isocitrate Dehydrogenase -- genetics KW - Cholangiocarcinoma -- enzymology KW - Cholangiocarcinoma -- pathology KW - Hepatocyte Nuclear Factor 4 -- genetics KW - Cell Differentiation -- genetics KW - Hepatocytes -- pathology KW - Bile Duct Neoplasms -- enzymology KW - Hepatocyte Nuclear Factor 4 -- metabolism KW - Hepatocytes -- enzymology KW - Mutant Proteins -- genetics KW - Cholangiocarcinoma -- genetics KW - Hepatocyte Nuclear Factor 4 -- biosynthesis KW - Bile Duct Neoplasms -- pathology KW - Isocitrate Dehydrogenase -- metabolism KW - Hepatocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560581844?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Mutant+IDH+inhibits+HNF-4%CE%B1+to+block+hepatocyte+differentiation+and+promote+biliary+cancer.&rft.au=Saha%2C+Supriya+K%3BParachoniak%2C+Christine+A%3BGhanta%2C+Krishna+S%3BFitamant%2C+Julien%3BRoss%2C+Kenneth+N%3BNajem%2C+Mortada+S%3BGurumurthy%2C+Sushma%3BAkbay%2C+Esra+A%3BSia%2C+Daniela%3BCornella%2C+Helena%3BMiltiadous%2C+Oriana%3BWalesky%2C+Chad%3BDeshpande%2C+Vikram%3BZhu%2C+Andrew+X%3BHezel%2C+Aram+F%3BYen%2C+Katharine+E%3BStraley%2C+Kimberly+S%3BTravins%2C+Jeremy%3BPopovici-Muller%2C+Janeta%3BGliser%2C+Camelia%3BFerrone%2C+Cristina+R%3BApte%2C+Udayan%3BLlovet%2C+Josep+M%3BWong%2C+Kwok-Kin%3BRamaswamy%2C+Sridhar%3BBardeesy%2C+Nabeel&rft.aulast=Saha&rft.aufirst=Supriya&rft.date=2014-09-04&rft.volume=513&rft.issue=7516&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=1476-4687&rft_id=info:doi/10.1038%2Fnature13441 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-24 N1 - Date created - 2014-09-04 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE57002; GEO N1 - SuppNotes - Cited By: Br J Cancer. 2011 Jan 4;104(1):24-32 [21102585] Cancer Cell. 2011 Jan 18;19(1):17-30 [21251613] Genes Dev. 2011 Jun 1;25(11):1185-92 [21632825] Nucleic Acids Res. 2005;33(5):e51 [15784609] Lab Invest. 1999 Feb;79(2):103-9 [10068199] Pharmacol Ther. 1996;71(1-2):57-81 [8910949] Nature. 1992 Jan 30;355(6359):457-61 [1734282] Nat Genet. 2002 Oct;32(2):312-5 [12355088] Hepatology. 2002 Oct;36(4 Pt 1):794-804 [12297826] Mech Dev. 2001 Dec;109(2):183-93 [11731232] Genesis. 2000 Feb;26(2):149-50 [10686614] J Clin Oncol. 2010 Jul 20;28(21):3531-40 [20547994] Leukemia. 2010 Jul;24(7):1302-9 [20508616] Dev Cell. 2010 Feb 16;18(2):175-89 [20159590] Nature. 2009 Dec 10;462(7274):739-44 [19935646] Mol Cell Biol. 2009 Jun;29(11):2945-59 [19289501] Am J Pathol. 2009 Apr;174(4):1149-53 [19246647] J Biol Chem. 2014 May 16;289(20):13717-25 [24668804] J Clin Invest. 2011 Dec;121(12):4850-60 [22105172] Oncogene. 2013 Jun 20;32(25):3091-100 [22824796] Hum Pathol. 2013 Jul;44(7):1216-22 [23391413] Hepatology. 2013 Jun;57(6):2480-90 [23315968] N Engl J Med. 2013 May 30;368(22):2059-74 [23634996] Compr Physiol. 2013 Jan;3(1):485-513 [23720294] Genes Dev. 2013 Apr 15;27(8):836-52 [23630074] Genes Dev. 2013 Apr 1;27(7):719-24 [23520387] Gastroenterology. 2013 Apr;144(4):829-40 [23295441] Hepatology. 2012 Nov;56(5):1792-803 [22707408] Nature. 2012 Aug 30;488(7413):656-9 [22763442] Lancet. 2014 Jun 21;383(9935):2168-79 [24581682] Nat Genet. 2006 May;38(5):500-1 [16642009] Genesis. 2006 Jan;44(1):23-8 [16400644] Nature. 2012 Mar 22;483(7390):474-8 [22343901] Cancer Res. 2012 Mar 15;72(6):1557-67 [22266220] J Biol Chem. 2012 Mar 2;287(10):7345-56 [22241473] Oncologist. 2012;17(1):72-9 [22180306] Cancer Res. 2007 Dec 1;67(23):11141-6 [18056438] Proc Natl Acad Sci U S A. 2007 Feb 6;104(6):1931-6 [17267601] Comment In: Cancer Discov. 2014 Sep;4(9):OF9 [25185208] Erratum In: Nature. 2015 Dec 3;528(7580):152 [26580013] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nature13441 ER - TY - JOUR T1 - Understanding the Role of mHealth and Other Media Interventions for Behavior Change to Enhance Child Survival and Development in Low- and Middle-Income Countries: An Evidence Review AN - 1727697830; 20864202 AB - Given the high morbidity and mortality among children in low- and middle-income countries as a result of preventable causes, the U.S. government and the United Nations Children's Fund convened an Evidence Summit on Enhancing Child Survival and Development in Lower- and Middle-Income Countries by Achieving Population-Level Behavior Change on June 3-4, 2013, in Washington, D.C. This article summarizes evidence for technological advances associated with population-level behavior changes necessary to advance child survival and healthy development in children under 5 years of age in low- and middle-income countries. After a rigorous evidence selection process, the authors assessed science, technology, and innovation papers that used mHealth, social/transmedia, multiplatform media, health literacy, and devices for behavior changes supporting child survival and development. Because of an insufficient number of studies on health literacy and devices that supported causal attribution of interventions to outcomes, the review focused on mHealth, social/transmedia, and multiplatform media. Overall, this review found that some mHealth interventions have sufficient evidence to make topic-specific recommendations for broader implementation, scaling, and next research steps (e.g., adherence to HIV/AIDS antiretroviral therapy, uptake and demand of maternal health service, and compliance with malaria treatment guidelines). While some media evidence demonstrates effectiveness in changing cognitive abilities, knowledge, and attitudes, evidence is minimal on behavioral endpoints linked to child survival. Population level behavior change is necessary to end preventable child deaths. Donors and low- and middle-income countries are encouraged to implement recommendations for informing practice, policy, and research decisions to fully maximize the impact potential of mHealth and multimedia for child survival and development. JF - Journal of Health Communication AU - Higgs, Elizabeth S AU - Goldberg, Allison B AU - Labrique, Alain B AU - Cook, Stephanie H AU - Schmid, Carina AU - Cole, Charlotte F AU - Obregon, Rafael A AD - Division of Clinical Research, National Institute for Allergy and Infectious Diseases, Bethesda, Maryland, USA, ehiggs@niaid.nih.gov Y1 - 2014/09/02/ PY - 2014 DA - 2014 Sep 02 SP - 164 EP - 189 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 19 IS - sup1 SN - 1081-0730, 1081-0730 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources KW - Policies KW - Human diseases KW - Human immunodeficiency virus KW - International organizations KW - Environmental impact KW - Therapy KW - Survival KW - Malaria KW - INE, USA, Washington KW - Mortality causes KW - Ecosystem disturbance KW - Q1 08604:Stock assessment and management KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727697830?accountid=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+Health+Communication&rft.atitle=Understanding+the+Role+of+mHealth+and+Other+Media+Interventions+for+Behavior+Change+to+Enhance+Child+Survival+and+Development+in+Low-+and+Middle-Income+Countries%3A+An+Evidence+Review&rft.au=Higgs%2C+Elizabeth+S%3BGoldberg%2C+Allison+B%3BLabrique%2C+Alain+B%3BCook%2C+Stephanie+H%3BSchmid%2C+Carina%3BCole%2C+Charlotte+F%3BObregon%2C+Rafael+A&rft.aulast=Higgs&rft.aufirst=Elizabeth&rft.date=2014-09-02&rft.volume=19&rft.issue=sup1&rft.spage=164&rft.isbn=&rft.btitle=&rft.title=Journal+of+Health+Communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2014.929763 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Human diseases; Policies; International organizations; Therapy; Environmental impact; Survival; Malaria; Ecosystem disturbance; Mortality causes; Human immunodeficiency virus; INE, USA, Washington DO - http://dx.doi.org/10.1080/10810730.2014.929763 ER - TY - JOUR T1 - Making Sense of the Undue Burden Interpretation of Minimal Risk AN - 1611637063; 20660684 JF - American Journal of Bioethics AU - Resnik, David B AD - National Institute of Environmental Health Sciences Y1 - 2014/09/02/ PY - 2014 DA - 2014 Sep 02 SP - 1 EP - 2 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 14 IS - 9 SN - 1526-5161, 1526-5161 KW - Environment Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611637063?accountid=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=American+Journal+of+Bioethics&rft.atitle=Making+Sense+of+the+Undue+Burden+Interpretation+of+Minimal+Risk&rft.au=Resnik%2C+David+B&rft.aulast=Resnik&rft.aufirst=David&rft.date=2014-09-02&rft.volume=14&rft.issue=9&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Bioethics&rft.issn=15265161&rft_id=info:doi/10.1080%2F15265161.2014.935880 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-10-01 N1 - Last updated - 2014-10-15 DO - http://dx.doi.org/10.1080/15265161.2014.935880 ER - TY - JOUR T1 - Duration and intensity of tobacco smoking and the risk of papillary and non-papillary transitional cell carcinoma of the bladder AN - 1842507920; 20695225 AB - Purpose: To evaluate the impact of tobacco smoking on specific histological subtypes of transitional cell carcinoma of the bladder (TCC). Methods: Between 2003 and 2009, we conducted a hospital-based case-control study in Italy, enrolling 531 incident TCC cases and 524 cancer-free matched patients. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were estimated through multiple logistic regression models. Results: Compared to never smokers, TCC risk was threefold higher in former smokers (95% CI 2.07-4.18) and more than sixfold higher in current smokers (95% CI 4.54-9.85). TCC risk steadily increased with increasing intensity (OR for greater than or equal to 25 cigarettes/day 8.75; 95% CI 3.40-22.55) and duration of smoking (OR for greater than or equal to 50 years 5.46; 95% CI 2.60-11.49). No heterogeneity emerged between papillary and non-papillary TCCs for smoking intensity and duration, but the risk for those who had smoked for greater than or equal to 50 years was twice for non-papillary TCC (OR 10.88) compared with papillary one (OR 4.76). Among current smokers, the risk for a 10-year increase in duration grew across strata of intensity (p-trend = 0.046). Conversely, the risk for a 5-cigarette/day increase in smoking intensity was quite steady across strata of duration (p-trend = 0.18). Conclusions: Study results suggested that duration of smoking outweighs intensity in determining TCC risk, with limited differences across histological subtypes. Elimination of tobacco smoking may prevent about 65 % of TCCs. JF - Cancer Causes & Control AU - Polesel, Jerry AU - Bosetti, Cristina AU - di Maso, Matteo AU - Montella, Maurizio AU - Libra, Massimo AU - Garbeglio, Antonio AU - Zucchetto, Antonella AU - Turati, Federica AU - Talamini, Renato AU - La Vecchia, Carlo AU - Serraino, Diego AD - Unit of Epidemiology and Biostatistics, IRCCS - CRO Aviano National Cancer Institute, Via F. Gallini 2, 33081, Aviano, PN, Italy, polesel@cro.it Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 1151 EP - 1158 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 25 IS - 9 SN - 0957-5243, 0957-5243 KW - Toxicology Abstracts KW - Tobacco smoking KW - Cigarettes KW - Urinary bladder KW - Risk factors KW - Regression analysis KW - transitional cell carcinoma KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842507920?accountid=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=Duration+and+intensity+of+tobacco+smoking+and+the+risk+of+papillary+and+non-papillary+transitional+cell+carcinoma+of+the+bladder&rft.au=Polesel%2C+Jerry%3BBosetti%2C+Cristina%3Bdi+Maso%2C+Matteo%3BMontella%2C+Maurizio%3BLibra%2C+Massimo%3BGarbeglio%2C+Antonio%3BZucchetto%2C+Antonella%3BTurati%2C+Federica%3BTalamini%2C+Renato%3BLa+Vecchia%2C+Carlo%3BSerraino%2C+Diego&rft.aulast=Polesel&rft.aufirst=Jerry&rft.date=2014-09-01&rft.volume=25&rft.issue=9&rft.spage=1151&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-014-0416-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-11-01 N1 - Number of references - 27 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Tobacco smoking; Cigarettes; Urinary bladder; Risk factors; Regression analysis; transitional cell carcinoma DO - http://dx.doi.org/10.1007/s10552-014-0416-0 ER - TY - JOUR T1 - State‐Level School Competitive Food and Beverage Laws Are Associated With Children's Weight Status AN - 1748688066 AB - This study attempted to determine whether state laws regulating low nutrient, high energy‐dense foods and beverages sold outside of the reimbursable school meals program (referred to as “competitive foods”) are associated with children's weight status. We use the Classification of Laws Associated with School Students (CLASS) database of state codified law(s) relevant to school nutrition. States were classified as having strong, weak, or no competitive food laws in 2005 based on strength and comprehensiveness. Parent‐reported height and weight along with demographic, behavioral, family, and household characteristics were obtained from the 2007 National Survey of Children's Health. Bivariate and logistic regression analyses estimated the association between states' competitive food laws and children's overweight and obesity status (body mass index [BMI]‐for‐age ≥85th percentile). Children (N = 16,271) between the ages of 11‐14 years with a BMI for age ≥5th percentile who attended public school were included. Children living in states with weak competitive food laws for middle schools had over a 20% higher odds of being overweight or obese than children living in states with either no or strong school competitive food laws. State‐level school competitive food and beverage laws merit attention with efforts to address the childhood obesity epidemic. Attention to the specificity and requirements of these laws should also be considered. JF - The Journal of School Health AU - Hennessy, Erin AU - Oh, April AU - Agurs‐Collins, Tanya AU - Chriqui, Jamie F AU - Msse, Louise C AU - Moser, Richard P AU - Perna, Frank AD - Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Support to Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute erin.hennessy@fnlcr.nih.gov; Health Communication and Informatics Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute ohay@mail.nih.gov; Health Behaviors Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute collinsta@mail.nih.gov pernafm@mail.nih.gov; Institute for Health Research and Policy. University of Illinois at Chicago (MC 275) jchriqui@uic.edu; School of Population and Public Health, University of British Columbia. BC Children's Hospital and BC Women's Hospital & Health Centre lmasse@cfri.ubc.ca; Science of Research and Technology Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute moserr@mail.nih.gov; Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Support to Behavioral Research Program, Division of Cancer Control and Population Sciences. National Cancer Institute Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 609 EP - 616 CY - Kent PB - Wiley Subscription Services, Inc. VL - 84 IS - 9 SN - 0022-4391 KW - Physical Fitness And Hygiene KW - Body mass KW - Attention KW - Codification KW - Obesity KW - School meals KW - Body Mass Index KW - Body weight KW - Childhood KW - Children KW - Classification KW - Demographic aspects KW - Drinks KW - Food KW - Health KW - Healthy food KW - Meals KW - Middle schools KW - Nutrition KW - Obese children UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1748688066?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+School+Health&rft.atitle=State%E2%80%90Level+School+Competitive+Food+and+Beverage+Laws+Are+Associated+With+Children%27s+Weight+Status&rft.au=Hennessy%2C+Erin%3BOh%2C+April%3BAgurs%E2%80%90Collins%2C+Tanya%3BChriqui%2C+Jamie+F%3BMsse%2C+Louise+C%3BMoser%2C+Richard+P%3BPerna%2C+Frank&rft.aulast=Hennessy&rft.aufirst=Erin&rft.date=2014-09-01&rft.volume=84&rft.issue=9&rft.spage=609&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+School+Health&rft.issn=00224391&rft_id=info:doi/10.1111%2Fjosh.12181 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-10-14 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1111/josh.12181 ER - TY - JOUR T1 - In Vivo Imaging of Tumor Physiological, Metabolic, and Redox Changes in Response to the Anti-Angiogenic Agent Sunitinib: Longitudinal Assessment to Identify Transient Vascular Renormalization AN - 1746891209; PQ0001373072 AB - Aims: The tumor microenvironment is characterized by a highly reducing redox status, a low pH, and hypoxia. Anti-angiogenic therapies for solid tumors frequently function in two steps: the transient normalization of structurally and functionally aberrant tumor blood vessels with increased blood perfusion, followed by the pruning of tumor blood vessels and the resultant cessation of nutrients and oxygen delivery required for tumor growth. Conventional anatomic or vascular imaging is impractical or insufficient to distinguish between the two steps of tumor response to anti-angiogenic therapies. Here, we investigated whether the noninvasive imaging of the tumor redox state and energy metabolism could be used to characterize anti-angiogenic drug-induced transient vascular normalization. Results: Daily treatment of squamous cell carcinoma (SCCVII) tumor-bearing mice with the multi-tyrosine kinase inhibitor sunitinib resulted in a rapid decrease in tumor microvessel density and the suppression of tumor growth. Tumor pO sub(2) imaging by electron paramagnetic resonance imaging showed a transient increase in tumor oxygenation after 2-4 days of sunitinib treatment, implying improved tumor perfusion. During this window of vascular normalization, magnetic resonance imaging of the redox status using an exogenously administered nitroxide probe and hyperpolarized super(13)C MRI of the metabolic flux of pyruvate/lactate couple revealed an oxidative shift in tumor redox status. Innovation: Redox-sensitive metabolic couples can serve as noninvasive surrogate markers to identify the vascular normalization window in tumors with imaging techniques. Conclusion: A multimodal imaging approach to characterize physiological, metabolic, and redox changes in tumors is useful to distinguish between the different stages of anti-angiogenic treatment. JF - Antioxidants and Redox Signaling AU - Matsumoto, Shingo AU - Saito, Keita AU - Takakusagi, Yoichi AU - Matsuo, Masayuki AU - Munasinghe, Jeeva P AU - Morris, Herman D AU - Lizak, Martin J AU - Merkle, Hellmut AU - Yasukawa, Keiji AU - Devasahayam, Nallathamby AU - Suburamanian, Sankaran AU - Mitchell, James B AU - Krishna, Murali C AD - Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, murali@helix.nih.gov PY - 2014 SP - 1145 EP - 1155 PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538-1962 United States VL - 21 IS - 8 SN - 1523-0864, 1523-0864 KW - Toxicology Abstracts KW - Redox properties KW - Antioxidants KW - Perfusion KW - Energy metabolism KW - Solid tumors KW - Magnetic resonance imaging KW - Probes KW - Nutrients KW - squamous cell carcinoma KW - Tumors KW - Oxygen KW - Pyruvic acid KW - Blood vessels KW - Lactic acid KW - Microenvironments KW - Pruning KW - Nitroxide KW - pH effects KW - metabolic flux KW - X 24390:Radioactive Materials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746891209?accountid=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=Antioxidants+and+Redox+Signaling&rft.atitle=In+Vivo+Imaging+of+Tumor+Physiological%2C+Metabolic%2C+and+Redox+Changes+in+Response+to+the+Anti-Angiogenic+Agent+Sunitinib%3A+Longitudinal+Assessment+to+Identify+Transient+Vascular+Renormalization&rft.au=Matsumoto%2C+Shingo%3BSaito%2C+Keita%3BTakakusagi%2C+Yoichi%3BMatsuo%2C+Masayuki%3BMunasinghe%2C+Jeeva+P%3BMorris%2C+Herman+D%3BLizak%2C+Martin+J%3BMerkle%2C+Hellmut%3BYasukawa%2C+Keiji%3BDevasahayam%2C+Nallathamby%3BSuburamanian%2C+Sankaran%3BMitchell%2C+James+B%3BKrishna%2C+Murali+C&rft.aulast=Matsumoto&rft.aufirst=Shingo&rft.date=2014-09-01&rft.volume=21&rft.issue=8&rft.spage=1145&rft.isbn=&rft.btitle=&rft.title=Antioxidants+and+Redox+Signaling&rft.issn=15230864&rft_id=info:doi/10.1089%2Fars.2013.5725 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Redox properties; Perfusion; Antioxidants; Energy metabolism; Solid tumors; Magnetic resonance imaging; Probes; squamous cell carcinoma; Nutrients; Tumors; Oxygen; Pyruvic acid; Blood vessels; Lactic acid; Microenvironments; Pruning; pH effects; Nitroxide; metabolic flux DO - http://dx.doi.org/10.1089/ars.2013.5725 ER - TY - JOUR T1 - Correlates of Current Smoking Among Malaysian Secondary School Children AN - 1701480360; PQ0001677906 AB - Cigarette smoking in adolescent is a significant public health problem, leading to the risk of addiction, morbidity, and mortality in the long term. This study determined the prevalence and correlates of current smoking among adolescent school children. A nationwide school-based survey among 25 507 students between Forms 1 to 5 (aged 12-17) was conducted using a 2-stage cluster sampling design. The prevalence of current smoking was 11.5%. Multivariable logistic regression analysis revealed that current smoking was significantly associated with males (adjusted odds ratio [aOR] = 3.25; 95% confidence interval [CI] = 1.87, 4.98), current drinking (aOR = 2.34; 95% CI = 1.46, 3.74), drug used (aOR = 2.97; 95% CI = 1.24, 7.11), and being bullied (aOR = 1.41; 95% CI = 1.00, 1.98) at least once in the past 12 months. Smoking is associated with several behaviors that pose risks to adolescents, such as social issues and smoking-related health problems. Thus, early and integrated prevention programs that address multiple risk behaviors simultaneously are required. JF - Asia-Pacific Journal of Public Health AU - Tee, Guat Hiong AU - Kaur, Gurpreet AD - Institute for Public Health, National Institutes of Health, Ministry of Health, Kuala Lumpur, Malaysia Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 70S EP - 80S PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 26 IS - 5 SN - 1010-5395, 1010-5395 KW - Risk Abstracts; Health & Safety Science Abstracts KW - smoking KW - drinking alcohol KW - substance use KW - bullying KW - Global School Health Survey (GSHS) KW - Malaysia KW - adolescent KW - Mortality KW - Health problems KW - Cigarettes KW - Risk taking KW - Children KW - Morbidity KW - Public health KW - Prevention KW - Behavior KW - Drugs KW - Adolescents KW - Bullying 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/1701480360?accountid=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=Asia-Pacific+Journal+of+Public+Health&rft.atitle=Correlates+of+Current+Smoking+Among+Malaysian+Secondary+School+Children&rft.au=Tee%2C+Guat+Hiong%3BKaur%2C+Gurpreet&rft.aulast=Tee&rft.aufirst=Guat&rft.date=2014-09-01&rft.volume=26&rft.issue=5&rft.spage=70S&rft.isbn=&rft.btitle=&rft.title=Asia-Pacific+Journal+of+Public+Health&rft.issn=10105395&rft_id=info:doi/10.1177%2F1010539514540468 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Number of references - 30 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Mortality; Health problems; Prevention; Cigarettes; Behavior; Risk taking; Children; Drugs; Bullying; Morbidity; Adolescents; Public health DO - http://dx.doi.org/10.1177/1010539514540468 ER - TY - JOUR T1 - Time Perspective and Exercise, Obesity, and Smoking: Moderation of Associations by Age AN - 1665152161 AB - Purpose. Time perspective, a psychological construct denoting subjective orientation to either present or future concerns, has been inconsistently associated with healthy behaviors in adults. We hypothesized that associations would be stronger in young adults, who are first developing independent attitudes, than in older adults. Design. Cross-sectional survey. Setting. The study was conducted in three cities in the Mid-Atlantic region. Subjects. Subjects were 790 patrons of barber and beauty shops. Measures. Measures used were the Zimbardo Time Perspective Inventory future, present-fatalistic, and present-hedonistic subscales and current smoking, days per week of recreational exercise, and height and weight, by self-report. Analysis. We tested if associations between time perspective and exercise, obesity, and current smoking differed by age group (18-24 years, 25-34 years, and 35 years and older) using analysis of variance and logistic regression. Results. Higher future time perspective scores, indicating greater focus on future events, ivas associated with more frequent exercise, whereas higher present-fatalistic time perspective scores, indicating more hopelessness, was associated with less frequent exercise in 18- to 24-year-olds, but not in older individuals. Lower future time perspective scores, and higher present-hedonistic time perspective scores, indicating interest in pleasure-seeking, were also associated with obesity only in 18- to 24-year-olds. Current smoking was not related to time perspective in any age group. Conclusion. Time perspective has age-specific associations with exercise and obesity, suggesting stages when lime perspective may influence health behavior decision making. JF - American Journal of Health Promotion : AJHP. AU - Guthrie, Lori C AU - Butler, Stephen C AU - Lessl, Kristen AU - Ochi, Onyinyechukwu AU - Ward, Michael M AD - National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland ; National Institutes of Health, Building 10 CRC, Room 4-1339, Bethesda, MD, 20892 ; National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland Y1 - 2014///Sep/Oct PY - 2014 DA - Sep/Oct 2014 SP - 9 EP - 16 CY - Birmingham PB - Mosby-Year Book, Inc. VL - 29 IS - 1 SN - 0890-1171 KW - Physical Fitness And Hygiene KW - Age differences KW - Associations KW - Selfreport KW - Shops KW - Smoking KW - Young adults KW - Attitudes KW - Beauty KW - Decision making KW - Elderly people KW - Exercise KW - Future events KW - Health behaviour KW - Healthy habits KW - Hopelessness KW - Moderation KW - Obesity KW - Older people KW - Patrons KW - Pleasure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665152161?accountid=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=American+Journal+of+Health+Promotion+%3A+AJHP.&rft.atitle=Time+Perspective+and+Exercise%2C+Obesity%2C+and+Smoking%3A+Moderation+of+Associations+by+Age&rft.au=Guthrie%2C+Lori+C%3BButler%2C+Stephen+C%3BLessl%2C+Kristen%3BOchi%2C+Onyinyechukwu%3BWard%2C+Michael+M&rft.aulast=Guthrie&rft.aufirst=Lori&rft.date=2014-09-01&rft.volume=29&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Health+Promotion+%3A+AJHP.&rft.issn=08901171&rft_id=info:doi/10.4278%2Fajhp.130122-QUAN-39 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.4278/ajhp.130122-QUAN-39 ER - TY - JOUR T1 - Clear Water Flows from Its Origin: Congratulations on the 30 super(th) Anniversary Celebration of Journal of Environmental and Occupational Medicine AN - 1654666361; 21198189 AB - Abstract not available. JF - Huanjing yu Zhiye Yixue AU - HU, Hui AD - Environmental Health Perspectives, National Institute of Environmental Health Sciences, NC 27709, USA, hu@niehs.nih.gov Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 686 PB - Shanghai Shi Jibing Fangkongzhi Zhongxin, 1105 Zhongxing Lu Shanghai 200070 China VL - 31 IS - 9 SN - 1006-3617, 1006-3617 KW - Health & Safety Science Abstracts; Environment Abstracts KW - Journal of Environmental and Occupational Medicine KW - public health KW - Environmental Health Perspectives(EHP) KW - Water flow 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/1654666361?accountid=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=Huanjing+yu+Zhiye+Yixue&rft.atitle=Clear+Water+Flows+from+Its+Origin%3A+Congratulations+on+the+30+super%28th%29+Anniversary+Celebration+of+Journal+of+Environmental+and+Occupational+Medicine&rft.au=HU%2C+Hui&rft.aulast=HU&rft.aufirst=Hui&rft.date=2014-09-01&rft.volume=31&rft.issue=9&rft.spage=686&rft.isbn=&rft.btitle=&rft.title=Huanjing+yu+Zhiye+Yixue&rft.issn=10063617&rft_id=info:doi/10.13213%2Fj.cnki.jeom.2014.0166 LA - Chinese DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-04-16 N1 - SubjectsTermNotLitGenreText - Water flow DO - http://dx.doi.org/10.13213/j.cnki.jeom.2014.0166 ER - TY - JOUR T1 - Nonmedical Prescription Drug Use Comorbidity: Developing a Cohesive Risk Model AN - 1627733707 AB - Nonmedical Prescription Drug Use (NMPDU) is a growing issue world-wide. Previously, NMPDU comorbidity has been investigated using bivariate approaches, providing a piecemeal understanding of NMPDU’s relationship to other mental disorders. We investigate how NMPDU fits within the multivariate meta-structure of psychiatric comorbidity and how this might vary as a function of gender. Data were collected as part of the National Epidemiological Survey on Alcohol and Related Conditions (NESARC) in 2001–2002 on 43,093 individuals 18 years or older living in the US. The Alcohol Use Disorder and Associated Disabilities Interview Schedule DSM-IV version IV (AUDADIS-IV) assessed psychiatric diagnoses and sedative, tranquilizer, opioid, and amphetamine NMPDU. Using confirmatory factor analysis, NMPDU was introduced into the internalizing-externalizing model of common mental disorders to determine where it best fits. Models were examined separately for men and women and tested for gender invariance. NMPDU was strongly associated with the externalizing factor, and also showed a very small secondary association with the fear subfactor of internalizing. This structure was gender invariant. Differences between men and women’s prevalence rates originate at the level of the latent factors. Results indicate a shared liability to NMPDU and other forms of externalizing psychopathology such as other substance use disorders, as well as antisocial behaviors. Research on NMPDU can benefit from focusing on the externalizing factor, aiming to understand how risk factors for diverse externalizing disorders may also manifest as NMPDU. Prescribers should be particularly attentive to the presence of the entire spectrum of externalizing disorders, as they may signal risk for NMPDU. JF - Journal of Psychopathology and Behavioral Assessment AU - Ofrat, Shani AU - Krueger, Robert F AU - Eaton, Nicholas R AU - Keyes, Katherine M AU - Skodol, Andrew E AU - Grant, Bridget F AU - Hasin, Deborah S AD - Department of Psychology, University of Minnesota, 75 East River Road, Minneapolis, MN, 55455, USA krueg038@umn.edu krueg038@umn.edu; Stony Brook University, Stony Brook, NY, USA ; Columbia University, New York, NY, USA ; Columbia University, New York, NY, USA, University of Arizona, Phoenix, AZ, USA ; National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA ; Department of Psychology, University of Minnesota, 75 East River Road, Minneapolis, MN, 55455, USA Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 371 EP - 379 CY - New York PB - Springer Science & Business Media VL - 36 IS - 3 SN - 0882-2689 KW - Psychology KW - Alcohol consumption KW - Alcohol related disorders KW - Amphetamines KW - Antisocial behaviour KW - Risk factors KW - Substance abuse disorders KW - Comorbidity KW - Confirmatory factor analysis KW - Drug abuse KW - Externalizing behaviour KW - Externalizing problems KW - Factor analysis KW - Fear KW - Gender KW - Gender differences KW - Internalization KW - Liability KW - Prevalence KW - Psychiatric disorders KW - Psychopathology KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627733707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Psychopathology+and+Behavioral+Assessment&rft.atitle=Nonmedical+Prescription+Drug+Use+Comorbidity%3A+Developing+a+Cohesive+Risk+Model&rft.au=Ofrat%2C+Shani%3BKrueger%2C+Robert+F%3BEaton%2C+Nicholas+R%3BKeyes%2C+Katherine+M%3BSkodol%2C+Andrew+E%3BGrant%2C+Bridget+F%3BHasin%2C+Deborah+S&rft.aulast=Ofrat&rft.aufirst=Shani&rft.date=2014-09-01&rft.volume=36&rft.issue=3&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=Journal+of+Psychopathology+and+Behavioral+Assessment&rft.issn=08822689&rft_id=info:doi/10.1007%2Fs10862-014-9409-2 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-10-14 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1007/s10862-014-9409-2 ER - TY - JOUR T1 - Regulation of Motor Function and Behavior by Atypical Chemokine Receptor 1 AN - 1627730456 AB - Atypical Chemokine Receptor 1 (ACKR1), previously known as Duffy Antigen Receptor for Chemokines, stands out among chemokine receptors for high selective expression on cerebellar Purkinje neurons. Although ACKR1 ligands activate Purkinje cells in vitro, evidence for ACKR1 regulation of brain function in vivo is lacking. Here we demonstrate that Ackr1 −/− mice have markedly impaired balance and ataxia on a rotating rod and increased tremor when injected with harmaline, which induces whole-body tremor by activating Purkinje cells. Ackr1 −/− mice also exhibited impaired exploratory behavior, increased anxiety-like behavior and frequent episodes of marked hypoactivity under low-stress conditions. Surprisingly, Ackr1 + /− had similar behavioral abnormalities, indicating pronounced haploinsufficiency. The behavioral phenotype of Ackr1 − /− mice was the opposite of mouse models of cerebellar degeneration, and the defects persisted when Ackr1 was deficient only on non-hematopoietic cells. Together, the results suggest that normal motor function and behavior may partly depend on negative regulation of Purkinje cell activity by Ackr1. JF - Behavior Genetics AU - Schneider, Erich H AU - Fowler, Stephen C AU - Lionakis, Michail S AU - Swamydas, Muthulekha AU - Holmes, Gibran AU - Diaz, Vivian AU - Munasinghe, Jeeva AU - Peiper, Stephen C AU - Gao, Ji-Liang AU - Murphy, Philip M AD - Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA, Institute of Pharmacology, Hannover Medical School, Hannover, Germany ; Department of Pharmacology and Toxicology, University of Kansas, Lawrence, KS, USA ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA, Fungal Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, NIAID/NIH, Bethesda, MD, USA ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA ; In Vivo NMR Center, National Institute of Neurological Diseases and Stroke (NINDS)/NIH, Bethesda, MD, USA ; Institute of Pathology, Anatomy and Cell Biology, Jefferson Medical College, Philadelphia, PA, USA ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA, Bldg 10, Room 11N113, NIH, Bethesda, MD, 20892, USA ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases (NIAID)/NIH, Bethesda, MD, USA; Institute of Pharmacology, Hannover Medical School, Hannover, Germany Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 498 EP - 515 CY - New York PB - Springer Science & Business Media VL - 44 IS - 5 SN - 0001-8244 KW - Biology KW - Animals KW - Behaviour KW - Anxiety KW - Ataxia KW - Brain KW - Defects KW - Motor performance KW - Neurons KW - Regulation KW - Stress UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627730456?accountid=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=Behavior+Genetics&rft.atitle=Regulation+of+Motor+Function+and+Behavior+by+Atypical+Chemokine+Receptor+1&rft.au=Schneider%2C+Erich+H%3BFowler%2C+Stephen+C%3BLionakis%2C+Michail+S%3BSwamydas%2C+Muthulekha%3BHolmes%2C+Gibran%3BDiaz%2C+Vivian%3BMunasinghe%2C+Jeeva%3BPeiper%2C+Stephen+C%3BGao%2C+Ji-Liang%3BMurphy%2C+Philip+M&rft.aulast=Schneider&rft.aufirst=Erich&rft.date=2014-09-01&rft.volume=44&rft.issue=5&rft.spage=498&rft.isbn=&rft.btitle=&rft.title=Behavior+Genetics&rft.issn=00018244&rft_id=info:doi/10.1007%2Fs10519-014-9665-7 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-11-10 N1 - Last updated - 2016-05-24 DO - http://dx.doi.org/10.1007/s10519-014-9665-7 ER - TY - JOUR T1 - Dark matter in archaeal genomes: a rich source of novel mobile elements, defense systems and secretory complexes AN - 1618155698; 20849255 AB - Microbial genomes encompass a sizable fraction of poorly characterized, narrowly spread fast-evolving genes. Using sensitive methods for sequences comparison and protein structure prediction, we performed a detailed comparative analysis of clusters of such genes, which we denote "dark matter islands", in archaeal genomes. The dark matter islands comprise up to 20 % of archaeal genomes and show remarkable heterogeneity and diversity. Nevertheless, three classes of entities are common in these genomic loci: (a) integrated viral genomes and other mobile elements; (b) defense systems, and (c) secretory and other membrane-associated systems. The dark matter islands in the genome of thermophiles and mesophiles show similar general trends of gene content, but thermophiles are substantially enriched in predicted membrane proteins whereas mesophiles have a greater proportion of recognizable mobile elements. Based on this analysis, we predict the existence of several novel groups of viruses and mobile elements, previously unnoticed variants of CRISPR-Cas immune systems, and new secretory systems that might be involved in stress response, intermicrobial conflicts and biogenesis of novel, uncharacterized membrane structures. JF - Extremophiles AU - Makarova, Kira S AU - Wolf, Yuri I AU - Forterre, Patrick AU - Prangishvili, David AU - Krupovic, Mart AU - Koonin, Eugene V AD - National Center for Biotechnology Information, National Library of Medicine, Bethesda, MD, 20894, USA, koonin@ncbi.nlm.nih.gov Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 877 EP - 893 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 18 IS - 5 SN - 1431-0651, 1431-0651 KW - ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts B: Bacteriology KW - Genomes KW - Membrane structure KW - Immune system KW - Viruses KW - Membrane proteins KW - Protein structure KW - Islands KW - Genes KW - Biogenesis KW - genomics KW - New species KW - Q1 08205:Genetics and evolution KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618155698?accountid=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=Extremophiles&rft.atitle=Dark+matter+in+archaeal+genomes%3A+a+rich+source+of+novel+mobile+elements%2C+defense+systems+and+secretory+complexes&rft.au=Makarova%2C+Kira+S%3BWolf%2C+Yuri+I%3BForterre%2C+Patrick%3BPrangishvili%2C+David%3BKrupovic%2C+Mart%3BKoonin%2C+Eugene+V&rft.aulast=Makarova&rft.aufirst=Kira&rft.date=2014-09-01&rft.volume=18&rft.issue=5&rft.spage=877&rft.isbn=&rft.btitle=&rft.title=Extremophiles&rft.issn=14310651&rft_id=info:doi/10.1007%2Fs00792-014-0672-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-10-01 N1 - Number of references - 73 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Genomes; Genes; Viruses; Biogenesis; New species; Protein structure; Islands; Immune system; Membrane structure; Membrane proteins; genomics DO - http://dx.doi.org/10.1007/s00792-014-0672-7 ER - TY - JOUR T1 - Structural enzymology and inhibition of the bi-functional folate pathway enzyme HPPK-DHPS from the biowarfare agent Francisella tularensis AN - 1618150282; 20761541 AB - Two valid targets for antibiotic development, 6-hydroxymethyl-7,8-dihydropterin pyrophosphokinase (HPPK) and dihydropteroate synthase (DHPS), catalyze consecutive reactions in folate biosynthesis. In Francisella tularensis (Ft), these two activities are contained in a single protein, FtHPPK-DHPS. Although Pemble et al. (PLoS One 5, e14165) determined the structure of FtHPPK-DHPS, they were unable to measure the kinetic parameters of the enzyme. In this study, we elucidated the binding and inhibitory activities of two HPPK inhibitors (HP-18 and HP-26) against FtHPPK-DHPS, determined the structure of FtHPPK-DHPS in complex with HP-26, and measured the kinetic parameters for the dual enzymatic activities of FtHPPK-DHPS. The biochemical analyses showed that HP-18 and HP-26 have significant isozyme selectivity, and that FtHPPK-DHPS is unique in that the catalytic efficiency of its DHPS activity is only 1/260,000 of that of Escherichia coli DHPS. Sequence and structural analyses suggest that HP-26 is an excellent lead for developing therapeutic agents for tularemia, and that the very low DHPS activity is due, at least in part, to the lack of a key residue that interacts with the substrate p-aminobenzoic acid (pABA). A BLAST search of the genomes of ten F. tularensis strains indicated that the bacterium contains a single FtHPPK-DHPS. The marginal DHPS activity and the single copy existence of FtHPPK-DHPS in F. tularensis make this bacterium more vulnerable to DHPS inhibitors. Current sulfa drugs are ineffective against tularemia; new inhibitors targeting the unique pABA-binding pocket may be effective and less subject to resistance because any mutations introducing resistance may make the marginal DHPS activity unable to support the growth of F. tularensis. The coordinates and structure factors have been deposited in the Protein Data Bank under accession code 4PZV. In Francisella tularensis (Ft), 6-hydroxymethyl-7,8-dihydropterin pyrophosphokinase (HPPK) and dihydropteroate synthase (DHPS) form the bifunctional enzyme FtHPPK-DHPS. Here, we report the activities of two HPPK inhibitors (HP-18 and HP-26) against FtHPPK-DHPS, the structure of FtHPPK-DHPS in complex with HP-26, and the kinetic parameters of FtHPPK-DHPS. The catalytic efficiency of FtDHPS is unique, which is only 1/2.6 105 that of Escherichia coli DHPS. JF - FEBS Journal AU - Shaw, Gary X AU - Li, Yue AU - Shi, Genbin AU - Wu, Yan AU - Cherry, Scott AU - Needle, Danielle AU - Zhang, Di AU - Tropea, Joseph E AU - Waugh, David S AU - Yan, Honggao AU - Ji, Xinhua AD - Macromolecular Crystallography Laboratory. National Cancer Institute Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 4123 EP - 4137 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 281 IS - 18 SN - 1742-464X, 1742-464X KW - Microbiology Abstracts B: Bacteriology KW - Genomes KW - Bifunctional enzymes KW - Biochemical analysis KW - Francisella tularensis KW - Antibiotics KW - Dihydropteroate synthase KW - p-Aminobenzoic acid KW - Data banks KW - Tularemia KW - Kinetics KW - Escherichia coli KW - Isoenzymes KW - Enzymatic activity KW - Folic acid KW - Mutation KW - J 02310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618150282?accountid=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+Journal&rft.atitle=Structural+enzymology+and+inhibition+of+the+bi-functional+folate+pathway+enzyme+HPPK-DHPS+from+the+biowarfare+agent+Francisella+tularensis&rft.au=Shaw%2C+Gary+X%3BLi%2C+Yue%3BShi%2C+Genbin%3BWu%2C+Yan%3BCherry%2C+Scott%3BNeedle%2C+Danielle%3BZhang%2C+Di%3BTropea%2C+Joseph+E%3BWaugh%2C+David+S%3BYan%2C+Honggao%3BJi%2C+Xinhua&rft.aulast=Shaw&rft.aufirst=Gary&rft.date=2014-09-01&rft.volume=281&rft.issue=18&rft.spage=4123&rft.isbn=&rft.btitle=&rft.title=FEBS+Journal&rft.issn=1742464X&rft_id=info:doi/10.1111%2Ffebs.12896 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-10-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Genomes; Biochemical analysis; Bifunctional enzymes; Antibiotics; Dihydropteroate synthase; p-Aminobenzoic acid; Data banks; Tularemia; Kinetics; Isoenzymes; Enzymatic activity; Folic acid; Mutation; Escherichia coli; Francisella tularensis DO - http://dx.doi.org/10.1111/febs.12896 ER - TY - JOUR T1 - Mn complex-mediated enhancement of antitumor response through modulating myeloid-derived suppressor cells in drug-resistant tumor. AN - 1614684093; 25189907 AB - The tumor microenvironment (TME) renders tumor cells more resistant to chemotherapy. However, effective immunomodulators for cancer therapy are still elusive. We hypothesized that Mn-N-(2-hydroxyacetophenone) glycinate (MnNG), reported to be an antitumor agent, can modulate the TME. Immunomodulatory effects of MnNG were performed through assessing Myeloid Derived Suppressor Cells (MDSCs), Interferon-γ (Ifnγ)- and Interleukin-4 (Il4)-secreting Cluster of Differentiation 4 (Cd4)(+) T-cells by annexin V-binding assay in drug-resistant TME and T-cell proliferation following in vitro co-culture assay by flow cytometry. MnNG induced infiltration of Ifnγ-secreting Cd4(+) T-cells and reduces MDSC numbers in vivo. Furthermore, it modulated differentiation of MDSCs towards dendritic cells with up-regulation of co-stimulatory molecules and reversed the suppressive function of MDSC's that enhances T-helper cell 1 (Th1) response. MnNG treatment resulted in reduced expression of IL4, but enhanced expression of Ifnγ when Cd4(+) T-cells were co-cultured with MDSCs. MnNG modulates MDSCs differentiaton towards dendritic cells and enhances Th1 response in drug-resistant TME, leading to immunomodulatory efficacy. Copyright © 2014 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved. JF - In vivo (Athens, Greece) AU - Das, Satyajit AU - Banerjee, Kaushik AU - Roy, Susmita AU - Majumder, Saikat AU - Chatterjee, Mitali AU - Majumdar, Subrata AU - Choudhuri, Soumitra Kumar AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India. ; Department of Pharmacology, Institute of Postgraduate Medical Education and Research, Kolkata, India. ; Division of Molecular Medicine, Bose Institute, Kolkata, India. ; Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India soumitra01@yahoo.com. PY - 2014 SP - 909 EP - 918 VL - 28 IS - 5 KW - Cytokines KW - 0 KW - Immunologic Factors KW - Manganese KW - 42Z2K6ZL8P KW - Index Medicus KW - myeloid derived suppressor cells KW - MDR KW - Mn complex KW - Th1 response KW - immunomodulation KW - T-Lymphocyte Subsets -- metabolism KW - Animals KW - Lymphocytes, Tumor-Infiltrating -- immunology KW - CD4-Positive T-Lymphocytes -- metabolism KW - T-Lymphocyte Subsets -- drug effects KW - T-Lymphocyte Subsets -- immunology KW - Disease Models, Animal KW - CD4-Positive T-Lymphocytes -- immunology KW - Mice KW - Cytokines -- metabolism KW - CD4-Positive T-Lymphocytes -- drug effects KW - Immunophenotyping KW - Male KW - Lymphocytes, Tumor-Infiltrating -- metabolism KW - Female KW - Manganese -- pharmacology KW - Neoplasms -- pathology KW - Manganese -- chemistry KW - Immunologic Factors -- pharmacology KW - Myeloid Cells -- immunology KW - Immunologic Factors -- chemistry KW - Drug Resistance, Neoplasm KW - Neoplasms -- therapy KW - Myeloid Cells -- drug effects KW - Immunomodulation -- drug effects KW - Neoplasms -- metabolism KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1614684093?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=In+vivo+%28Athens%2C+Greece%29&rft.atitle=Mn+complex-mediated+enhancement+of+antitumor+response+through+modulating+myeloid-derived+suppressor+cells+in+drug-resistant+tumor.&rft.au=Das%2C+Satyajit%3BBanerjee%2C+Kaushik%3BRoy%2C+Susmita%3BMajumder%2C+Saikat%3BChatterjee%2C+Mitali%3BMajumdar%2C+Subrata%3BChoudhuri%2C+Soumitra+Kumar&rft.aulast=Das&rft.aufirst=Satyajit&rft.date=2014-09-01&rft.volume=28&rft.issue=5&rft.spage=909&rft.isbn=&rft.btitle=&rft.title=In+vivo+%28Athens%2C+Greece%29&rft.issn=1791-7549&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-22 N1 - Date created - 2014-09-05 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - The role of health systems and policy in producing behavior and social change to enhance child survival and development in low- and middle-income countries: an examination of the evidence AN - 1613947810; 4608959 AB - Evidence-based behavior change interventions addressing health systems must be identified and disseminated to improve child health outcomes. Studies of the efficacy of such interventions were identified from systematic searches of the published literature. Two hundred twenty-nine of the initially identified references were judged to be relevant and were further reviewed for the quality and strength of the evidence. Studies were eligible if an intervention addressed policy or health systems interventions, measured relevant behavioral or health outcomes (e.g., nutrition, childhood immunization, malaria prevention and treatment), used at least a moderate quality research design, and were implemented in low- or middle-income countries. Policy or systems interventions able to produce behavior change reviewed included media (e.g., mass media, social media), community mobilization, educational programs (for caregivers, communities, or providers), social marketing, opinion leadership, economic incentives (for both caregiver and provider), health systems strengthening/policy/legislation, and others. Recommendations for policy, practice, and research are given based on fairly strong data across the areas of health service delivery, health workforce, health financing, governance and leadership, and research. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Vélez, Luis F AU - Sanitato, Mary AU - Barry, Donna AU - Alilio, Martin AU - Apfel, Franklin AU - Coe, Gloria AU - Garcia, Amparo AU - Kaufman, Michelle AU - Klein, Jonathan AU - Kutlesic, Vesna AU - Meadowcroft, Lisa AU - Nilsen, Wendy AU - O'Sullivan, Gael AU - Peterson, Stefan AU - Raiten, Daniel AU - Vorkoper, Susan AD - DePelchin Children's Center ; US Agency for International Development ; Center for American Progress ; World Health Communication Associates ; US Forest Service ; Johns Hopkins Bloomberg School of Public Health ; American Academy of Pediatrics ; National Institutes of Health ; African Medical and Research Foundation ; ABT Associates ; Karolinska Institute Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 89 EP - 121 VL - 19 IS - Supp.1 SN - 1081-0730, 1081-0730 KW - Sociology KW - Political Science KW - Child mortality KW - Social change KW - Health KW - U.S.A. KW - Public policy KW - Child development KW - Low income KW - Community care KW - Policy consultation KW - Health policy KW - Evidence KW - Infants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1613947810?accountid=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=The+role+of+health+systems+and+policy+in+producing+behavior+and+social+change+to+enhance+child+survival+and+development+in+low-+and+middle-income+countries%3A+an+examination+of+the+evidence&rft.au=V%C3%A9lez%2C+Luis+F%3BSanitato%2C+Mary%3BBarry%2C+Donna%3BAlilio%2C+Martin%3BApfel%2C+Franklin%3BCoe%2C+Gloria%3BGarcia%2C+Amparo%3BKaufman%2C+Michelle%3BKlein%2C+Jonathan%3BKutlesic%2C+Vesna%3BMeadowcroft%2C+Lisa%3BNilsen%2C+Wendy%3BO%27Sullivan%2C+Gael%3BPeterson%2C+Stefan%3BRaiten%2C+Daniel%3BVorkoper%2C+Susan&rft.aulast=V%C3%A9lez&rft.aufirst=Luis&rft.date=2014-09-01&rft.volume=19&rft.issue=Supp.1&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2014.939313 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-10-20 N1 - Last updated - 2014-10-20 N1 - SubjectsTermNotLitGenreText - 7553 6271; 5788 11888 10472; 2604 11949 13521; 2203 2212 8291 3409 6306; 4560; 2197 2212 6075 3483; 11783; 6495 2212; 5772; 10472; 9619 9628 9625; 433 293 14 DO - http://dx.doi.org/10.1080/10810730.2014.939313 ER - TY - JOUR T1 - Caregiver behavior change for child survival and development in low- and middle-income countries: an examination of the evidence AN - 1613947546; 4608960 AB - In June of 2012, representatives from more than 80 countries promulgated a Child Survival Call to Action, which called for reducing child mortality to 20 or fewer child deaths per 1,000 live births in every country by 2035. To address the problem of ending preventable child deaths, the U.S. Agency for International Development and the United Nations Children's Fund convened, on June 3-4, 2013, an Evidence Summit on Enhancing Child Survival and Development in Lower- and Middle-Income Countries by Achieving Population-Level Behavior Change. Six evidence review teams were established on different topics related to child survival and healthy development to identify the relevant evidence-based interventions and to prepare reports. This article was developed by the evidence review team responsible for identifying the research literature on caregiver change for child survival and development. This article is organized into childhood developmental periods and cross-cutting issues that affect child survival and healthy early development across all these periods. On the basis of this review, the authors present evidence-based recommendations for programs focused on caregivers to increase child survival and promote healthy development. Last, promising directions for future research to change caregivers' behaviors are given. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Elder, John P AU - Pequegnat, Willo AU - Ahmed, Saifuddin AU - Bachman, Gretchen AU - Bullock, Merry AU - Carlo, Waldemar A AU - Chandra-Mouli, Venkatraman AU - Fox, Nathan A AU - Harkness, Sara AU - Huebner, Gillian AU - Lombardi, Joan AU - Murry, Velma McBride AU - Moran, Allisyn AU - Norton, Maureen AU - Mulik, Jennifer AU - Parks, Will AU - Raikes, Helen H AU - Smyser, Joseph AU - Sugg, Caroline AU - Sweat, Michael AD - Diego State University ; National Institute of Mental Health ; Johns Hopkins Bloomberg School of Public Health ; US Agency for International Development ; American Psychological Association ; University of Alabama, Birmingham ; World Health Organization ; University of Maryland ; University of Connecticut ; Bernard van Leer Foundation ; Vanderbilt University ; United States Agency for International Development ; UNICEF ; University of Nebraska ; British Broadcasting Company ; Medical University of South Carolina Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 25 EP - 66 VL - 19 IS - Supp.1 SN - 1081-0730, 1081-0730 KW - Sociology KW - Political Science KW - Child mortality KW - Policy consultation KW - Social change KW - Health KW - U.S.A. KW - Evidence KW - Public policy KW - Child development KW - Low income KW - Infants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1613947546?accountid=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=Caregiver+behavior+change+for+child+survival+and+development+in+low-+and+middle-income+countries%3A+an+examination+of+the+evidence&rft.au=Elder%2C+John+P%3BPequegnat%2C+Willo%3BAhmed%2C+Saifuddin%3BBachman%2C+Gretchen%3BBullock%2C+Merry%3BCarlo%2C+Waldemar+A%3BChandra-Mouli%2C+Venkatraman%3BFox%2C+Nathan+A%3BHarkness%2C+Sara%3BHuebner%2C+Gillian%3BLombardi%2C+Joan%3BMurry%2C+Velma+McBride%3BMoran%2C+Allisyn%3BNorton%2C+Maureen%3BMulik%2C+Jennifer%3BParks%2C+Will%3BRaikes%2C+Helen+H%3BSmyser%2C+Joseph%3BSugg%2C+Caroline%3BSweat%2C+Michael&rft.aulast=Elder&rft.aufirst=John&rft.date=2014-09-01&rft.volume=19&rft.issue=Supp.1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2014.940477 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-10-20 N1 - Last updated - 2014-10-20 N1 - SubjectsTermNotLitGenreText - 7553 6271; 2203 2212 8291 3409 6306; 4560; 2197 2212 6075 3483; 11783; 6495 2212; 5772; 10472; 9619 9628 9625; 433 293 14 DO - http://dx.doi.org/10.1080/10810730.2014.940477 ER - TY - JOUR T1 - US lung cancer trends by histologic type AN - 1611613985; 20690441 AB - BACKGROUND Lung cancer incidence rates overall are declining in the United States. This study investigated the trends by histologic type and demographic characteristics. METHODS Surveillance, Epidemiology, and End Results (SEER) program rates of microscopically confirmed lung cancer overall and squamous cell, small cell, adenocarcinoma, large cell, other, and unspecified carcinomas among US whites and blacks diagnosed from 1977 to 2010 and white non-Hispanics, Asian/Pacific Islanders, and white Hispanics diagnosed from 1992 to 2010 were analyzed by sex and age. RESULTS Squamous and small cell carcinoma rates declined since the 1990s, although less rapidly among females than males. Adenocarcinoma rates decreased among males and only through 2005, after which they then rose during 2006 to 2010 among every racial/ethnic/sex group; rates for unspecified type declined. Male/female rate ratios declined among whites and blacks more than among other groups. Recent rates among young females were higher than among males for adenocarcinoma among all racial/ethnic groups and for other specified carcinomas among whites. CONCLUSIONS US lung cancer trends vary by sex, histologic type, racial/ethnic group, and age, reflecting historical cigarette smoking rates, duration, cessation, cigarette composition, and exposure to other carcinogens. Substantial excesses among males have diminished and higher rates of adenocarcinoma among young females have emerged as rates among males declined more rapidly. The recognition of EGFR mutation and ALK rearrangements that occur primarily in adenocarcinomas are the primary basis for the molecular revolution that has transformed lung cancer diagnosis and treatment over the past decade, and these changes have affected recent type-specific trends. Cancer 2014; 120:2883-2892. copyright 2014 American Cancer Society. This analysis of lung cancer trends by histologic type represents a fresh classification of lung cancer histology and reveals several new incidence trends by sex and race/ethnicity. This new analysis by histologic type is important in the context of molecular-based diagnosis and should inform additional research that will direct therapy appropriate to the specific lung cancer type. JF - Cancer AU - Lewis, Denise Riedel AU - Check, David P AU - Caporaso, Neil E AU - Travis, William D AU - Devesa, Susan S AD - Surveillance Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, Maryland. Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 2883 EP - 2892 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 120 IS - 18 SN - 0008-543X, 0008-543X KW - Health & Safety Science Abstracts KW - Demography KW - Historical account KW - USA KW - Age KW - Cigarettes KW - Classification KW - Histology KW - I, Pacific KW - Carcinogens KW - Mutation KW - Ethnic groups KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611613985?accountid=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&rft.atitle=US+lung+cancer+trends+by+histologic+type&rft.au=Lewis%2C+Denise+Riedel%3BCheck%2C+David+P%3BCaporaso%2C+Neil+E%3BTravis%2C+William+D%3BDevesa%2C+Susan+S&rft.aulast=Lewis&rft.aufirst=Denise&rft.date=2014-09-01&rft.volume=120&rft.issue=18&rft.spage=2883&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.28749 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-10-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Demography; Historical account; Age; Histology; Classification; Cigarettes; Carcinogens; Mutation; Ethnic groups; USA; I, Pacific DO - http://dx.doi.org/10.1002/cncr.28749 ER - TY - JOUR T1 - Antiretroviral therapy: current drugs. AN - 1609306097; 25151562 AB - The rapid advances in drug discovery and the development of antiretroviral therapy is unprecedented in the history of modern medicine. The administration of chronic combination antiretroviral therapy targeting different stages of the human immunodeficiency virus' replicative life cycle allows for durable and maximal suppression of plasma viremia. This suppression has resulted in dramatic improvement of patient survival. This article reviews the history of antiretroviral drug development and discusses the clinical pharmacology, efficacy, and toxicities of the antiretroviral agents most commonly used in clinical practice to date. Published by Elsevier Inc. JF - Infectious disease clinics of North America AU - Pau, Alice K AU - George, Jomy M AD - Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11C103 (MSC 1880), Bethesda, MD 20892, USA. Electronic address: apau@niaid.nih.gov. ; Department of Pharmacy Practice and Administration, Philadelphia College of Pharmacy, University of the Sciences in Philadelphia, 600 South 43rd Street, GH-108K, Philadelphia, PA 19104, USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 371 EP - 402 VL - 28 IS - 3 KW - Anti-Retroviral Agents KW - 0 KW - Index Medicus KW - Non-nucleoside reverse transcriptase inhibitors KW - Fusion inhibitor KW - CCR5 antagonist KW - Protease inhibitors KW - Nucleoside/nucleotide reverse transcriptase inhibitors KW - Integrase strand transfer inhibitors KW - Antiretroviral therapy KW - HIV KW - History, 21st Century KW - History, 20th Century KW - Humans KW - Drug Discovery -- trends KW - Antiretroviral Therapy, Highly Active -- adverse effects KW - Anti-Retroviral Agents -- pharmacokinetics KW - HIV Infections -- drug therapy KW - Anti-Retroviral Agents -- adverse effects KW - Antiretroviral Therapy, Highly Active -- history KW - Antiretroviral Therapy, Highly Active -- methods KW - Anti-Retroviral Agents -- pharmacology KW - Anti-Retroviral Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1609306097?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infectious+disease+clinics+of+North+America&rft.atitle=Antiretroviral+therapy%3A+current+drugs.&rft.au=Pau%2C+Alice+K%3BGeorge%2C+Jomy+M&rft.aulast=Pau&rft.aufirst=Alice&rft.date=2014-09-01&rft.volume=28&rft.issue=3&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=Infectious+disease+clinics+of+North+America&rft.issn=1557-9824&rft_id=info:doi/10.1016%2Fj.idc.2014.06.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-23 N1 - Date created - 2014-08-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):15109-14 [10611346] J Infect Dis. 2014 Aug 1;210(3):354-62 [24446523] AIDS. 2001 Jan 26;15(2):289 [11216946] J Natl Cancer Inst Monogr. 2001;(28):44-9 [11158206] Clin Ther. 2001 Oct;23(10):1603-14 [11726000] N Engl J Med. 2004 Apr 29;350(18):1850-61 [15115831] N Engl J Med. 1987 Jul 23;317(4):185-91 [3299089] N Engl J Med. 1994 Nov 3;331(18):1173-80 [7935654] N Engl J Med. 1998 Mar 26;338(13):853-60 [9516219] J Infect Dis. 1998 Jul;178(1):70-9 [9652425] AIDS. 1999 May 28;13(8):999-1000 [10371187] Antivir Ther. 2004 Dec;9(6):849-63 [15651744] Antivir Ther. 2005;10 Suppl 2:M47-52 [16152705] Am J Med Sci. 2007 Nov;334(5):334-41 [18004087] N Engl J Med. 2008 Feb 7;358(6):568-79 [18256392] Lancet. 2008 Apr 26;371(9622):1417-26 [18387667] Clin Infect Dis. 2008 Apr 1;46(7):1111-8 [18444831] N Engl J Med. 2008 Jul 24;359(4):339-54 [18650512] AIDS Patient Care STDS. 2008 Nov;22(11):843-50 [19025478] HIV Med. 2009 Jan;10(1):12-8 [18795964] Clin Infect Dis. 2009 Apr 1;48(7):931-9 [19231980] J Clin Rheumatol. 2009 Mar;15(2):72-4 [19265350] J Acquir Immune Defic Syndr. 2010 Sep;55(1):39-48 [20404738] Am J Kidney Dis. 2011 May;57(5):773-80 [21435764] AIDS. 2011 Aug 24;25(13):1671-3 [21716074] Scand J Infect Dis. 2011 Oct;43(10):821-6 [21563880] J Clin Pharmacol. 2012 Apr;52(4):520-9 [21558456] AIDS. 2012 Sep 24;26(15):1907-15 [22824630] J Acquir Immune Defic Syndr. 2012 Dec 1;61(4):441-7 [22932321] HIV Med. 2013 Jan;14(1):49-59 [23088336] Top Antivir Med. 2013 Feb-Mar;21(1):6-14 [23596273] AIDS. 2013 Mar 27;27(6):879-87 [23262501] J Acquir Immune Defic Syndr. 2013 Apr 15;62(5):525-33 [23274936] PLoS One. 2013;8(6):e66223 [23776637] HIV Clin Trials. 2013 May-Jun;14(3):81-91 [23835510] Antimicrob Agents Chemother. 2013 Nov;57(11):5619-28 [24002093] HIV Clin Trials. 2013 Sep-Oct;14(5):224-34 [24144899] J Antimicrob Chemother. 2014 May;69(5):1385-9 [24379301] J Infect Dis. 2000 Oct;182(4):1077-83 [10979902] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.idc.2014.06.001 ER - TY - JOUR T1 - Jonathan Silvertown The Long and the Short of It: The Science of Life Span and Aging AN - 1566851757; 20739526 JF - Population And Development Review AU - Haaga, John G AD - National Institute on Aging. Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 565 EP - 566 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 40 IS - 3 SN - 0098-7921, 0098-7921 KW - Sustainability Science Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566851757?accountid=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+And+Development+Review&rft.atitle=Jonathan+Silvertown+The+Long+and+the+Short+of+It%3A+The+Science+of+Life+Span+and+Aging&rft.au=Haaga%2C+John+G&rft.aulast=Haaga&rft.aufirst=John&rft.date=2014-09-01&rft.volume=40&rft.issue=3&rft.spage=565&rft.isbn=&rft.btitle=&rft.title=Population+And+Development+Review&rft.issn=00987921&rft_id=info:doi/10.1111%2Fj.1728-4457.2014.00701.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-10-02 DO - http://dx.doi.org/10.1111/j.1728-4457.2014.00701.x ER - TY - JOUR T1 - Ebola Virus Modulates Transforming Growth Factor beta Signaling and Cellular Markers of Mesenchyme-Like Transition in Hepatocytes AN - 1566850801; 20698556 AB - Ebola virus (EBOV) causes a severe hemorrhagic disease in humans and nonhuman primates, with a median case fatality rate of 78.4%. Although EBOV is considered a public health concern, there is a relative paucity of information regarding the modulation of the functional host response during infection. We employed temporal kinome analysis to investigate the relative early, intermediate, and late host kinome responses to EBOV infection in human hepatocytes. Pathway overrepresentation analysis and functional network analysis of kinome data revealed that transforming growth factor (TGF- beta )-mediated signaling responses were temporally modulated in response to EBOV infection. Upregulation of TGF- beta signaling in the kinome data sets correlated with the upregulation of TGF- beta secretion from EBOV-infected cells. Kinase inhibitors targeting TGF- beta signaling, or additional cell receptors and downstream signaling pathway intermediates identified from our kinome analysis, also inhibited EBOV replication. Further, the inhibition of select cell signaling intermediates identified from our kinome analysis provided partial protection in a lethal model of EBOV infection. To gain perspective on the cellular consequence of TGF- beta signaling modulation during EBOV infection, we assessed cellular markers associated with upregulation of TGF- beta signaling. We observed upregulation of matrix metalloproteinase 9, N-cadherin, and fibronectin expression with concomitant reductions in the expression of E-cadherin and claudin-1, responses that are standard characteristics of an epithelium-to-mesenchyme-like transition. Additionally, we identified phosphorylation events downstream of TGF- beta that may contribute to this process. From these observations, we propose a model for a broader role of TGF- beta -mediated signaling responses in the pathogenesis of Ebola virus disease. IMPORTANCE Ebola virus (EBOV), formerly Zaire ebolavirus, causes a severe hemorrhagic disease in humans and nonhuman primates and is the most lethal Ebola virus species, with case fatality rates of up to 90%. Although EBOV is considered a worldwide concern, many questions remain regarding EBOV molecular pathogenesis. As it is appreciated that many cellular processes are regulated through kinase-mediated phosphorylation events, we employed temporal kinome analysis to investigate the functional responses of human hepatocytes to EBOV infection. Administration of kinase inhibitors targeting signaling pathway intermediates identified in our kinome analysis inhibited viral replication in vitro and reduced EBOV pathogenesis in vivo. Further analysis of our data also demonstrated that EBOV infection modulated TGF- beta -mediated signaling responses and promoted "mesenchyme-like" phenotypic changes. Taken together, these results demonstrated that EBOV infection specifically modulates TGF- beta -mediated signaling responses in epithelial cells and may have broader implications in EBOV pathogenesis. JF - Journal of Virology AU - Kindrachuk, Jason AU - Wahl-Jensen, Victoria AU - Safronetz, David AU - Trost, Brett AU - Hoenen, Thomas AU - Arsenault, Ryan AU - Feldmann, Friederike AU - Traynor, Dawn AU - Postnikova, Elena AU - Kusalik, Anthony AD - Emerging Viral Pathogens Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, kindrachuk.kenneth@nih.gov. Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 9877 EP - 9892 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 88 IS - 17 SN - 0022-538X, 0022-538X KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Transforming growth factor KW - Epithelial cells KW - Hepatocytes KW - Fibronectin KW - Secretion KW - Animal models KW - Matrix metalloproteinase KW - Ebola virus KW - Infection KW - Angola, Zaire KW - Public health KW - Phosphorylation KW - Downstream KW - Growth factors KW - Mortality KW - Data processing KW - Replication KW - Primates KW - E-Cadherin KW - N-Cadherin KW - Transforming growth factor- beta KW - Hemorrhagic disease KW - Signal transduction KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22320:Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566850801?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Ebola+Virus+Modulates+Transforming+Growth+Factor+beta+Signaling+and+Cellular+Markers+of+Mesenchyme-Like+Transition+in+Hepatocytes&rft.au=Kindrachuk%2C+Jason%3BWahl-Jensen%2C+Victoria%3BSafronetz%2C+David%3BTrost%2C+Brett%3BHoenen%2C+Thomas%3BArsenault%2C+Ryan%3BFeldmann%2C+Friederike%3BTraynor%2C+Dawn%3BPostnikova%2C+Elena%3BKusalik%2C+Anthony&rft.aulast=Kindrachuk&rft.aufirst=Jason&rft.date=2014-09-01&rft.volume=88&rft.issue=17&rft.spage=9877&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.01410-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 68 N1 - Last updated - 2015-11-25 N1 - SubjectsTermNotLitGenreText - Epithelial cells; Transforming growth factor; Data processing; Hepatocytes; Replication; Secretion; Fibronectin; Animal models; Matrix metalloproteinase; Infection; E-Cadherin; Public health; Phosphorylation; N-Cadherin; Transforming growth factor- beta; Hemorrhagic disease; Signal transduction; Mortality; Downstream; Growth factors; Primates; Ebola virus; Angola, Zaire DO - http://dx.doi.org/10.1128/JVI.01410-14 ER - TY - JOUR T1 - Introductions and Evolution of Human-Origin Seasonal Influenza A Viruses in Multinational Swine Populations AN - 1566846982; 20698539 AB - The capacity of influenza A viruses to cross species barriers presents a continual threat to human and animal health. Knowledge of the human-swine interface is particularly important for understanding how viruses with pandemic potential evolve in swine hosts. We sequenced the genomes of 141 influenza viruses collected from North American swine during 2002 to 2011 and identified a swine virus that possessed all eight genome segments of human seasonal A/H3N2 virus origin. A molecular clock analysis indicates that this virus-A/sw/Saskatchewan/02903/2009(H3N2)-has likely circulated undetected in swine for at least 7 years. For historical context, we performed a comprehensive phylogenetic analysis of an additional 1,404 whole-genome sequences from swine influenza A viruses collected globally during 1931 to 2013. Human-to-swine transmission occurred frequently over this time period, with 20 discrete introductions of human seasonal influenza A viruses showing sustained onward transmission in swine for at least 1 year since 1965. Notably, human-origin hemagglutinin (H1 and H3) and neuraminidase (particularly N2) segments were detected in swine at a much higher rate than the six internal gene segments, suggesting an association between the acquisition of swine-origin internal genes via reassortment and the adaptation of human influenza viruses to new swine hosts. Further understanding of the fitness constraints on the adaptation of human viruses to swine, and vice versa, at a genomic level is central to understanding the complex multihost ecology of influenza and the disease threats that swine and humans pose to each other. IMPORTANCE The swine origin of the 2009 A/H1N1 pandemic virus underscored the importance of understanding how influenza A virus evolves in these animals hosts. While the importance of reassortment in generating genetically diverse influenza viruses in swine is well documented, the role of human-to-swine transmission has not been as intensively studied. Through a large-scale sequencing effort, we identified a novel influenza virus of wholly human origin that has been circulating undetected in swine for at least 7 years. In addition, we demonstrate that human-to-swine transmission has occurred frequently on a global scale over the past decades but that there is little persistence of human virus internal gene segments in swine. JF - Journal of Virology AU - Nelson, Martha I AU - Wentworth, David E AU - Culhane, Marie R AU - Vincent, Amy L AU - Viboud, Cecile AU - LaPointe, Matthew P AU - Lin, Xudong AU - Holmes, Edward C AU - Detmer, Susan E AD - Fogarty International Center, National Institutes of Health, Bethesda, Maryland, USA, nelsonma@mail.nih.gov. Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 10110 EP - 10119 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 88 IS - 17 SN - 0022-538X, 0022-538X KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Genomes KW - Fitness KW - Phylogeny KW - Historical account KW - Adaptations KW - Canada, Saskatchewan KW - Influenza A KW - Hemagglutinins KW - Viruses KW - Swine influenza KW - Influenza KW - Ecology KW - Adaptability KW - pandemics KW - Sulfur dioxide KW - Influenza A virus KW - genomics KW - Exo- alpha -sialidase KW - Seasonal variations KW - Evolution KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22310:Genetics, Taxonomy & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566846982?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Introductions+and+Evolution+of+Human-Origin+Seasonal+Influenza+A+Viruses+in+Multinational+Swine+Populations&rft.au=Nelson%2C+Martha+I%3BWentworth%2C+David+E%3BCulhane%2C+Marie+R%3BVincent%2C+Amy+L%3BViboud%2C+Cecile%3BLaPointe%2C+Matthew+P%3BLin%2C+Xudong%3BHolmes%2C+Edward+C%3BDetmer%2C+Susan+E&rft.aulast=Nelson&rft.aufirst=Martha&rft.date=2014-09-01&rft.volume=88&rft.issue=17&rft.spage=10110&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.01080-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 46 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Phylogeny; Fitness; Genomes; pandemics; Adaptations; Hemagglutinins; Influenza A; Swine influenza; Exo- alpha -sialidase; genomics; Evolution; Ecology; Influenza; Historical account; Adaptability; Sulfur dioxide; Viruses; Seasonal variations; Influenza A virus; Canada, Saskatchewan DO - http://dx.doi.org/10.1128/JVI.01080-14 ER - TY - CONF T1 - Cancer treatment-related cardiotoxicity: current state of knowledge and future research priorities. AN - 1561972361; 25210198 AB - Cardiotoxicity resulting from direct myocyte damage has been a known complication of cancer treatment for decades. More recently, the emergence of hypertension as a clinically significant side effect of several new agents has been recognized as adversely affecting cancer treatment outcomes. With cancer patients living longer, in part because of treatment advances, these adverse events have become increasingly important to address. However, little is known about the cardiovascular pathogenic mechanisms associated with cancer treatment and even less about how to optimally prevent and manage short- and long-term cardiovascular complications, leading to improved patient safety and clinical outcomes. To identify research priorities, allocate resources, and establish infrastructure required to address cardiotoxicity associated with cancer treatment, the National Cancer Institute (NCI) and National Heart, Lung and Blood Institute (NHLBI) sponsored a two-day workshop, "Cancer treatment-related cardiotoxicity: Understanding the current state of knowledge and future research priorities," in March 2013 in Bethesda, MD. Participants included leading oncology and cardiology researchers and health professionals, patient advocates and industry representatives, with expertise ranging from basic to clinical science. Attendees were charged with identifying research opportunities to advance the understanding of cancer treatment-related cardiotoxicity across basic and clinical science. This commentary highlights the key discussion points and overarching recommendations from that workshop. Published by Oxford University Press 2014. JF - Journal of the National Cancer Institute AU - Shelburne, Nonniekaye AU - Adhikari, Bishow AU - Brell, Joanna AU - Davis, Myrtle AU - Desvigne-Nickens, Patrice AU - Freedman, Andrew AU - Minasian, Lori AU - Force, Thomas AU - Remick, Scot C Y1 - 2014/09// PY - 2014 DA - September 2014 VL - 106 IS - 9 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - United States KW - Health Personnel -- education KW - National Cancer Institute (U.S.) KW - Humans KW - Muscle Cells -- drug effects KW - National Heart, Lung, and Blood Institute (U.S.) KW - Neoplasms -- drug therapy KW - Antineoplastic Agents -- administration & dosage KW - Heart Diseases -- chemically induced KW - Heart -- drug effects KW - Heart Diseases -- prevention & control KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561972361?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Journal+of+the+National+Cancer+Institute&rft.atitle=Cancer+treatment-related+cardiotoxicity%3A+current+state+of+knowledge+and+future+research+priorities.&rft.au=Shelburne%2C+Nonniekaye%3BAdhikari%2C+Bishow%3BBrell%2C+Joanna%3BDavis%2C+Myrtle%3BDesvigne-Nickens%2C+Patrice%3BFreedman%2C+Andrew%3BMinasian%2C+Lori%3BForce%2C+Thomas%3BRemick%2C+Scot+C&rft.aulast=Shelburne&rft.aufirst=Nonniekaye&rft.date=2014-09-01&rft.volume=106&rft.issue=9&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju232 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-14 N1 - Date created - 2014-09-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Circ Res. 2013 Aug 30;113(6):754-64 [23989717] Circulation. 2013 Jul 9;128(2):152-61 [23757312] Int J Cardiovasc Imaging. 2013 Oct;29(7):1459-76 [23744127] Circulation. 2013 Oct 22;128(17):1927-95 [24081971] J Cardiovasc Transl Res. 2014 Mar;7(2):250-61 [24309956] J Am Coll Cardiol. 2014 Mar 4;63(8):809-16 [24291281] Toxicol Sci. 2014 Aug 1;140(2):445-61 [24812011] J Am Coll Cardiol. 2000 Sep;36(3):959-69 [10987628] J Clin Oncol. 2001 Jul 1;19(13):3163-72 [11432882] Ann Oncol. 2002 Jun;13(6):819-29 [12123328] Int J Cancer. 2003 Apr 20;104(4):488-95 [12584748] Cancer. 2003 Jun 1;97(11):2869-79 [12767102] Circulation. 2004 Jun 8;109(22):2749-54 [15148277] Semin Oncol. 1998 Aug;25(4 Suppl 10):10-4 [9768818] Mol Pharmacol. 2005 Aug;68(2):261-71 [15883202] J Clin Oncol. 2006 Jul 20;24(21):3509-10; author reply 3510-1 [16849773] J Clin Oncol. 2009 May 10;27(14):2339-55 [19364955] J Am Coll Cardiol. 2009 Jun 16;53(24):2231-47 [19520246] Cancer Epidemiol Biomarkers Prev. 2010 Jan;19(1):170-81 [20056636] J Natl Cancer Inst. 2010 May 5;102(9):596-604 [20351338] BMC Cancer. 2010;10:337 [20587042] Prog Cardiovasc Dis. 2010 Sep-Oct;53(2):94-104 [20728696] Prog Cardiovasc Dis. 2010 Sep-Oct;53(2):173-9 [20728705] Eur J Heart Fail. 2011 Jan;13(1):1-10 [21169385] Am J Cardiol. 2011 May 1;107(9):1375-80 [21371685] Am Heart J. 2012 Feb;163(2):156-63 [22305831] J Natl Cancer Inst. 2012 Mar 7;104(5):357-70 [22312134] J Nucl Cardiol. 2012 Apr;19(2):377-88 [22351492] Cancer. 2012 Apr 15;118(8 Suppl):2270-6 [22488701] Cochrane Database Syst Rev. 2012;4:CD006243 [22513938] BMC Physiol. 2012;12:3 [22449203] Curr Cardiol Rev. 2011 Nov;7(4):234-44 [22758624] CA Cancer J Clin. 2012 Jul-Aug;62(4):220-41 [22700443] Eur Heart J. 2012 Jul;33(14):1787-847 [22611136] Circ Cardiovasc Imaging. 2012 Sep 1;5(5):596-603 [22744937] J Transl Med. 2012;10:140 [22768802] Curr Cardiol Rep. 2013 Jan;15(1):326 [23250662] Circulation. 2013 Apr 23;127(16):1677-91 [23519760] Circulation. 2013 Jul 9;128(2):98-100 [23757311] J Nucl Med Technol. 2013 Sep;41(3):170-81 [23929800] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/dju232 ER - TY - JOUR T1 - Effects of methylprednisolone and 4-chloro-3-hydroxyanthranilic acid in experimental spinal cord injury in the guinea pig appear to be mediated by different and potentially complementary mechanisms. AN - 1560585260; 25047053 AB - Blinded, placebo-controlled, parallel treatment group studies of the effects of methylprednisolone (MP) or 4-chloro-3-hydroxyanthranilate (4-Cl-3-HAA) on behavioral outcome and quinolinic acid tissue levels from experimental thoracic spinal cord injury in adult guinea pigs. To compare the effects of treatment with high-dose MP, a corticosteroid, and 4-Cl-3-HAA, a compound that inhibits synthesis of the neurotoxin quinolinic acid (QUIN) by activated macrophages. To explore the effect of different times of treatment using these two approaches to ameliorating secondary tissue damage. Laboratory animal studies at the University of North Carolina, Chapel Hill, NC, USA. Standardized spinal cord injuries were produced in anesthetized guinea pigs, using lateral compression of the spinal cord. Behavioral impairment and recovery were measured by placing and toe-spread responses (motor function), cutaneus trunci muscle reflex receptive field areas and somatosensory-evoked potentials (sensory function). Tissue quinolinic acid levels were measured by gas chromatograph/mass spectrometry. The current experiments showed a reduction in delayed loss of motor and sensory function in the guinea pig with MP (150 mg kg(-1), intraperitoneally in split doses between 0.5 and 6 h), but no significant reduction in tissue QUIN. Improved sensory function was seen with a single dose of 60 mg kg(-1) MP intraperitoneally at 5 h after injury, but not at 10 h after injury. A single dose of 4-Cl-3-HAA at 5 h in the guinea pig did not produce the sensory and motor improvements seen in previous studies with 12 days of dosing, beginning at 5 h. These studies, together with earlier findings, indicate that both drugs can attenuate secondary pathologic damage after SCI, but through separate mechanisms. These are most likely an acute reduction by MP of oxidative processes and reduction by 4-Cl-3-HAA of QUIN synthesis. JF - Spinal cord AU - Yates, J R AU - Gay, E A AU - Heyes, M P AU - Blight, A R AD - 1] Curriculum in Neurobiology and Division of Neurosurgery, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA [2] Acorda Therapeutics Inc., Ardsley, NY, USA [3] Department of Psychology, Ohio Wesleyan University, Delaware, OH, USA. ; Curriculum in Neurobiology and Division of Neurosurgery, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Laboratory of Neurotoxicology, National Institute of Mental Health, Chapel Hill, NC, USA. ; 1] Curriculum in Neurobiology and Division of Neurosurgery, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA [2] Acorda Therapeutics Inc., Ardsley, NY, USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 662 EP - 666 VL - 52 IS - 9 KW - 3-Hydroxyanthranilic Acid KW - 1UQB1BT4OT KW - 4-chloro-3-hydroxyanthranilic acid KW - 23219-33-2 KW - Quinolinic Acid KW - F6F0HK1URN KW - Methylprednisolone KW - X4W7ZR7023 KW - Index Medicus KW - Animals KW - Quinolinic Acid -- metabolism KW - Guinea Pigs KW - Disease Models, Animal KW - Evoked Potentials, Somatosensory KW - Female KW - Spinal Cord Injuries -- metabolism KW - 3-Hydroxyanthranilic Acid -- pharmacology KW - Methylprednisolone -- pharmacology KW - Spinal Cord Injuries -- drug therapy KW - Behavior, Animal -- physiology KW - Spinal Cord Injuries -- physiopathology KW - 3-Hydroxyanthranilic Acid -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560585260?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Spinal+cord&rft.atitle=Effects+of+methylprednisolone+and+4-chloro-3-hydroxyanthranilic+acid+in+experimental+spinal+cord+injury+in+the+guinea+pig+appear+to+be+mediated+by+different+and+potentially+complementary+mechanisms.&rft.au=Yates%2C+J+R%3BGay%2C+E+A%3BHeyes%2C+M+P%3BBlight%2C+A+R&rft.aulast=Yates&rft.aufirst=J&rft.date=2014-09-01&rft.volume=52&rft.issue=9&rft.spage=662&rft.isbn=&rft.btitle=&rft.title=Spinal+cord&rft.issn=1476-5624&rft_id=info:doi/10.1038%2Fsc.2014.118 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-12 N1 - Date created - 2014-09-05 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/sc.2014.118 ER - TY - JOUR T1 - Reliability of triclosan measures in repeated urine samples from Norwegian pregnant women AN - 1560138677; 20621177 AB - Triclosan (TCS) is a synthetic antibacterial chemical that is used in personal care products and is measurable in urine. Urinary TCS has been associated with allergy in children in Norway and the United States. A reasonable degree of temporal reliability of TCS urinary concentrations has been reported among US children as well as for Puerto Rican pregnant women. We examined the reliability of TCS measures in urine among Norwegian pregnant women. TCS was measured in spot urine samples collected in gestational weeks 17, 23, and 29 from 45 women in The Norwegian Mother and Child Cohort Study (MoBa) enrolled in 2007 and 2008. Spearman's rank correlation coefficient (r sub(s)) and intraclass correlation coefficient (ICC) statistics were calculated. Fifty-six percent of the 45 women had a least one sample with a value above the method limit of detection (2.3 mu g/l). The correlation coefficients were 0.61 for TCS concentrations at 17 and 23 weeks and 0.49 for concentrations at 17 and 29 weeks. For the three time points, the ICC was 0.49. The reliability of TCS concentrations in repeated urine samples from pregnant Norwegian women was reasonably good, suggesting a single urine sample can adequately represent TCS exposure during pregnancy. JF - Journal of Exposure Science and Environmental Epidemiology AU - Bertelsen, Randi J AU - Engel, Stephanie M AU - Jusko, Todd A AU - Calafat, Antonia M AU - Hoppin, Jane A AU - London, Stephanie J AU - Eggesboe, Merete AU - Aase, Heidi AU - Zeiner, Pal AU - Reichborn-Kjennerud, Ted AU - Knudsen, Gun P AU - Guidry, Virginia T AU - Longnecker, Matthew P AD - 1] Epidemiology Branch, National Institute of Environmental Health Sciences (NIEHS/NIH), Research Triangle Park, North Cardina, USA [2] Department of food, water and cosmetics, Norwegian Institute of Public Health, Oslo, Norway Y1 - 2014/09// PY - 2014 DA - Sep 2014 SP - 517 EP - 521 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 24 IS - 5 SN - 1559-0631, 1559-0631 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Statistics KW - Consumer products KW - Children KW - Allergies KW - Pregnancy KW - USA KW - Hypersensitivity KW - Urine KW - Females KW - Norway KW - Triclosan KW - H 12000:Epidemiology and Public Health KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560138677?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.atitle=Reliability+of+triclosan+measures+in+repeated+urine+samples+from+Norwegian+pregnant+women&rft.au=Bertelsen%2C+Randi+J%3BEngel%2C+Stephanie+M%3BJusko%2C+Todd+A%3BCalafat%2C+Antonia+M%3BHoppin%2C+Jane+A%3BLondon%2C+Stephanie+J%3BEggesboe%2C+Merete%3BAase%2C+Heidi%3BZeiner%2C+Pal%3BReichborn-Kjennerud%2C+Ted%3BKnudsen%2C+Gun+P%3BGuidry%2C+Virginia+T%3BLongnecker%2C+Matthew+P&rft.aulast=Bertelsen&rft.aufirst=Randi&rft.date=2014-09-01&rft.volume=24&rft.issue=5&rft.spage=517&rft.isbn=&rft.btitle=&rft.title=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.issn=15590631&rft_id=info:doi/10.1038%2Fjes.2013.95 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Hypersensitivity; Statistics; Urine; Children; Triclosan; Pregnancy; Consumer products; Females; Allergies; USA; Norway DO - http://dx.doi.org/10.1038/jes.2013.95 ER - TY - JOUR T1 - Isolation of rare recombinants without using selectable markers for one-step seamless BAC mutagenesis. AN - 1558529894; 25028895 AB - Current methods to isolate rare (1:10,000-1:100,000) bacterial artificial chromosome (BAC) recombinants require selectable markers. For seamless BAC mutagenesis, selectable markers need to be removed after isolation of recombinants through counterselection. Here we illustrate founder principle-driven enrichment (FPE), a simple method to rapidly isolate rare recombinants without using selectable markers, allowing one-step seamless BAC mutagenesis. As proof of principle, we isolated 1:100,000 seamless fluorescent protein-modified Nodal BACs and confirmed BAC functionality by generating fluorescent reporter mice. We also isolated small indel P1 phage-derived artificial chromosome (PAC) and BAC recombinants. Statistical analysis revealed that 1:100,000 recombinants can be isolated with <40 PCRs, and we developed a web-based calculator to optimize FPE. JF - Nature methods AU - Lyozin, George T AU - Bressloff, Paul C AU - Kumar, Amit AU - Kosaka, Yasuhiro AU - Demarest, Bradley L AU - Yost, H Joseph AU - Kuehn, Michael R AU - Brunelli, Luca AD - Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah, USA. ; 1] Department of Mathematics, University of Utah, Salt Lake City, Utah, USA. [2]. ; 1] Laboratory of Protein Dynamics and Signaling, National Cancer Institute, Frederick, Maryland, USA. [2]. ; Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, Utah, USA. ; 1] Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah, USA. [2] Department of Neurobiology and Anatomy, University of Utah School of Medicine, Salt Lake City, Utah, USA. ; Laboratory of Protein Dynamics and Signaling, National Cancer Institute, Frederick, Maryland, USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 966 EP - 970 VL - 11 IS - 9 KW - Genetic Markers KW - 0 KW - Recombinant Proteins KW - Index Medicus KW - Animals KW - Genetic Markers -- genetics KW - Mice KW - Recombinant Proteins -- isolation & purification KW - Mutagenesis, Site-Directed -- methods KW - Protein Engineering -- methods KW - Chromosomes, Artificial, Bacterial -- genetics KW - Recombinant Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558529894?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+methods&rft.atitle=Isolation+of+rare+recombinants+without+using+selectable+markers+for+one-step+seamless+BAC+mutagenesis.&rft.au=Lyozin%2C+George+T%3BBressloff%2C+Paul+C%3BKumar%2C+Amit%3BKosaka%2C+Yasuhiro%3BDemarest%2C+Bradley+L%3BYost%2C+H+Joseph%3BKuehn%2C+Michael+R%3BBrunelli%2C+Luca&rft.aulast=Lyozin&rft.aufirst=George&rft.date=2014-09-01&rft.volume=11&rft.issue=9&rft.spage=966&rft.isbn=&rft.btitle=&rft.title=Nature+methods&rft.issn=1548-7105&rft_id=info:doi/10.1038%2Fnmeth.3030 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-04 N1 - Date created - 2014-08-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2000 May 23;97(11):5978-83 [10811905] Nat Biotechnol. 2013 Mar;31(3):233-9 [23360965] Genome Res. 2003 Mar;13(3):476-84 [12618378] Nat Biotechnol. 2003 Jun;21(6):652-9 [12730667] Gene. 2003 Oct 2;315:63-9 [14557065] Dev Cell. 2004 Jan;6(1):7-28 [14723844] J Exp Med. 1980 Jun 1;151(6):1372-85 [6445930] Methods Enzymol. 1983;101:202-11 [6310324] Nature. 1988 Sep 8;335(6186):142-5 [3045565] Genetics. 1989 Mar;121(3):395-9 [2653959] Res Microbiol. 1992 Sep;143(7):711-9 [1488555] Nature. 1993 Feb 11;361(6412):543-7 [8429908] Science. 1994 Feb 11;263(5148):802-5 [8303295] Nat Genet. 1994 Jan;6(1):84-9 [8136839] Nat Genet. 1996 Dec;14(4):450-6 [8944025] J Bacteriol. 1998 Apr;180(8):2063-71 [9555887] Nat Genet. 1998 Oct;20(2):123-8 [9771703] Genes Dev. 1999 Jun 15;13(12):1575-88 [10385626] BMC Mol Biol. 2004 Dec 13;5(1):22 [15596011] Nat Methods. 2006 Oct;3(10):839-44 [16990816] Plasmid. 2007 Sep;58(2):148-58 [17434584] Nat Methods. 2008 May;5(5):409-15 [18391959] Nat Protoc. 2009;4(2):206-23 [19180090] Nat Biotechnol. 2009 Apr;27(4):369-77 [19349972] Nature. 2009 Aug 13;460(7257):894-8 [19633652] Mol Microbiol. 2010 Jan;75(1):138-48 [19943907] Science. 2010 Feb 12;327(5967):818-22 [20150489] Nat Biotechnol. 2010 Aug;28(8):856-62 [20639866] J Mol Biol. 2011 Mar 18;407(1):45-59 [21256136] Biotechnol Bioeng. 2011 Aug;108(8):1872-82 [21351074] Nature. 2011 Jun 16;474(7351):337-42 [21677750] PLoS One. 2011;6(8):e23457 [21858126] Nat Methods. 2011 Dec;8(12):1078-82 [22020067] Nat Methods. 2012 Jan;9(1):103-9 [22138824] Genesis. 2001 Jan;29(1):14-21 [11135458] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nmeth.3030 ER - TY - JOUR T1 - Transforming growth factor alpha is a critical mediator of radiation lung injury. AN - 1558524652; 25117621 AB - Radiation fibrosis of the lung is a late toxicity of thoracic irradiation. Epidermal growth factor (EGF) signaling has previously been implicated in radiation lung injury. We hypothesized that TGF-α, an EGF receptor ligand, plays a key role in radiation-induced fibrosis in lung. Mice deficient in transforming growth factor (TGF-α(-/-)) and control C57Bl/6J (C57-WT) mice were exposed to thoracic irradiation in 5 daily fractions of 6 Gy. Cohorts of mice were followed for survival (n ≥ 5 per group) and tissue collection (n = 3 per strain and time point). Collagen accumulation in irradiated lungs was assessed by Masson's trichrome staining and analysis of hydroxyproline content. Cytokine levels in lung tissue were assessed with ELISA. The effects of TGF-α on pneumocyte and fibroblast proliferation and collagen production were analyzed in vitro. Lysyl oxidase (LOX) expression and activity were measured in vitro and in vivo. Irradiated C57-WT mice had a median survival of 24.4 weeks compared to 48.2 weeks for irradiated TGF-α(-/-) mice (P = 0.001). At 20 weeks after irradiation, hydroxyproline content was markedly increased in C57-WT mice exposed to radiation compared to TGF-α(-/-) mice exposed to radiation or unirradiated C57-WT mice (63.0, 30.5 and 37.6 μg/lung, respectively, P = 0.01). C57-WT mice exposed to radiation had dense foci of subpleural fibrosis at 20 weeks after exposure, whereas the lungs of irradiated TGF-α (-/-) mice were largely devoid of fibrotic foci. Lung tissue concentrations of IL-1β, IL-4, TNF-α, TGF-β and EGF at multiple time points after irradiation were similar in C57-WT and TGF-α(-/-) mice. TGF-α in lung tissue of C57-WT mice rose rapidly after irradiation and remained elevated through 20 weeks. TGF-α(-/-) mice had lower basal LOX expression than C57-WT mice. Both LOX expression and LOX activity were increased after irradiation in all mice but to a lesser degree in TGF-α(-/-) mice. Treatment of NIH-3T3 fibroblasts with TGF-α resulted in increases in proliferation, collagen production and LOX activity. These studies identify TGF-α as a critical mediator of radiation-induced lung injury and a novel therapeutic target in this setting. Further, these data implicate TGF-α as a mediator of collagen maturation through a TGF-β independent activation of lysyl oxidase. JF - Radiation research AU - Chung, Eun Joo AU - Hudak, Kathryn AU - Horton, Jason A AU - White, Ayla AU - Scroggins, Bradley T AU - Vaswani, Shiva AU - Citrin, Deborah AD - Radiation Oncology Branch, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 350 EP - 362 VL - 182 IS - 3 KW - Cytokines KW - 0 KW - Transforming Growth Factor alpha KW - Collagen KW - 9007-34-5 KW - Protein-Lysine 6-Oxidase KW - EC 1.4.3.13 KW - Index Medicus KW - Space life sciences KW - Animals KW - Pulmonary Fibrosis -- etiology KW - Collagen -- metabolism KW - Cytokines -- biosynthesis KW - Mice, Inbred C57BL KW - Mice KW - Protein-Lysine 6-Oxidase -- metabolism KW - NIH 3T3 Cells KW - Female KW - Transforming Growth Factor alpha -- physiology KW - Radiation Injuries -- metabolism KW - Radiation Injuries -- pathology KW - Radiation Injuries -- etiology KW - Lung -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558524652?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transforming+growth+factor+alpha+is+a+critical+mediator+of+radiation+lung+injury.&rft.au=Chung%2C+Eun+Joo%3BHudak%2C+Kathryn%3BHorton%2C+Jason+A%3BWhite%2C+Ayla%3BScroggins%2C+Bradley+T%3BVaswani%2C+Shiva%3BCitrin%2C+Deborah&rft.aulast=Chung&rft.aufirst=Eun&rft.date=2014-09-01&rft.volume=182&rft.issue=3&rft.spage=350&rft.isbn=&rft.btitle=&rft.title=Radiation+research&rft.issn=1938-5404&rft_id=info:doi/10.1667%2FRR13625.1 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-24 N1 - Date created - 2014-08-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lab Invest. 1999 Dec;79(12):1655-67 [10616214] Clin Oral Investig. 2015 Mar;19(2):209-20 [24802627] J Cell Biochem. 2002;85(4):775-84 [11968017] Cancer Res. 2003 Aug 15;63(16):5054-9 [12941834] Int J Radiat Oncol Biol Phys. 2004 Feb 1;58(2):463-9 [14751516] FASEB J. 2004 May;18(7):926-8 [15033924] J Biol Chem. 2004 Jun 4;279(23):24307-12 [15039441] J Invest Dermatol. 2004 Nov;123(5):982-9 [15482488] Proc Natl Acad Sci U S A. 1976 Jan;73(1):183-7 [1061114] Am J Pathol. 1986 Jan;122(1):92-100 [2934989] Lab Invest. 1991 Apr;64(4):538-45 [2016859] Exp Cell Res. 1994 Feb;210(2):166-71 [8299714] Am J Physiol. 1994 Jan;266(1 Pt 1):L17-22 [8304465] J Clin Invest. 1994 Apr;93(4):1691-9 [8163670] J Biol Chem. 1994 Oct 7;269(40):25057-61 [7929192] Am J Respir Cell Mol Biol. 1994 Nov;11(5):540-51 [7524566] Am J Physiol. 1994 Dec;267(6 Pt 1):L728-38 [7810677] Exp Lung Res. 1995 May-Jun;21(3):407-21 [7621777] J Vasc Surg. 1997 Mar;25(3):446-52 [9081125] Exp Lung Res. 1998 Jan-Feb;24(1):27-39 [9457467] Am J Respir Cell Mol Biol. 1999 May;20(5):924-34 [10226062] J Immunol. 2005 Apr 15;174(8):5047-56 [15814736] Cancer Res. 2006 Apr 1;66(7):3802-12 [16585207] J Biol Chem. 2008 Apr 18;283(16):10226-31 [18182394] J Nippon Med Sch. 2008 Apr;75(2):96-105 [18475030] Am J Physiol Lung Cell Mol Physiol. 2008 Jun;294(6):L1217-25 [18424623] Curr Med Chem. 2009;16(2):130-43 [19149566] Clin Colorectal Cancer. 2009 Apr;8(2):118-20 [19739274] Am J Respir Cell Mol Biol. 2009 Nov;41(5):562-72 [19244201] Acta Biomater. 2010 Aug;6(8):3146-51 [20144751] J Vis Exp. 2010;(44). pii: 2033. doi: 10.3791/2033 [20972406] Am J Respir Crit Care Med. 2011 Mar 15;183(6):743-51 [20935109] Radiat Res. 2011 May;175(5):657-64 [21342009] Cytokine. 2011 Jul;55(1):90-7 [21498085] Am J Respir Cell Mol Biol. 2011 Jul;45(1):127-35 [20870892] Biochem Biophys Res Commun. 2011 Sep 23;413(2):370-5 [21893029] Target Oncol. 2011 Dec;6(4):235-43 [22076388] J Med Invest. 2012;59(1-2):174-85 [22450006] Onkologie. 2012;35(4):191-4 [22488089] Am J Ther. 2011 Jan;18(1):e19-21 [20019587] Clin Cancer Res. 2012 Jul 1;18(13):3616-27 [22547771] Proc Natl Acad Sci U S A. 2012 Nov 20;109(47):19392-6 [23129611] Cancer Res. 2013 Mar 15;73(6):1721-32 [23345161] Cytokine. 2013 Apr;62(1):22-33 [23481102] Biomed Res Int. 2013;2013:654354 [23841084] Oncol Res. 2013;20(7):303-17 [23879171] J Natl Cancer Inst. 2013 Oct 2;105(19):1474-84 [24052614] FASEB J. 2000 Jul;14(10):1362-74 [10877829] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1667/RR13625.1 ER - TY - JOUR T1 - Transarterial embolization (TAE) is equally effective and slightly safer than transarterial chemoembolization (TACE) to manage liver metastases in neuroendocrine tumors. AN - 1558521613; 24385266 AB - Liver metastases from neuroendocrine tumor (NET) can be treated by transarterial embolization (TAE) or transarterial chemoembolization (TACE). The goal of TAE and TACE is to reduce blood flow to the tumor resulting in tumor ischemia and necrosis. In this retrospective study, the effectiveness and safety of TAE-TACE in the treatment of liver metastases in patients with NET was compared. Thirty patients with a histologically confirmed gastro-entero-pancreatic NET with liver metastases were retrospectively investigated. Seventeen patients underwent TAE, while 13 patients underwent TACE. Tumor response, degree of devascularization in treated lesions, and progression free survival (PFS) were evaluated in the whole population and then separately in TAE and TACE subgroups. In all patients treated with TAE and TACE, there was a significant size reduction of lesions as compared to baseline. Per lesion reduction was 2.2 ± 1.4 versus 3.3 ± 1.5 cm for TAE (p < 0.001) and 2.2 ± 1.5 versus 3.4 ± 1.7 cm for TACE (p < 0.001). In the whole population, the median PFS for all patients was 36 months (16.2-55.7 CI), without significant difference between TAE and TACE. In no patient did adverse events grade 3 and 4 as well as TAE/TACE-related death occurred, while the post-embolization syndrome occurred in 41 % of patients treated with TAE and 61 % of those treated with TACE. TAE and TACE are both effective in NET patients with liver metastases. TAE should be preferred to TACE in light of its similar anti-tumor effects and slightly better toxicity profile. JF - Endocrine AU - Fiore, Francesco AU - Del Prete, Michela AU - Franco, Renato AU - Marotta, Vincenzo AU - Ramundo, Valeria AU - Marciello, Francesca AU - Di Sarno, Antonella AU - Carratù, Anna Chiara AU - de Luca di Roseto, Chiara AU - Colao, Annamaria AU - Faggiano, Antongiulio AD - Interventional Radiology, National Cancer Institute, Fondazione "G. Pascale", Naples, Italy, doc.fiore@virgilio.it. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 177 EP - 182 VL - 47 IS - 1 KW - Index Medicus KW - Young Adult KW - Disease-Free Survival KW - Humans KW - Aged KW - Gastrointestinal Neoplasms -- therapy KW - Chemoembolization, Therapeutic -- adverse effects KW - Pancreatic Neoplasms -- pathology KW - Pancreatic Neoplasms -- therapy KW - Aged, 80 and over KW - Chemoembolization, Therapeutic -- methods KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Gastrointestinal Neoplasms -- pathology KW - Female KW - Male KW - Neuroendocrine Tumors -- therapy KW - Neuroendocrine Tumors -- pathology KW - Embolization, Therapeutic -- methods KW - Liver Neoplasms -- therapy KW - Liver Neoplasms -- secondary KW - Embolization, Therapeutic -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558521613?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrine&rft.atitle=Transarterial+embolization+%28TAE%29+is+equally+effective+and+slightly+safer+than+transarterial+chemoembolization+%28TACE%29+to+manage+liver+metastases+in+neuroendocrine+tumors.&rft.au=Fiore%2C+Francesco%3BDel+Prete%2C+Michela%3BFranco%2C+Renato%3BMarotta%2C+Vincenzo%3BRamundo%2C+Valeria%3BMarciello%2C+Francesca%3BDi+Sarno%2C+Antonella%3BCarrat%C3%B9%2C+Anna+Chiara%3Bde+Luca+di+Roseto%2C+Chiara%3BColao%2C+Annamaria%3BFaggiano%2C+Antongiulio&rft.aulast=Fiore&rft.aufirst=Francesco&rft.date=2014-09-01&rft.volume=47&rft.issue=1&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Endocrine&rft.issn=1559-0100&rft_id=info:doi/10.1007%2Fs12020-013-0130-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-08 N1 - Date created - 2014-08-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s12020-013-0130-9 ER - TY - JOUR T1 - Joint analysis of three genome-wide association studies of esophageal squamous cell carcinoma in Chinese populations. AN - 1558519653; 25129146 AB - We conducted a joint (pooled) analysis of three genome-wide association studies (GWAS) of esophageal squamous cell carcinoma (ESCC) in individuals of Chinese ancestry (5,337 ESCC cases and 5,787 controls) with 9,654 ESCC cases and 10,058 controls for follow-up. In a logistic regression model adjusted for age, sex, study and two eigenvectors, two new loci achieved genome-wide significance, marked by rs7447927 at 5q31.2 (per-allele odds ratio (OR) = 0.85, 95% confidence interval (CI) = 0.82-0.88; P = 7.72 × 10(-20)) and rs1642764 at 17p13.1 (per-allele OR = 0.88, 95% CI = 0.85-0.91; P = 3.10 × 10(-13)). rs7447927 is a synonymous SNP in TMEM173, and rs1642764 is an intronic SNP in ATP1B2, near TP53. Furthermore, a locus in the HLA class II region at 6p21.32 (rs35597309) achieved genome-wide significance in the two populations at highest risk for ESSC (OR = 1.33, 95% CI = 1.22-1.46; P = 1.99 × 10(-10)). Our joint analysis identifies new ESCC susceptibility loci overall as well as a new locus unique to the population in the Taihang Mountain region at high risk of ESCC. JF - Nature genetics AU - Wu, Chen AU - Wang, Zhaoming AU - Song, Xin AU - Feng, Xiao-Shan AU - Abnet, Christian C AU - He, Jie AU - Hu, Nan AU - Zuo, Xian-Bo AU - Tan, Wen AU - Zhan, Qimin AU - Hu, Zhibin AU - He, Zhonghu AU - Jia, Weihua AU - Zhou, Yifeng AU - Yu, Kai AU - Shu, Xiao-Ou AU - Yuan, Jian-Min AU - Zheng, Wei AU - Zhao, Xue-Ke AU - Gao, She-Gan AU - Yuan, Zhi-Qing AU - Zhou, Fu-You AU - Fan, Zong-Min AU - Cui, Ji-Li AU - Lin, Hong-Li AU - Han, Xue-Na AU - Li, Bei AU - Chen, Xi AU - Dawsey, Sanford M AU - Liao, Linda AU - Lee, Maxwell P AU - Ding, Ti AU - Qiao, You-Lin AU - Liu, Zhihua AU - Liu, Yu AU - Yu, Dianke AU - Chang, Jiang AU - Wei, Lixuan AU - Gao, Yu-Tang AU - Koh, Woon-Puay AU - Xiang, Yong-Bing AU - Tang, Ze-Zhong AU - Fan, Jin-Hu AU - Han, Jing-Jing AU - Zhou, Sheng-Li AU - Zhang, Peng AU - Zhang, Dong-Yun AU - Yuan, Yuan AU - Huang, Ying AU - Liu, Chunling AU - Zhai, Kan AU - Qiao, Yan AU - Jin, Guangfu AU - Guo, Chuanhai AU - Fu, Jianhua AU - Miao, Xiaoping AU - Lu, Changdong AU - Yang, Haijun AU - Wang, Chaoyu AU - Wheeler, William A AU - Gail, Mitchell AU - Yeager, Meredith AU - Yuenger, Jeff AU - Guo, Er-Tao AU - Li, Ai-Li AU - Zhang, Wei AU - Li, Xue-Min AU - Sun, Liang-Dan AU - Ma, Bao-Gen AU - Li, Yan AU - Tang, Sa AU - Peng, Xiu-Qing AU - Liu, Jing AU - Hutchinson, Amy AU - Jacobs, Kevin AU - Giffen, Carol AU - Burdette, Laurie AU - Fraumeni, Joseph F AU - Shen, Hongbing AU - Ke, Yang AU - Zeng, Yixin AU - Wu, Tangchun AU - Kraft, Peter AU - Chung, Charles C AU - Tucker, Margaret A AU - Hou, Zhi-Chao AU - Liu, Ya-Li AU - Hu, Yan-Long AU - Wang, Li AU - Yuan, Guo AU - Chen, Li-Sha AU - Liu, Xiao AU - Ma, Teng AU - Meng, Hui AU - Sun, Li AU - Li, Xin-Min AU - Li, Xiu-Min AU - Ku, Jian-Wei AU - Zhou, Ying-Fa AU - Yang, Liu-Qin AU - Wang, Zhou AU - Li, Yin AU - Qige, Qirenwang AU - Yang, Wen-Jun AU - Lei, Guang-Yan AU - Chen, Long-Qi AU - Li, En-Min AU - Yuan, Ling AU - Yue, Wen-Bin AU - Wang, Ran AU - Wang, Lu-Wen AU - Fan, Xue-Ping AU - Zhu, Fang-Heng AU - Zhao, Wei-Xing AU - Mao, Yi-Min AU - Zhang, Mei AU - Xing, Guo-Lan AU - Li, Ji-Lin AU - Han, Min AU - Ren, Jing-Li AU - Liu, Bin AU - Ren, Shu-Wei AU - Kong, Qing-Peng AU - Li, Feng AU - Sheyhidin, Ilyar AU - Wei, Wu AU - Zhang, Yan-Rui AU - Feng, Chang-Wei AU - Wang, Jin AU - Yang, Yu-Hua AU - Hao, Hong-Zhang AU - Bao, Qi-De AU - Liu, Bao-Chi AU - Wu, Ai-Qun AU - Xie, Dong AU - Yang, Wan-Cai AU - Wang, Liang AU - Zhao, Xiao-Hang AU - Chen, Shu-Qing AU - Hong, Jun-Yan AU - Zhang, Xue-Jun AU - Freedman, Neal D AU - Goldstein, Alisa M AU - Lin, Dongxin AU - Taylor, Philip R AU - Wang, Li-Dong AU - Chanock, Stephen J AD - 1] State Key Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. [2]. ; 1] Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. [2] Cancer Genome Research Laboratory, Division of Cancer Epidemiology and Genetics, Advanced Technology Program, SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland, USA. [3]. ; 1] Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. [2] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [3]. ; 1] Department of Oncology, Pathology, Clinical Laboratory and Respiratory Medicine, The First Affiliated Hospital, Henan University of Science and Technology, Luoyang, China. [2]. ; 1] Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. [2]. ; 1] Department of Thoracic Surgery, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. [2]. ; 1] Key Laboratory of Dermatology, Anhui Medical University, Anhui, China. [2]. ; State Key Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. ; Department of Epidemiology and Biostatistics, Cancer Center, Nanjing Medical University, Nanjing, China. ; Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University School of Oncology, Beijing Cancer Hospital and Institute, Beijing, China. ; 1] State Key Laboratory of Oncology in Southern China, Sun Yat-Sen University Cancer Center, Guangzhou, China. [2] Department of Experimental Research, Sun Yat-Sen University Cancer Center, Guangzhou, China. ; Laboratory of Cancer Molecular Genetics, Medical College of Soochow University, Suzhou, China. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. ; 1] Department of Medicine, Vanderbilt University, Nashville, Tennessee, USA. [2] Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, Tennessee, USA. ; University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania, USA. ; Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. ; Department of Oncology, Pathology, Clinical Laboratory and Respiratory Medicine, The First Affiliated Hospital, Henan University of Science and Technology, Luoyang, China. ; Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. ; Anyang Tumor Hospital, Anyang, China. ; 1] Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. [2] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Basic Oncology and Pathology at the College of Medicine, Zhengzhou University, Zhengzhou, China. ; Center for Cancer Research, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. ; Shanxi Cancer Hospital, Taiyuan, China. ; Department of Epidemiology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. ; Shanghai Cancer Institute, Shanghai, China. ; Duke-National University of Singapore Graduate Medical School, Singapore. ; Key Laboratory for Environment and Health (Ministry of Education), School of Public Health, Huazhong University of Sciences and Technology, Wuhan, China. ; Information Management Services, Inc., Silver Spring, Maryland, USA. ; 1] Division of Cancer Epidemiology and Genetics, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. [2] Cancer Genome Research Laboratory, Division of Cancer Epidemiology and Genetics, Advanced Technology Program, SAIC-Frederick, Inc., NCI-Frederick, Frederick, Maryland, USA. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Medical Oncology, Tumor Hospital of Linzhou, Linzhou, China. ; Department of Pathology and Thoracic Surgery, Centre for Health Screening and Endoscopy, Cixian Hospital, Cixian, China. ; Key Laboratory of Dermatology, Anhui Medical University, Anhui, China. ; 1] Department of Gastroenterology, Henan Provincial People's Hospital, Zhengzhou, China. [2] Department of Hematology, Henan Provincial People's Hospital, Zhengzhou, China. [3] Central Laboratory, Henan Provincial People's Hospital, Zhengzhou, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Oncology, Pathology, Clinical Laboratory and Respiratory Medicine, The First Affiliated Hospital, Henan University of Science and Technology, Luoyang, China. ; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA. ; 1] Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. [2] Department of Basic Oncology, Pathology and Gastroenterology, The Second Affiliated Hospital, Zhengzhou University, Zhengzhou, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Oncology, The Second Affiliated Hospital of Nanyang Medical College, Nanyang, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA. ; Department of Radiotherapy, Pathology and Pediatrics, Central Hospital of Xinxiang, Xinxiang, China. ; Department of Thoracic Surgery, Provincial Hospital affiliated to Shandong University, Jinan, China. ; Department of Thoracic Surgery and Radiotherapy, Cancer Hospital of Henan Province, Zhengzhou, China. ; Department of Internal Mongolia Medicine, The Affiliated Hospital, Inner Mongolia Medical College, Hohhot, China. ; Department of Biotechnology, Ningxia Medical University, Yinchuan, China. ; Department of Thoracic Surgery, Tumor Hospital of Shaanxi Province, Xi'an, China. ; Department of Thoracic and Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu, China. ; 1] Department of Oncologic Pathology, Medical College of Shantou University, Shantou, China. [2] Department of Biochemistry and Molecular Biology, Medical College of Shantou University, Shantou, China. ; 1] Henan Key Laboratory for Esophageal Cancer Research of The First Affiliated Hospital, Zhengzhou University, Zhengzhou, China. [2] Department of Oncology, Puyang City Oil Field General Hospital, Puyang, China. ; Department of Pathology and Thoracic Surgery, Linzhou Esophageal Cancer Hospital, Linzhou, China. ; Department of Gastroenterology and Thoracic Surgery, The First People's Hospital of Shangqiu, Shangqiu, China. ; Department of Basic Oncology, Pathology and Gastroenterology, The Second Affiliated Hospital, Zhengzhou University, Zhengzhou, China. ; Department of Gastroenterology, Beijing Tongren Hospital affiliated to Capital Medical University, Beijing, China. ; Department of Oncology, Xinyang Central Hospital, Xinyang, China. ; State Key Laboratory of Genetic Resource and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China. ; Department of Pathology, Shihezi University School of Medicine, Shihezi, China. ; 1] Department of Thoracic Surgery, The First Affiliated Hospital, Xinjiang Medical University, Urumqi, China. [2] Medical Research Center, The First Affiliated Hospital, Xinjiang Medical University, Urumqi, China. ; 1] Institute of Hematologic Disease, Changzhi Medical University, Changzhi, China. [2] Department of Pathology, Changzhi Medical University, Changzhi, China. ; Department of Surgery, Hebi Dahejian Hospital, Hebi, China. ; Anyang District Hospital, Anyang, China. ; Surgical Department of the Shanghai Public Health Clinical Center, Fudan University, Shanghai, China. ; Department of Anatomy, the Second Military Medical University of the Chinese People's Liberation Army, Shanghai, China. ; Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. ; 1] Department of Pathology, Cancer Research Center, Basic Medical College, Xinxiang Medical University, Xinxiang, China. [2] Medical College of Wisconsin, Cancer Research Center, Milwaukee, Wisconsin, USA. ; National Laboratory of Molecular Oncology, Cancer Institute and Hospital, Chinese Academy of Medical Sciences, Beijing, China. ; College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China. ; 1] College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China. [2] Department of Environmental and Occupational Health, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 1001 EP - 1006 VL - 46 IS - 9 KW - Index Medicus KW - Genotype KW - Risk KW - Polymorphism, Single Nucleotide KW - Alleles KW - Genetic Loci KW - Humans KW - Case-Control Studies KW - Middle Aged KW - Genetic Predisposition to Disease KW - Genome-Wide Association Study -- methods KW - Male KW - Female KW - Esophageal Neoplasms -- genetics KW - Carcinoma, Squamous Cell -- genetics KW - Asian Continental Ancestry Group -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558519653?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+genetics&rft.atitle=Joint+analysis+of+three+genome-wide+association+studies+of+esophageal+squamous+cell+carcinoma+in+Chinese+populations.&rft.au=Wu%2C+Chen%3BWang%2C+Zhaoming%3BSong%2C+Xin%3BFeng%2C+Xiao-Shan%3BAbnet%2C+Christian+C%3BHe%2C+Jie%3BHu%2C+Nan%3BZuo%2C+Xian-Bo%3BTan%2C+Wen%3BZhan%2C+Qimin%3BHu%2C+Zhibin%3BHe%2C+Zhonghu%3BJia%2C+Weihua%3BZhou%2C+Yifeng%3BYu%2C+Kai%3BShu%2C+Xiao-Ou%3BYuan%2C+Jian-Min%3BZheng%2C+Wei%3BZhao%2C+Xue-Ke%3BGao%2C+She-Gan%3BYuan%2C+Zhi-Qing%3BZhou%2C+Fu-You%3BFan%2C+Zong-Min%3BCui%2C+Ji-Li%3BLin%2C+Hong-Li%3BHan%2C+Xue-Na%3BLi%2C+Bei%3BChen%2C+Xi%3BDawsey%2C+Sanford+M%3BLiao%2C+Linda%3BLee%2C+Maxwell+P%3BDing%2C+Ti%3BQiao%2C+You-Lin%3BLiu%2C+Zhihua%3BLiu%2C+Yu%3BYu%2C+Dianke%3BChang%2C+Jiang%3BWei%2C+Lixuan%3BGao%2C+Yu-Tang%3BKoh%2C+Woon-Puay%3BXiang%2C+Yong-Bing%3BTang%2C+Ze-Zhong%3BFan%2C+Jin-Hu%3BHan%2C+Jing-Jing%3BZhou%2C+Sheng-Li%3BZhang%2C+Peng%3BZhang%2C+Dong-Yun%3BYuan%2C+Yuan%3BHuang%2C+Ying%3BLiu%2C+Chunling%3BZhai%2C+Kan%3BQiao%2C+Yan%3BJin%2C+Guangfu%3BGuo%2C+Chuanhai%3BFu%2C+Jianhua%3BMiao%2C+Xiaoping%3BLu%2C+Changdong%3BYang%2C+Haijun%3BWang%2C+Chaoyu%3BWheeler%2C+William+A%3BGail%2C+Mitchell%3BYeager%2C+Meredith%3BYuenger%2C+Jeff%3BGuo%2C+Er-Tao%3BLi%2C+Ai-Li%3BZhang%2C+Wei%3BLi%2C+Xue-Min%3BSun%2C+Liang-Dan%3BMa%2C+Bao-Gen%3BLi%2C+Yan%3BTang%2C+Sa%3BPeng%2C+Xiu-Qing%3BLiu%2C+Jing%3BHutchinson%2C+Amy%3BJacobs%2C+Kevin%3BGiffen%2C+Carol%3BBurdette%2C+Laurie%3BFraumeni%2C+Joseph+F%3BShen%2C+Hongbing%3BKe%2C+Yang%3BZeng%2C+Yixin%3BWu%2C+Tangchun%3BKraft%2C+Peter%3BChung%2C+Charles+C%3BTucker%2C+Margaret+A%3BHou%2C+Zhi-Chao%3BLiu%2C+Ya-Li%3BHu%2C+Yan-Long%3BWang%2C+Li%3BYuan%2C+Guo%3BChen%2C+Li-Sha%3BLiu%2C+Xiao%3BMa%2C+Teng%3BMeng%2C+Hui%3BSun%2C+Li%3BLi%2C+Xin-Min%3BLi%2C+Xiu-Min%3BKu%2C+Jian-Wei%3BZhou%2C+Ying-Fa%3BYang%2C+Liu-Qin%3BWang%2C+Zhou%3BLi%2C+Yin%3BQige%2C+Qirenwang%3BYang%2C+Wen-Jun%3BLei%2C+Guang-Yan%3BChen%2C+Long-Qi%3BLi%2C+En-Min%3BYuan%2C+Ling%3BYue%2C+Wen-Bin%3BWang%2C+Ran%3BWang%2C+Lu-Wen%3BFan%2C+Xue-Ping%3BZhu%2C+Fang-Heng%3BZhao%2C+Wei-Xing%3BMao%2C+Yi-Min%3BZhang%2C+Mei%3BXing%2C+Guo-Lan%3BLi%2C+Ji-Lin%3BHan%2C+Min%3BRen%2C+Jing-Li%3BLiu%2C+Bin%3BRen%2C+Shu-Wei%3BKong%2C+Qing-Peng%3BLi%2C+Feng%3BSheyhidin%2C+Ilyar%3BWei%2C+Wu%3BZhang%2C+Yan-Rui%3BFeng%2C+Chang-Wei%3BWang%2C+Jin%3BYang%2C+Yu-Hua%3BHao%2C+Hong-Zhang%3BBao%2C+Qi-De%3BLiu%2C+Bao-Chi%3BWu%2C+Ai-Qun%3BXie%2C+Dong%3BYang%2C+Wan-Cai%3BWang%2C+Liang%3BZhao%2C+Xiao-Hang%3BChen%2C+Shu-Qing%3BHong%2C+Jun-Yan%3BZhang%2C+Xue-Jun%3BFreedman%2C+Neal+D%3BGoldstein%2C+Alisa+M%3BLin%2C+Dongxin%3BTaylor%2C+Philip+R%3BWang%2C+Li-Dong%3BChanock%2C+Stephen+J&rft.aulast=Wu&rft.aufirst=Chen&rft.date=2014-09-01&rft.volume=46&rft.issue=9&rft.spage=1001&rft.isbn=&rft.btitle=&rft.title=Nature+genetics&rft.issn=1546-1718&rft_id=info:doi/10.1038%2Fng.3064 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-15 N1 - Date created - 2014-08-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Cancer Res. 2001 Apr;7(4):883-91 [11309337] Br J Cancer. 2013 Apr 2;108(6):1378-86 [23361049] Cancer Lett. 1995 Jun 29;93(1):17-48 [7600541] Int J Cancer. 2005 Jan 20;113(3):456-63 [15455378] Nature. 2008 Oct 2;455(7213):674-8 [18724357] Gastroenterol Clin North Am. 2009 Mar;38(1):27-57, vii [19327566] Nat Genet. 2009 Aug;41(8):920-5 [19578364] Nat Genet. 2009 Nov;41(11):1234-7 [19838193] Cancer. 2010 Mar 15;116(6):1572-81 [20186831] Nat Genet. 2010 Jun;42(6):492-4 [20453839] Nat Genet. 2010 Jul;42(7):599-603 [20512145] Nat Genet. 2010 Sep;42(9):764-7 [20729852] Nat Genet. 2010 Sep;42(9):759-63 [20729853] Blood. 2011 Feb 10;117(6):1911-6 [21131588] Med Oncol. 2011 Mar;28(1):188-93 [20195802] Nat Genet. 2011 Jul;43(7):679-84 [21642993] Br J Cancer. 2013 May 28;108(10):2178-85 [23571737] Nat Genet. 2013 Aug;45(8):868-76 [23770605] Gastroenterology. 2011 Sep;141(3):864-871.e1-5 [21699788] Nucleic Acids Res. 2012 Jan;40(Database issue):D930-4 [22064851] Hum Mol Genet. 2012 May 1;21(9):2132-41 [22323360] PLoS Genet. 2012;8(7):e1002791 [22807686] PLoS Genet. 2012;8(7):e1002805 [22829776] Hum Genet. 2012 Sep;131(9):1403-21 [22610502] Genome Res. 2012 Sep;22(9):1790-7 [22955989] Nat Genet. 2012 Oct;44(10):1090-7 [22960999] Nat Genet. 2012 Oct;44(10):1131-6 [22961001] Hum Genet. 2012 Dec;131(12):1877-88 [22886559] Nat Genet. 2012 Dec;44(12):1330-5 [23143601] Curr Opin Cell Biol. 2013 Feb;25(1):63-71 [23219370] Cancer Res. 1980 Aug;40(8 Pt 1):2633-44 [6992989] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ng.3064 ER - TY - JOUR T1 - Cross-cancer pleiotropic analysis of endometrial cancer: PAGE and E2C2 consortia. AN - 1558519031; 24832084 AB - Genome-wide association studies (GWAS) have identified a large number of cancer-associated single nucleotide polymorphisms (SNPs), several of which have been associated with multiple cancer sites suggesting pleiotropic effects and shared biological mechanisms across some cancers. We hypothesized that SNPs associated with other cancers may be additionally associated with endometrial cancer. We examined 213 SNPs previously associated with 14 other cancers for their associations with endometrial cancer in 3758 endometrial cancer cases and 5966 controls of European ancestry from two consortia: Population Architecture Using Genomics and Epidemiology and the Epidemiology of Endometrial Cancer Consortium. Study-specific logistic regression estimates adjusted for age, body mass index and the most significant principal components of genetic ancestry were combined using fixed-effect meta-analysis to evaluate the association between each SNP and endometrial cancer risk. A Bonferroni-corrected P value of 2.35×10(-4) was used to determine statistical significance of the associations. SNP rs7679673, ~6.3kb upstream of TET2 and previously reported to be associated with prostate cancer risk, was associated with endometrial cancer risk in the direction opposite to that for prostate cancer [meta-analysis odds ratio = 0.87 (per copy of the C allele), 95% confidence interval = 0.81, 0.93; P = 7.37×10(-5)] with no evidence of heterogeneity across studies (P heterogeneity = 0.66). This pleiotropic analysis is the first to suggest TET2 as a susceptibility locus for endometrial cancer. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Setiawan, Veronica Wendy AU - Schumacher, Fredrick AU - Prescott, Jennifer AU - Haessler, Jeffrey AU - Malinowski, Jennifer AU - Wentzensen, Nicolas AU - Yang, Hannah AU - Chanock, Stephen AU - Brinton, Louise AU - Hartge, Patricia AU - Lissowska, Jolanta AU - Park, S Lani AU - Cheng, Iona AU - Bush, William S AU - Crawford, Dana C AU - Ursin, Giske AU - Horn-Ross, Pamela AU - Bernstein, Leslie AU - Lu, Lingeng AU - Risch, Harvey AU - Yu, Herbert AU - Sakoda, Lori C AU - Doherty, Jennifer AU - Chen, Chu AU - Jackson, Rebecca AU - Yasmeen, Shagufta AU - Cote, Michele AU - Kocarnik, Jonathan M AU - Peters, Ulrike AU - Kraft, Peter AU - De Vivo, Immaculata AU - Haiman, Christopher A AU - Kooperberg, Charles AU - Le Marchand, Loic AD - Department of Preventive Medicine, Keck School of Medicine, and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Center for Human Genetics Research, Vanderbilt University, Nashville, TN 37235, USA, National Cancer Institute, Bethesda, MD 20892, USA, M.Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, 02-781 Warsaw, Poland, Cancer Prevention Institute of California, Fremont, CA 94538, USA, Institute of Population Based Cancer Research, Cancer Registry of Norway, N-0304 Oslo, Norway, Division of Cancer Etiology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA, Department of Epidemiology, Yale School of Public Health, New Haven CT 06520, USA, Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA, Division of Research, Kaiser Permanente Northern California, Oakland, CA 94611, USA, Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, NH 03756, USA, Division of Endocrinology, Diabetes and Metabolism, Ohio State University, Columbus, OH 43210, USA, Department of Obstetrics and Gynecology, University of California, Davis, CA 95616, USA, Department of Oncology, Wayne State University School of Medicine and Population Studies and Disparities Research, Karmanos Cancer Institute, Detroit, MI 48202, USA and Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA vsetiawa@usc.edu. ; Department of Preventive Medicine, Keck School of Medicine, and Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90089, USA, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Center for Human Genetics Research, Vanderbilt University, Nashville, TN 37235, USA, National Cancer Institute, Bethesda, MD 20892, USA, M.Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, 02-781 Warsaw, Poland, Cancer Prevention Institute of California, Fremont, CA 94538, USA, Institute of Population Based Cancer Research, Cancer Registry of Norway, N-0304 Oslo, Norway, Division of Cancer Etiology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA, Department of Epidemiology, Yale School of Public Health, New Haven CT 06520, USA, Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA, Division of Research, Kaiser Permanente Northern California, Oakland, CA 94611, USA, Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, NH 03756, USA, Division of Endocrinology, Diabetes and Metabolism, Ohio State University, Columbus, OH 43210, USA, Department of Obstetrics and Gynecology, University of California, Davis, CA 95616, USA, Department of Oncology, Wayne State University School of Medicine and Population Studies and Disparities Research, Karmanos Cancer Institute, Detroit, MI 48202, USA and Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA. ; Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. ; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. ; Center for Human Genetics Research, Vanderbilt University, Nashville, TN 37235, USA. ; National Cancer Institute, Bethesda, MD 20892, USA. ; M.Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, 02-781 Warsaw, Poland. ; Cancer Prevention Institute of California, Fremont, CA 94538, USA. ; Institute of Population Based Cancer Research, Cancer Registry of Norway, N-0304 Oslo, Norway. ; Division of Cancer Etiology, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA. ; Department of Epidemiology, Yale School of Public Health, New Haven CT 06520, USA. ; Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA. ; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Division of Research, Kaiser Permanente Northern California, Oakland, CA 94611, USA. ; Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Section of Biostatistics and Epidemiology, Department of Community and Family Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, NH 03756, USA. ; Division of Endocrinology, Diabetes and Metabolism, Ohio State University, Columbus, OH 43210, USA. ; Department of Obstetrics and Gynecology, University of California, Davis, CA 95616, USA. ; Department of Oncology, Wayne State University School of Medicine and Population Studies and Disparities Research, Karmanos Cancer Institute, Detroit, MI 48202, USA and. ; Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA, Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 2068 EP - 2073 VL - 35 IS - 9 KW - DNA-Binding Proteins KW - 0 KW - Proto-Oncogene Proteins KW - TET2 protein, human KW - Index Medicus KW - Genetic Pleiotropy KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Genetic Predisposition to Disease KW - Female KW - Genome-Wide Association Study KW - Polymorphism, Single Nucleotide KW - DNA-Binding Proteins -- genetics KW - Endometrial Neoplasms -- genetics KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558519031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cross-cancer+pleiotropic+analysis+of+endometrial+cancer%3A+PAGE+and+E2C2+consortia.&rft.au=Setiawan%2C+Veronica+Wendy%3BSchumacher%2C+Fredrick%3BPrescott%2C+Jennifer%3BHaessler%2C+Jeffrey%3BMalinowski%2C+Jennifer%3BWentzensen%2C+Nicolas%3BYang%2C+Hannah%3BChanock%2C+Stephen%3BBrinton%2C+Louise%3BHartge%2C+Patricia%3BLissowska%2C+Jolanta%3BPark%2C+S+Lani%3BCheng%2C+Iona%3BBush%2C+William+S%3BCrawford%2C+Dana+C%3BUrsin%2C+Giske%3BHorn-Ross%2C+Pamela%3BBernstein%2C+Leslie%3BLu%2C+Lingeng%3BRisch%2C+Harvey%3BYu%2C+Herbert%3BSakoda%2C+Lori+C%3BDoherty%2C+Jennifer%3BChen%2C+Chu%3BJackson%2C+Rebecca%3BYasmeen%2C+Shagufta%3BCote%2C+Michele%3BKocarnik%2C+Jonathan+M%3BPeters%2C+Ulrike%3BKraft%2C+Peter%3BDe+Vivo%2C+Immaculata%3BHaiman%2C+Christopher+A%3BKooperberg%2C+Charles%3BLe+Marchand%2C+Loic&rft.aulast=Setiawan&rft.aufirst=Veronica&rft.date=2014-09-01&rft.volume=35&rft.issue=9&rft.spage=2068&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu107 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-21 N1 - Date created - 2014-08-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hum Mutat. 2009 Jan;30(1):69-78 [18683858] Gut. 2014 May;63(5):800-7 [23935004] Nat Genet. 2009 May;41(5):579-84 [19330030] N Engl J Med. 2009 May 28;360(22):2289-301 [19474426] Proc Natl Acad Sci U S A. 2009 Jun 9;106(23):9362-7 [19474294] Nat Genet. 2009 Jul;41(7):807-10 [19483681] Nat Genet. 2009 Oct;41(10):1116-21 [19767753] PLoS One. 2010;5(5):e10858 [20526366] Am J Epidemiol. 2000 Feb 15;151(4):346-57 [10695593] Control Clin Trials. 2000 Dec;21(6 Suppl):251S-272S [11189683] Control Clin Trials. 2000 Dec;21(6 Suppl):273S-309S [11189684] Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12263-8 [12218173] Control Clin Trials. 1998 Feb;19(1):61-109 [9492970] Nat Cell Biol. 2005 Nov;7(11):1074-82 [16244670] Nat Genet. 2006 Aug;38(8):904-9 [16862161] Nat Genet. 2007 Jul;39(7):870-4 [17529973] Nature. 2007 Jun 28;447(7148):1087-93 [17529967] BMC Med Genet. 2007;8 Suppl 1:S6 [17903305] J Natl Cancer Inst. 2008 Jul 2;100(13):962-6 [18577746] Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):242-7 [19124504] Carcinogenesis. 2010 Aug;31(8):1392-9 [20547493] PLoS One. 2010;5(7):e11824 [20686608] Bioinformatics. 2010 Sep 1;26(17):2190-1 [20616382] Nat Genet. 2010 Sep;42(9):751-4 [20676098] Nat Genet. 2010 Sep;42(9):764-7 [20729852] Nat Genet. 2010 Nov;42(11):973-7 [20972440] Hum Mol Genet. 2010 Dec 15;19(24):4948-54 [20876614] Nat Genet. 2011 May;43(5):451-4 [21499250] Int J Cancer. 2011 Sep 1;129(5):1237-43 [21387312] Cancer Epidemiol Biomarkers Prev. 2011 Sep;20(9):1873-82 [21750170] Am J Epidemiol. 2011 Oct 1;174(7):849-59 [21836165] Am J Hum Genet. 2011 Nov 11;89(5):607-18 [22077970] Clin Cancer Res. 2012 Jan 15;18(2):577-84 [22142827] PLoS One. 2012;7(1):e30390 [22299039] J Natl Cancer Inst. 2012 Jun 6;104(11):840-54 [22523397] Cancer Epidemiol Biomarkers Prev. 2012 Jun;21(6):980-7 [22426144] Pac Symp Biocomput. 2013;:373-84 [23424142] Nat Commun. 2013;4:1627 [23535648] Nat Genet. 2013 Apr;45(4):345-8 [23535722] Nat Genet. 2013 Apr;45(4):353-61, 361e1-2 [23535729] Nucleic Acids Res. 2014 Jan;42(Database issue):D1001-6 [24316577] Hum Genet. 2014 Feb;133(2):211-24 [24096698] Cancer Causes Control. 2009 May;20(4):491-6 [19132539] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu107 ER - TY - JOUR T1 - Fecal metabolomics: assay performance and association with colorectal cancer. AN - 1558518851; 25037050 AB - Metabolomic analysis of feces may provide insights on colorectal cancer (CRC) if assay performance is satisfactory. In lyophilized feces from 48 CRC cases, 102 matched controls, and 48 masked quality control specimens, 1043 small molecules were detected with a commercial platform. Assay reproducibility was good for 527 metabolites [technical intraclass correlation coefficient (ICC) >0.7 in quality control specimens], but reproducibility in 6-month paired specimens was lower for the majority of metabolites (within-subject ICC ≤0.5). In the CRC cases and controls, significant differences (false discovery rate ≤0.10) were found for 41 of 1043 fecal metabolites. Direct cancer association was found with three fecal heme-related molecules [covariate-adjusted 90th versus 10th percentile odds ratio (OR) = 17-345], 18 peptides/amino acids (OR = 3-14), palmitoyl-sphingomyelin (OR = 14), mandelate (OR = 3) and p-hydroxy-benzaldehyde (OR = 4). Conversely, cancer association was inverse with acetaminophen metabolites (OR <0.1), tocopherols (OR = 0.3), sitostanol (OR = 0.2), 3-dehydrocarnitine (OR = 0.4), pterin (OR = 0.3), conjugated-linoleate-18-2N7 (OR = 0.2), N-2-furoyl-glycine (OR = 0.3) and p-aminobenzoate (PABA, OR = 0.2). Correlations suggested an independent role for palmitoyl-sphingomyelin and a central role for PABA (which was stable over 6 months, within-subject ICC 0.67) modulated by p-hydroxy-benzaldehyde. Power calculations based on ICCs indicate that only 45% of metabolites with a true relative risk 5.0 would be found in prospectively collected, prediagnostic specimens from 500 cases and 500 controls. Thus, because fecal metabolites vary over time, very large studies will be needed to reliably detect associations of many metabolites that potentially contribute to CRC. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Goedert, James J AU - Sampson, Joshua N AU - Moore, Steven C AU - Xiao, Qian AU - Xiong, Xiaoqin AU - Hayes, Richard B AU - Ahn, Jiyoung AU - Shi, Jianxin AU - Sinha, Rashmi AD - Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Bethesda, MD 20892-9704, USA, Information Management Services, 6110 Executive Boulevard, Rockville, MD 20852, USA and Division of Epidemiology, Department of Population Health, New York University School of Medicine, 650 First Avenue, #518, New York, NY 10016, USA goedertj@mail.nih.gov. ; Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Bethesda, MD 20892-9704, USA, Information Management Services, 6110 Executive Boulevard, Rockville, MD 20852, USA and Division of Epidemiology, Department of Population Health, New York University School of Medicine, 650 First Avenue, #518, New York, NY 10016, USA. ; Information Management Services, 6110 Executive Boulevard, Rockville, MD 20852, USA and. ; Division of Epidemiology, Department of Population Health, New York University School of Medicine, 650 First Avenue, #518, New York, NY 10016, USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 2089 EP - 2096 VL - 35 IS - 9 KW - Biomarkers, Tumor KW - 0 KW - Hippurates KW - Peptides KW - Heme KW - 42VZT0U6YR KW - salicylurate KW - 487-54-7 KW - Index Medicus KW - Humans KW - Reference Standards KW - Case-Control Studies KW - Peptides -- metabolism KW - Hippurates -- metabolism KW - Middle Aged KW - Heme -- metabolism KW - Metabolomics -- standards KW - Male KW - Female KW - Biomarkers, Tumor -- metabolism KW - Metabolome KW - Colorectal Neoplasms -- metabolism KW - Feces -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558518851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fecal+metabolomics%3A+assay+performance+and+association+with+colorectal+cancer.&rft.au=Goedert%2C+James+J%3BSampson%2C+Joshua+N%3BMoore%2C+Steven+C%3BXiao%2C+Qian%3BXiong%2C+Xiaoqin%3BHayes%2C+Richard+B%3BAhn%2C+Jiyoung%3BShi%2C+Jianxin%3BSinha%2C+Rashmi&rft.aulast=Goedert&rft.aufirst=James&rft.date=2014-09-01&rft.volume=35&rft.issue=9&rft.spage=2089&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu131 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-21 N1 - Date created - 2014-08-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 2007 Oct 3;99(19):1462-70 [17895475] BMC Genomics. 2007;8:180 [17578578] Mol Cancer. 2008;7:72 [18799019] Cancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):3233-40 [18990766] J Proteome Res. 2009 Jan;8(1):352-61 [19063642] NMR Biomed. 2009 Apr;22(3):342-8 [19006102] Cancer Res. 2009 Jun 1;69(11):4918-25 [19458066] NMR Biomed. 2009 Jul;22(6):593-600 [19259992] Cancer Epidemiol Biomarkers Prev. 2009 Aug;18(8):2195-201 [19661077] Nutrition. 2009 Nov-Dec;25(11-12):1193-201 [19619983] Magn Reson Chem. 2009 Dec;47 Suppl 1:S54-61 [19842159] Cancer Res. 2010 Mar 15;70(6):2406-14 [20215514] Anal Chem. 2009 Aug 15;81(16):6656-67 [19624122] FASEB J. 2010 Aug;24(8):2962-75 [20371621] J Proteome Res. 2010 Oct 1;9(10):5284-95 [20806900] Cancer Prev Res (Phila). 2011 Apr;4(4):530-43 [21321062] Annu Rev Plant Biol. 2011;62:105-25 [21275646] Ann Oncol. 2011 Sep;22(9):1958-72 [21307158] J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2011 Oct;29(4):324-57 [22107166] J Proteome Res. 2011 Dec 2;10(12):5512-22 [21970572] Am J Physiol Gastrointest Liver Physiol. 2012 Jan 1;302(1):G1-9 [22016433] Anticancer Agents Med Chem. 2012 May;12(4):340-63 [21707511] Am J Clin Nutr. 2012 Aug;96(2):374-81 [22695871] Biochim Biophys Acta. 2014 May;1841(5):773-82 [24060581] N Engl J Med. 2014 Apr 3;370(14):1287-97 [24645800] Cancer Biol Ther. 2014 Apr;15(4):389-97 [24424155] Clin Cancer Res. 2014 Apr 15;20(8):2136-46 [24526730] Biochem Biophys Res Commun. 2012 Nov 9;428(1):185-90 [23068102] Nutr Cancer. 2012;64(8):1279-87 [23163856] Cancer Epidemiol Biomarkers Prev. 2013 Apr;22(4):631-40 [23396963] Food Chem. 2013 Nov 15;141(2):1378-82 [23790927] PLoS One. 2013;8(8):e70803 [23940645] Nat Rev Cancer. 2013 Nov;13(11):800-12 [24132111] J Natl Cancer Inst. 2013 Dec 18;105(24):1907-11 [24316595] Cell Host Microbe. 2014 Mar 12;15(3):317-28 [24629338] Am J Clin Nutr. 1999 Nov;70(5):826-31 [10539742] Scand J Gastroenterol. 2001 Mar;36(3):291-6 [11305517] Physiol Rev. 2001 Jul;81(3):1031-64 [11427691] JAMA. 2003 Jul 23;290(4):476-85 [12876090] Environ Mol Mutagen. 2004;44(1):44-55 [15199546] Mutat Res. 1986 Dec;172(3):189-97 [3537775] Cancer Res. 1989 Mar 1;49(5):1322-6 [2917361] Cancer Res. 1989 Jun 15;49(12):3420-4 [2655896] Nutr Rev. 1995 Apr;53(4 Pt 1):83-9 [7624062] N Engl J Med. 1995 Nov 16;333(20):1308-12 [7566021] Eur J Cancer Prev. 1996 Sep;5 Suppl 1:131-6 [8972308] Cancer Res. 1997 Mar 15;57(6):1098-102 [9067278] Atherosclerosis. 1999 Aug;145(2):279-85 [10488954] Oncol Rep. 2005 Apr;13(4):559-83 [15756426] Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):856-62 [15824156] J Physiol Biochem. 2005 Sep;61(3):483-94 [16440602] J Proteome Res. 2006 Oct;5(10):2780-8 [17022649] Peptides. 2006 Nov;27(11):2706-14 [16797105] Carcinogenesis. 2007 Jun;28(6):1329-33 [17389616] Bioinformatics. 2008 Jan 1;24(1):78-85 [18024976] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu131 ER - TY - JOUR T1 - Elevated HERV-K mRNA expression in PBMC is associated with a prostate cancer diagnosis particularly in older men and smokers. AN - 1558518181; 24858205 AB - Aberrant expression of subgroup k human endogenous retroviruses (HERV-K) has been observed in prostate cancer. This subgroup is unique because it encodes sequences in the human genome containing open reading frames for near intact retroviruses. We hypothesized that HERV-K reactivation could serve as a non-invasive early disease detection marker for prostate cancer. We evaluated HERV-K gag messenger RNA (mRNA) expression in blood samples of African-American and European-American men using a case-control design via quantitative real-time PCR. Additionally, we examined HERV-K envelope protein expression in prostate tumors by immunohistochemistry. HERV-K envelope protein was commonly upregulated in prostate tumors, but more so in tumors of African-American than European-American patients (61% versus 40%, P 12-fold increased odds {odds ratio = 12.87 [95% confidence interval 6.3-26.25]} of being diagnosed with prostate cancer than those in the lowest quartile. Moreover, our results showed that HERV-K expression may perform better as a disease biomarker in older than younger men (whereas the sensitivity of prostate-specific antigen (PSA) testing decreases with age) and in men with a smoking history compared with never smokers. Combining non-invasive HERV-K testing with PSA testing may improve the efficacy of prostate cancer detection specifically among older men and smokers who tend to develop a more aggressive disease. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Wallace, Tiffany A AU - Downey, Ronan F AU - Seufert, Caleb J AU - Schetter, Aaron AU - Dorsey, Tiffany H AU - Johnson, Carol A AU - Goldman, Radoslav AU - Loffredo, Christopher A AU - Yan, Peisha AU - Sullivan, Francis J AU - Giles, Francis J AU - Wang-Johanning, Feng AU - Ambs, Stefan AU - Glynn, Sharon A AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA, Prostate Cancer Institute, Biosciences Research Building, National University of Ireland Galway, Dangan, Corrib Village, Galway, Ireland, Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057-1465, USA, Department of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA, Department of Radiation Oncology, Galway University Hospital, Galway, Ireland and Viral Oncology, Center for Cancer and Metabolism, Stanford Research Institute International, Menlo Park, CA 94025, USA. ; Prostate Cancer Institute, Biosciences Research Building, National University of Ireland Galway, Dangan, Corrib Village, Galway, Ireland. ; Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC 20057-1465, USA. ; Department of Pathology and Laboratory Medicine, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA. ; Prostate Cancer Institute, Biosciences Research Building, National University of Ireland Galway, Dangan, Corrib Village, Galway, Ireland, Department of Radiation Oncology, Galway University Hospital, Galway, Ireland and. ; Viral Oncology, Center for Cancer and Metabolism, Stanford Research Institute International, Menlo Park, CA 94025, USA. ; Prostate Cancer Institute, Biosciences Research Building, National University of Ireland Galway, Dangan, Corrib Village, Galway, Ireland, sharon.glynn@nuigalway.ie. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 2074 EP - 2083 VL - 35 IS - 9 KW - CXCL10 protein, human KW - 0 KW - Chemokine CXCL10 KW - Gene Products, gag KW - RNA, Messenger KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - RNA, Messenger -- blood KW - Chemokine CXCL10 -- blood KW - Risk Factors KW - Humans KW - Endogenous Retroviruses -- enzymology KW - Gene Expression KW - Interferon-gamma -- blood KW - RNA, Messenger -- genetics KW - Male KW - Adenocarcinoma -- diagnosis KW - Adenocarcinoma -- blood KW - Smoking -- blood KW - Prostatic Neoplasms -- diagnosis KW - Leukocytes, Mononuclear -- virology KW - Gene Products, gag -- blood KW - Prostatic Neoplasms -- virology KW - Prostatic Neoplasms -- blood KW - Leukocytes, Mononuclear -- metabolism KW - Adenocarcinoma -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558518181?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Elevated+HERV-K+mRNA+expression+in+PBMC+is+associated+with+a+prostate+cancer+diagnosis+particularly+in+older+men+and+smokers.&rft.au=Wallace%2C+Tiffany+A%3BDowney%2C+Ronan+F%3BSeufert%2C+Caleb+J%3BSchetter%2C+Aaron%3BDorsey%2C+Tiffany+H%3BJohnson%2C+Carol+A%3BGoldman%2C+Radoslav%3BLoffredo%2C+Christopher+A%3BYan%2C+Peisha%3BSullivan%2C+Francis+J%3BGiles%2C+Francis+J%3BWang-Johanning%2C+Feng%3BAmbs%2C+Stefan%3BGlynn%2C+Sharon+A&rft.aulast=Wallace&rft.aufirst=Tiffany&rft.date=2014-09-01&rft.volume=35&rft.issue=9&rft.spage=2074&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu114 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-21 N1 - Date created - 2014-08-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: JAMA. 2011 Jun 22;305(24):2548-55 [21693743] Cancer Epidemiol Biomarkers Prev. 2011 May;20(5):740-50 [21546365] Carcinogenesis. 2011 Oct;32(10):1484-92 [21828060] J Natl Cancer Inst. 2012 Feb 8;104(3):189-210 [22247020] Nucleic Acids Res. 2012 Apr;40(8):3689-703 [22210864] Cancer Discov. 2012 Nov;2(11):995-1003 [23093251] CA Cancer J Clin. 2013 Jan;63(1):11-30 [23335087] Curr Opin Oncol. 2013 May;25(3):235-41 [23399519] J Cancer Res Clin Oncol. 2013 May;139(5):755-63 [23358719] BJU Int. 2013 Sep;112(5):543-7 [23924423] Int J Cancer. 2014 Feb 1;134(3):587-95 [23873154] Clin Cancer Res. 2013 Nov 15;19(22):6112-25 [24081977] J Vis Exp. 2013;(81):e50713 [24300377] Am J Pathol. 2014 Jan;184(1):28-41 [24269592] Cancer. 2014 Jan 15;120(2):197-204 [24127391] Int J Cancer. 2015 Sep 15;137(6):1249-57 [24890612] Nature. 2001 Feb 15;409(6822):860-921 [11237011] Epidemiol Rev. 2001;23(1):115-25 [11588835] Ann Neurol. 2001 Oct;50(4):434-42 [11601494] Leukemia. 2002 Feb;16(2):254-9 [11840292] Nat Rev Immunol. 2002 Aug;2(8):569-79 [12154376] Oncogene. 2003 Mar 13;22(10):1528-35 [12629516] Lancet. 2003 Mar 8;361(9360):859-64 [12642065] Proc Natl Acad Sci U S A. 2004 Oct 5;101 Suppl 2:14572-9 [15310846] J Gen Virol. 1992 Sep;73 ( Pt 9):2463-6 [1402820] Leuk Lymphoma. 1993;11 Suppl 1:119-23 [7504541] Cancer Epidemiol Biomarkers Prev. 1999 Apr;8(4 Pt 1):277-82 [10207628] J Mol Evol. 2004 Nov;59(5):642-56 [15693620] AIDS Res Hum Retroviruses. 2006 Jan;22(1):52-6 [16438646] J Lab Clin Med. 2006 Mar;147(3):126-32 [16503242] Curr Top Microbiol Immunol. 2006;310:211-50 [16909913] Annu Rev Genomics Hum Genet. 2006;7:149-73 [16722807] Nat Rev Cancer. 2007 Apr;7(4):256-69 [17384581] Mol Med. 2007 Jan-Feb;13(1-2):79-88 [17515959] Trends Genet. 2007 Jul;23(7):326-33 [17524519] Trends Mol Med. 2007 Oct;13(10):422-32 [17919976] Cancer Res. 2008 Feb 1;68(3):927-36 [18245496] Cancer Res. 2008 Jul 15;68(14):5869-77 [18632641] Curr Urol Rep. 2008 May;9(3):243-9 [18765120] J Virol. 2008 Oct;82(19):9329-36 [18632860] Cell Mol Life Sci. 2008 Nov;65(21):3366-82 [18818873] Cancer Immun. 2008;8:15 [19006261] Exp Cell Res. 2009 Mar 10;315(5):849-62 [19167380] Mol Biol Evol. 2009 Nov;26(11):2617-26 [19666991] Crit Rev Oncol Hematol. 2010 Jan;73(1):10-22 [19328712] Am J Public Health. 2010 Apr;100(4):693-701 [19608952] AIDS Res Hum Retroviruses. 2010 Aug;26(8):883-8 [20666582] Nat Commun. 2011;2:180 [21285958] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu114 ER - TY - JOUR T1 - Identification of a melanoma susceptibility locus and somatic mutation in TET2. AN - 1558518161; 24980573 AB - Although genetic studies have reported a number of loci associated with melanoma risk, the complex genetic architecture of the disease is not yet fully understood. We sought to identify common genetic variants associated with melanoma risk in a genome-wide association study (GWAS) of 2298 cases and 6654 controls. Thirteen of 15 known loci were replicated with nominal significance. A total of 69 single-nucleotide polymorphisms (SNPs) were selected for in silico replication in two independent melanoma GWAS datasets (a total of 5149 cases and 12 795 controls). Seven novel loci were nominally significantly associated with melanoma risk. These seven SNPs were further genotyped in 234 melanoma cases and 238 controls. The SNP rs4698934 was nominally significantly associated with melanoma risk. The combined odds ratio per T allele = 1.18; 95% confidence interval (1.10-1.25); combined P = 7.70 × 10(-) (7). This SNP is located in the intron of the TET2 gene on chromosome 4q24. In addition, a novel somatic mutation of TET2 was identified by next-generation sequencing in 1 of 22 sporadic melanoma cases. TET2 encodes a member of TET family enzymes that oxidizes 5-methylcytosine to 5-hydroxymethylcytosine (5hmC). It is a putative epigenetic biomarker of melanoma as we previously reported, with observation of reduced TET2 transcriptional expression. This study is the first to implicate TET2 genetic variation and mutation in melanoma. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Song, Fengju AU - Amos, Christopher I AU - Lee, Jeffrey E AU - Lian, Christine G AU - Fang, Shenying AU - Liu, Hongliang AU - MacGregor, Stuart AU - Iles, Mark M AU - Law, Matthew H AU - Lindeman, Neal I AU - Montgomery, Grant W AU - Duffy, David L AU - Cust, Anne E AU - Jenkins, Mark A AU - Whiteman, David C AU - Kefford, Richard F AU - Giles, Graham G AU - Armstrong, Bruce K AU - Aitken, Joanne F AU - Hopper, John L AU - Brown, Kevin M AU - Martin, Nicholas G AU - Mann, Graham J AU - Bishop, D Timothy AU - Bishop, Julia A Newton AU - GenoMEL consortium AU - Kraft, Peter AU - Qureshi, Abrar A AU - Kanetsky, Peter A AU - Hayward, Nicholas K AU - Hunter, David J AU - Wei, Qingyi AU - Han, Jiali AD - Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, P.R. China. ; Department of Community and Family Medicine, Center for Genomic Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, NH 03755, USA. ; Department of Surgical Oncology, MD Anderson Cancer Center, Houston, TX 77030, USA. ; Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. ; Duke Cancer Institute, Duke University Medical Center, Durham, NC 27710, USA. ; Queensland Institute of Medical Research, Brisbane, Queensland 4029, Australia. ; Leeds Institute of Cancer and Pathology, University of Leeds, Leeds LS9 7TF, UK. ; Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, University of Melbourne, Melbourne, Victoria 3052, Australia, Cancer Epidemiology and Services Research, Sydney School of Public Health, University of Sydney, Sydney, New South Wales 2006, Australia. ; Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, School of Population Health, University of Melbourne, Melbourne, Victoria 3052, Australia. ; Westmead Institute of Cancer Research, University of Sydney at Westmead Millennium Institute and Melanoma Institute Australia, Westmead, New South Wales 2145, Australia. ; Cancer Epidemiology Centre, The Cancer Council Victoria, Carlton, Victoria 3053, Australia. ; Cancer Epidemiology and Services Research, Sydney School of Public Health, University of Sydney, Sydney, New South Wales 2006, Australia. ; Viertel Centre for Research in Cancer Control, Cancer Council Queensland, Brisbane, Queensland 4004, Australia. ; Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20852, USA. ; GenoMEL consortium ; Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA. ; Channing Division of Network Medicine and Department of Dermatology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. ; Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Oncogenomics Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Queensland 4029, Australia. ; Duke Cancer Institute, Duke University Medical Center, Durham, NC 27710, USA, jialhan@iu.edu qingyi.wei@duke.edu. ; Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center of Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, P.R. China, Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA, Channing Division of Network Medicine and Department of Dermatology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA, Department of Epidemiology, Fairbanks School of Public Health, Indiana University, Indianapolis, IN 46202, USA, Simon Cancer Center, Indiana University, Indianapolis, IN 46202, USA and Department of Dermatology, School of Medicine, Indiana University, Indianapolis, IN 46202, USA jialhan@iu.edu. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 2097 EP - 2101 VL - 35 IS - 9 KW - DNA-Binding Proteins KW - 0 KW - Proto-Oncogene Proteins KW - TET2 protein, human KW - Index Medicus KW - Polymorphism, Single Nucleotide KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Genetic Predisposition to Disease KW - Mutation KW - Genome-Wide Association Study KW - Skin Neoplasms -- genetics KW - Melanoma -- genetics KW - DNA-Binding Proteins -- genetics KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558518161?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification+of+a+melanoma+susceptibility+locus+and+somatic+mutation+in+TET2.&rft.au=Song%2C+Fengju%3BAmos%2C+Christopher+I%3BLee%2C+Jeffrey+E%3BLian%2C+Christine+G%3BFang%2C+Shenying%3BLiu%2C+Hongliang%3BMacGregor%2C+Stuart%3BIles%2C+Mark+M%3BLaw%2C+Matthew+H%3BLindeman%2C+Neal+I%3BMontgomery%2C+Grant+W%3BDuffy%2C+David+L%3BCust%2C+Anne+E%3BJenkins%2C+Mark+A%3BWhiteman%2C+David+C%3BKefford%2C+Richard+F%3BGiles%2C+Graham+G%3BArmstrong%2C+Bruce+K%3BAitken%2C+Joanne+F%3BHopper%2C+John+L%3BBrown%2C+Kevin+M%3BMartin%2C+Nicholas+G%3BMann%2C+Graham+J%3BBishop%2C+D+Timothy%3BBishop%2C+Julia+A+Newton%3BGenoMEL+consortium%3BKraft%2C+Peter%3BQureshi%2C+Abrar+A%3BKanetsky%2C+Peter+A%3BHayward%2C+Nicholas+K%3BHunter%2C+David+J%3BWei%2C+Qingyi%3BHan%2C+Jiali&rft.aulast=Song&rft.aufirst=Fengju&rft.date=2014-09-01&rft.volume=35&rft.issue=9&rft.spage=2097&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu140 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-21 N1 - Date created - 2014-08-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Dermatol Sci. 2014 Feb;73(2):161-3 [24169492] Mod Pathol. 2014 Jul;27(7):936-44 [24390216] Hum Genet. 2011 Mar;129(3):247-53 [21116649] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Hum Mol Genet. 2011 Jul 1;20(13):2673-9 [21478494] Hum Mol Genet. 2011 Sep 15;20(18):3718-24 [21700618] Oncotarget. 2011 Aug;2(8):627-37 [21896958] Nat Genet. 2011 Nov;43(11):1114-8 [21983785] Nat Genet. 2011 Nov;43(11):1108-13 [21983787] Hum Mol Genet. 2011 Dec 15;20(24):5012-23 [21926416] Eur J Cancer. 2005 Jan;41(1):28-44 [15617989] Cell. 2012 Sep 14;150(6):1135-46 [22980977] Bioanalysis. 2013 Apr;5(7):839-45 [23534428] Melanoma Res. 2013 Jun;23(3):218-20 [23458759] PLoS One. 2013;8(5):e62828 [23671639] Proc Natl Acad Sci U S A. 2013 Jun 11;110(24):9920-5 [23716660] Anticancer Res. 2013 Oct;33(10):4325-8 [24122999] Mod Pathol. 2013 Nov;26(11):1492-7 [23743927] Oncogene. 2003 May 19;22(20):3042-52 [12789279] Int J Cancer. 2012 Oct 1;131(7):1577-90 [22234893] Eur J Cancer. 2005 Sep;41(14):2040-59 [16125929] Expert Rev Anticancer Ther. 2006 May;6(5):657-70 [16759158] Nat Genet. 2008 Jul;40(7):838-40 [18488026] Nat Genet. 2008 Jul;40(7):886-91 [18488027] Br J Dermatol. 2008 Aug;159(2):286-91 [18547303] Nat Genet. 2008 Nov;40(11):1313-8 [18849993] Nat Genet. 2009 Feb;41(2):221-7 [19151717] Blood. 2009 Jul 2;114(1):144-7 [19420352] Ann Oncol. 2009 Aug;20 Suppl 6:vi1-7 [19617292] Nat Genet. 2009 Aug;41(8):920-5 [19578364] Nat Genet. 2009 Aug;41(8):915-9 [19578365] Blood. 2009 Aug 20;114(8):1628-32 [19564637] Hum Genet. 2009 Oct;126(4):499-510 [19585149] J Invest Dermatol. 2010 Feb;130(2):520-8 [19710684] Nature. 2010 Aug 26;466(7310):1129-33 [20639862] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu140 ER - TY - JOUR T1 - Modulation of miR-29 expression by α-fetoprotein is linked to the hepatocellular carcinoma epigenome. AN - 1557082548; 24798303 AB - Globally, hepatocellular carcinoma (HCC) accounts for 70%-85% of primary liver cancers and ranks as the second leading cause of male cancer death. Serum alpha-fetoprotein (AFP), normally highly expressed in the liver only during fetal development, is reactivated in 60% of HCC tumors and associated with poor patient outcome. We hypothesize that AFP+ and AFP- tumors differ biologically. Multivariable analysis in 237 HCC cases demonstrates that AFP level predicts poor survival independent of tumor stage (P<0.043). Using microarray-based global microRNA (miRNA) profiling, we found that miRNA-29 (miR-29) family members were the most significantly (P<0.001) down-regulated miRNAs in AFP+ tumors. Consistent with miR-29's role in targeting DNA methyltransferase 3A (DNMT3A), a key enzyme regulating DNA methylation, we found a significant inverse correlation (P<0.001) between miR-29 and DNMT3A gene expression, suggesting that they might be functionally antagonistic. Moreover, global DNA methylation profiling reveals that AFP+ and AFP- HCC tumors have distinct global DNA methylation patterns and that increased DNA methylation is associated with AFP+ HCC. Experimentally, we found that AFP expression in AFP- HCC cells induces cell proliferation, migration, and invasion. Overexpression of AFP, or conditioned media from AFP+ cells, inhibits miR-29a expression and induces DNMT3A expression in AFP- HCC cells. AFP also inhibited transcription of the miR-29a/b-1 locus, and this effect is mediated through c-MYC binding to the transcript of miR-29a/b-1. Furthermore, AFP expression promotes tumor growth of AFP- HCC cells in nude mice. Tumor biology differs considerably between AFP+ HCC and AFP- HCC; AFP is a functional antagonist of miR-29, which may contribute to global epigenetic alterations and poor prognosis in HCC. © 2014 by the American Association for the Study of Liver Diseases. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA. JF - Hepatology (Baltimore, Md.) AU - Parpart, Sonya AU - Roessler, Stephanie AU - Dong, Fei AU - Rao, Vinay AU - Takai, Atsushi AU - Ji, Junfang AU - Qin, Lun-Xiu AU - Ye, Qing-Hai AU - Jia, Hu-Liang AU - Tang, Zhao-You AU - Wang, Xin Wei AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD; Tumor Biology Department, Georgetown University, Washington, DC. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 872 EP - 883 VL - 60 IS - 3 KW - MIRN29 microRNA, human KW - 0 KW - MicroRNAs KW - alpha-Fetoproteins KW - Index Medicus KW - Animals KW - Liver Neoplasms, Experimental -- genetics KW - Humans KW - Liver Neoplasms, Experimental -- enzymology KW - Mice, Nude KW - Mice KW - Cell Line, Tumor KW - DNA Methylation -- genetics KW - Down-Regulation -- genetics KW - Liver Neoplasms, Experimental -- mortality KW - Adult KW - Cohort Studies KW - Middle Aged KW - Female KW - Male KW - MicroRNAs -- genetics KW - alpha-Fetoproteins -- biosynthesis KW - Liver Neoplasms -- enzymology KW - Liver Neoplasms -- mortality KW - MicroRNAs -- biosynthesis KW - MicroRNAs -- antagonists & inhibitors KW - Gene Expression Regulation, Neoplastic KW - Carcinoma, Hepatocellular -- genetics KW - Carcinoma, Hepatocellular -- enzymology KW - alpha-Fetoproteins -- genetics KW - Carcinoma, Hepatocellular -- mortality KW - Epigenomics KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1557082548?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modulation+of+miR-29+expression+by+%CE%B1-fetoprotein+is+linked+to+the+hepatocellular+carcinoma+epigenome.&rft.au=Parpart%2C+Sonya%3BRoessler%2C+Stephanie%3BDong%2C+Fei%3BRao%2C+Vinay%3BTakai%2C+Atsushi%3BJi%2C+Junfang%3BQin%2C+Lun-Xiu%3BYe%2C+Qing-Hai%3BJia%2C+Hu-Liang%3BTang%2C+Zhao-You%3BWang%2C+Xin+Wei&rft.aulast=Parpart&rft.aufirst=Sonya&rft.date=2014-09-01&rft.volume=60&rft.issue=3&rft.spage=872&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.27200 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-30 N1 - Date created - 2014-08-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hepatology. 2009 Aug;50(2):472-80 [19585654] Ann Surg Oncol. 2008 Apr;15(4):962-71 [18236113] Nat Rev Genet. 2009 Nov;10(11):805-11 [19789556] Cancer Biol Ther. 2009 Sep;8(18):1686-93 [19901517] Hepatology. 2010 Mar;51(3):836-45 [20041405] J Cell Biochem. 2010 Aug 1;110(5):1155-64 [20564213] BMC Cancer. 2010;10:399 [20678188] Adv Genet. 2010;70:27-56 [20920744] Adv Genet. 2010;70:87-99 [20920746] J Hematol Oncol. 2010;3:37 [20925959] Clin Liver Dis. 2001 Feb;5(1):145-59 [11218912] Cell. 2004 Jan 23;116(2):281-97 [14744438] Exp Biol Med (Maywood). 2004 Jun;229(6):439-63 [15169963] Cancer Res. 1983 Aug;43(8):3739-41 [6190555] Int J Cancer. 1985 Mar 15;35(3):315-8 [2579036] Biochem Biophys Res Commun. 1991 May 15;176(3):985-92 [1645550] J Formos Med Assoc. 1993 Oct;92(10):866-70 [7511953] Oncogene. 1997 Jan 30;14(4):395-404 [9053836] Mol Endocrinol. 1998 Oct;12(10):1551-7 [9773978] J Gastroenterol Hepatol. 1999 May;14 Suppl:S32-6 [10382636] J Hepatol. 1999 Jul;31(1):123-32 [10424292] Scand J Clin Lab Invest. 1957;9(3):277-86 [13495347] Transplantation. 1963 Apr;1:174-80 [14010646] Biochemistry (Mosc). 2006 Feb;71(2):120-32 [16489915] Cancer Res. 2010 Dec 15;70(24):10202-12 [21159642] Oncotarget. 2010 Jul;1(3):224-7 [20936047] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Gastroenterology. 2012 Apr;142(4):957-966.e12 [22202459] Gastroenterology. 2012 Jun;142(7):1431-43 [22504185] Ann Surg Oncol. 2013 Dec;20 Suppl 3:S625-35 [23864307] Cancer Res. 2006 Aug 1;66(15):7390-4 [16885332] Nat Rev Cancer. 2006 Sep;6(9):674-87 [16929323] Clin Cancer Res. 2007 Feb 1;13(3):944-52 [17289889] Clin Chem Lab Med. 2007;45(9):1169-79 [17635075] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317] Nat Genet. 2008 Jan;40(1):43-50 [18066065] Hepatology. 2008 Mar;47(3):897-907 [18176954] N Engl J Med. 2009 Oct 8;361(15):1437-47 [19812400] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/hep.27200 ER - TY - JOUR T1 - Carboplatin-Paclitaxel versus Cisplatin-Ifosfamide in the treatment of uterine carcinosarcoma: a retrospective cohort study. AN - 1557081203; 25078338 AB - Uterine carcinosarcoma (CS) is a rare neoplasm whose adjuvant treatment has not been yet defined. We report on the activity and toxicity of cisplatin-ifosfamide and carboplatin-paclitaxel as adjuvant treatments for patients with uterine CS. Data of International Federation of Gynecology and Obstetrics (FIGO) stage I to IV uterine CS patients treated between 2006 and 2012 with adjuvant chemotherapy (cisplatin 20 mg/mq and ifosfamide 1500 mg/mq day 1 to 4 every 3 weeks plus prophylactic Granulocyte colony-stimulating factor (G-CSF) support [group A] or carboplatin area under the curve -5 (AUC-5) and paclitaxel 175 mg/mq d1q21 [group B]) were retrospectively reviewed. Progression-free survival, overall survival, and chemotherapy-related toxicities were compared between the 2 groups. A subanalysis of oncologic outcomes according to the sarcomatous component (homologous vs heterologous) was performed. Forty-six women were evaluated-21 in group A and 25 in group B. At a median follow-up of 30 months, the median progression-free survival was 11.6 months (95% confidence interval [CI], 6.3-16.9) and 16.6 months (95% CI, 14.7-18.5) for group A and B, respectively (P = 0.20). The median overall survival was 17.1 months (95% CI, 12.6-21.5) and 35.1 months (95% CI, 26.3-43.7) for group A and B, respectively (P = 0.14). No differences were identified among heterologous or homologous components according to chemotherapy treatment. Toxicity profiles widely differ between treatment arms. Because of the super imposable activity and the better toxicity profile, carboplatin-paclitaxel may be a suitable alternative to cisplatin-ifosfamide in the treatment of uterine CS. JF - International journal of gynecological cancer : official journal of the International Gynecological Cancer Society AU - Lorusso, Domenica AU - Martinelli, Fabio AU - Mancini, Maria AU - Sarno, Italo AU - Ditto, Antonino AU - Raspagliesi, Francesco AD - Department of Gynecologic Oncology, IRCCS Foundation National Cancer Institute, Milan, Italy. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 1256 EP - 1261 VL - 24 IS - 7 KW - Carboplatin KW - BG3F62OND5 KW - Paclitaxel KW - P88XT4IS4D KW - Cisplatin KW - Q20Q21Q62J KW - Ifosfamide KW - UM20QQM95Y KW - Index Medicus KW - Paclitaxel -- administration & dosage KW - Aged, 80 and over KW - Humans KW - Adult KW - Retrospective Studies KW - Aged KW - Middle Aged KW - Carboplatin -- administration & dosage KW - Female KW - Survival Analysis KW - Ifosfamide -- administration & dosage KW - Cisplatin -- administration & dosage KW - Carcinosarcoma -- pathology KW - Uterine Neoplasms -- drug therapy KW - Carcinosarcoma -- drug therapy KW - Carcinosarcoma -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Uterine Neoplasms -- mortality KW - Uterine Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1557081203?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+gynecological+cancer+%3A+official+journal+of+the+International+Gynecological+Cancer+Society&rft.atitle=Carboplatin-Paclitaxel+versus+Cisplatin-Ifosfamide+in+the+treatment+of+uterine+carcinosarcoma%3A+a+retrospective+cohort+study.&rft.au=Lorusso%2C+Domenica%3BMartinelli%2C+Fabio%3BMancini%2C+Maria%3BSarno%2C+Italo%3BDitto%2C+Antonino%3BRaspagliesi%2C+Francesco&rft.aulast=Lorusso&rft.aufirst=Domenica&rft.date=2014-09-01&rft.volume=24&rft.issue=7&rft.spage=1256&rft.isbn=&rft.btitle=&rft.title=International+journal+of+gynecological+cancer+%3A+official+journal+of+the+International+Gynecological+Cancer+Society&rft.issn=1525-1438&rft_id=info:doi/10.1097%2FIGC.0000000000000215 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-02 N1 - Date created - 2014-08-26 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/IGC.0000000000000215 ER - TY - JOUR T1 - Relationship between characteristics of medications and drug-induced liver disease phenotype and outcome. AN - 1555619978; 24362054 AB - It is not known whether specific characteristics of medication are associated with type of drug-induced liver injury (DILI) or outcome. We examined the relationships among select characteristics of medications and DILI phenotype and outcome. We analyzed 383 cases of DILI caused by a single orally administered prescription agent from the DILI Network Prospective Study with causalities of definite, highly likely, or probable. Relationship of daily dosage (≥50 mg vs ≤49 mg), preponderance of hepatic metabolism (≥50% vs <50%), or Biopharmaceutics Drug Disposition Classification System (BDDCS) class (1-4, based on solubility and metabolism of the drug) were compared with clinical characteristics and outcomes. Compared with cases of DILI in the ≤49 mg/day group, those associated with daily dosages ≥50 mg had shorter latency (median, 38 days vs 56 days; P = .03) and a different biochemical pattern of liver injury (P = .04); no differences in recovery, severity, or outcome were observed. Patients with DILI caused by medications with or without preponderant hepatic metabolism did not differ in clinical characteristics or outcomes. Compared with other classes of BDDCS, DILI caused by BDDCS class 1 medications had significantly longer latency (P < .001) and greater proportion of hepatocellular injury (P = .001). However, peak liver biochemical values and patients' time to recovery, disease severity, and outcomes did not differ among the 4 BDDCS classes. Characteristics of medications (dosage, hepatic metabolism, and solubility) are associated with features of DILI such as latency and pattern of liver injury, but not with recovery, severity, or outcome. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved. JF - Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association AU - Vuppalanchi, Raj AU - Gotur, Raghavender AU - Reddy, K Rajender AU - Fontana, Robert J AU - Ghabril, Marwan AU - Kosinski, Andrzej S AU - Gu, Jiezhun AU - Serrano, Jose AU - Chalasani, Naga AD - Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. ; Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. ; Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan. ; Duke Clinical Research Institute, Durham, North Carolina. ; Liver Disease Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. ; Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: nchalasa@iu.edu. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 1550 EP - 1555 VL - 12 IS - 9 KW - Index Medicus KW - Overdose KW - ALT KW - Liver Toxicity KW - Side Effect KW - DILIN KW - Prospective Studies KW - Humans KW - Adult KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Male KW - Female KW - Chemical and Drug Induced Liver Injury -- etiology KW - Chemical and Drug Induced Liver Injury -- mortality KW - Chemical and Drug Induced Liver Injury -- pathology KW - Drug Therapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1555619978?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+gastroenterology+and+hepatology+%3A+the+official+clinical+practice+journal+of+the+American+Gastroenterological+Association&rft.atitle=Relationship+between+characteristics+of+medications+and+drug-induced+liver+disease+phenotype+and+outcome.&rft.au=Vuppalanchi%2C+Raj%3BGotur%2C+Raghavender%3BReddy%2C+K+Rajender%3BFontana%2C+Robert+J%3BGhabril%2C+Marwan%3BKosinski%2C+Andrzej+S%3BGu%2C+Jiezhun%3BSerrano%2C+Jose%3BChalasani%2C+Naga&rft.aulast=Vuppalanchi&rft.aufirst=Raj&rft.date=2014-09-01&rft.volume=12&rft.issue=9&rft.spage=1550&rft.isbn=&rft.btitle=&rft.title=Clinical+gastroenterology+and+hepatology+%3A+the+official+clinical+practice+journal+of+the+American+Gastroenterological+Association&rft.issn=1542-7714&rft_id=info:doi/10.1016%2Fj.cgh.2013.12.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-27 N1 - Date created - 2014-08-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Ann N Y Acad Sci. 1993 Jun 23;685:641-5 [8363271] Pharm Res. 2005 Jan;22(1):11-23 [15771225] Annu Rev Pharmacol Toxicol. 2007;47:513-39 [16879083] Pharm Res. 2008 Mar;25(3):483-8 [18236138] Hepatology. 2008 Jun;47(6):2003-9 [18454504] Bioorg Med Chem Lett. 2008 Sep 1;18(17):4872-5 [18691886] Gastroenterology. 2008 Dec;135(6):1924-34, 1934.e1-4 [18955056] Drug Saf. 2009;32(1):55-68 [19132805] Mol Pharm. 2009 Jan-Feb;6(1):74-81 [19132929] Nat Genet. 2009 Jul;41(7):816-9 [19483685] Hepatology. 2010 Feb;51(2):615-20 [19839004] Basic Clin Pharmacol Toxicol. 2010 Mar;106(3):162-7 [20002064] Dig Dis Sci. 2011 Apr;56(4):958-76 [21327704] Nat Rev Gastroenterol Hepatol. 2011 Apr;8(4):202-11 [21386809] Clin Pharmacol Ther. 2011 Jun;89(6):911-4 [21412230] Clin Pharmacol Ther. 2011 Jun;89(6):806-15 [21544079] Gastroenterology. 2011 Jul;141(1):338-47 [21570397] AAPS J. 2011 Dec;13(4):519-47 [21818695] Clin Pharmacol Ther. 2012 Sep;92(3):376-80 [22850601] Pharmacogenet Genomics. 2012 Nov;22(11):784-95 [22968431] J Pharm Sci. 2013 Jan;102(1):34-42 [23147500] Hepatology. 2013 Feb;57(2):727-39 [22987284] Hepatology. 2013 Jul;58(1):388-96 [23258593] Hepatology. 2013 Jul;58(1):15-7 [23390057] Eur J Haematol Suppl. 1996;60:89-92 [8987248] Comment In: Clin Gastroenterol Hepatol. 2014 Sep;12(9):1556-61 [24530601] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.cgh.2013.12.016 ER - TY - JOUR T1 - A new antiviral: chimeric 3TC-AZT phosphonate efficiently inhibits HIV-1 in human tissues ex vivo. AN - 1554469325; 25010891 AB - Although more-recently developed antivirals target different molecules in the HIV-1 replication cycle, nucleoside reverse transcriptase inhibitors (NRTIs) remain central for HIV-1 therapy. Here, we test the anti-HIV activity of a phosphonate chimera of two well-known NRTIs, namely AZT and 3TC. We show that this newly synthesized compound suppressed HIV-1 infection in lymphoid tissue ex vivo more efficiently than did other phosphonates of NRTIs. Moreover, the new compound was not toxic for tissue cells, thus making the chimeric phosphonate strategy a valid approach for the development of anti HIV-1 compound heterodimers. Published by Elsevier B.V. JF - Antiviral research AU - Vanpouille, Christophe AU - Khandazhinskaya, Anastasia AU - Karpenko, Inna AU - Zicari, Sonia AU - Barreto-de-Souza, Victor AU - Frolova, Svetlana AU - Margolis, Leonid AU - Kochetkov, Sergey AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, United States. ; Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russian Federation. ; Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, United States. Electronic address: margolis@helix.nih.gov. ; Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russian Federation. Electronic address: kochet@eimb.ru. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 125 EP - 131 VL - 109 KW - Anti-HIV Agents KW - 0 KW - Dideoxynucleotides KW - Thymine Nucleotides KW - Lamivudine KW - 2T8Q726O95 KW - Zidovudine KW - 4B9XT59T7S KW - 3'-azido-3'-deoxythymidine 5'-triphosphate KW - 6RGF96R053 KW - Index Medicus KW - Depot form KW - NRTI KW - HIV-1 KW - Virus Replication -- drug effects KW - Humans KW - In Vitro Techniques KW - Drug Evaluation, Preclinical KW - Zidovudine -- analogs & derivatives KW - Anti-HIV Agents -- chemistry KW - Dideoxynucleotides -- chemistry KW - HIV Infections -- virology KW - Zidovudine -- pharmacology KW - Lamivudine -- chemistry KW - Lamivudine -- pharmacology KW - HIV-1 -- physiology KW - Thymine Nucleotides -- chemistry KW - Anti-HIV Agents -- chemical synthesis KW - Palatine Tonsil -- drug effects KW - Dideoxynucleotides -- pharmacology KW - Anti-HIV Agents -- pharmacology KW - Thymine Nucleotides -- pharmacology KW - HIV Infections -- drug therapy KW - Zidovudine -- chemistry KW - HIV-1 -- drug effects KW - Palatine Tonsil -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554469325?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antiviral+research&rft.atitle=A+new+antiviral%3A+chimeric+3TC-AZT+phosphonate+efficiently+inhibits+HIV-1+in+human+tissues+ex+vivo.&rft.au=Vanpouille%2C+Christophe%3BKhandazhinskaya%2C+Anastasia%3BKarpenko%2C+Inna%3BZicari%2C+Sonia%3BBarreto-de-Souza%2C+Victor%3BFrolova%2C+Svetlana%3BMargolis%2C+Leonid%3BKochetkov%2C+Sergey&rft.aulast=Vanpouille&rft.aufirst=Christophe&rft.date=2014-09-01&rft.volume=109&rft.issue=&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Antiviral+research&rft.issn=1872-9096&rft_id=info:doi/10.1016%2Fj.antiviral.2014.06.019 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-06 N1 - Date created - 2014-08-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2002 May 2;417(6884):95-8 [11986671] Nucleosides Nucleotides Nucleic Acids. 2000 Oct-Dec;19(10-12):1795-804 [11200274] Curr Top Med Chem. 2003;3(13):1467-95 [14529522] Nucleosides Nucleotides Nucleic Acids. 2003 May-Aug;22(5-8):873-5 [14565300] Curr Drug Metab. 2003 Dec;4(6):461-85 [14683475] Antiviral Res. 1990 Jul;14(1):11-23 [1964371] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1934-8 [1371886] J Med Chem. 1995 May 12;38(10):1641-9 [7538589] Proc Natl Acad Sci U S A. 1998 Aug 4;95(16):9518-23 [9689112] J Hepatol. 1999 Jan;30(1):156-60 [9927163] Pharmacol Rep. 2006 Sep-Oct;58(5):599-613 [17085852] Cell Host Microbe. 2008 Sep 11;4(3):260-70 [18779052] Nat Protoc. 2009;4(2):256-69 [19197269] Drug Metab Dispos. 2009 Mar;37(3):494-501 [19106116] Int J Antimicrob Agents. 2009 Apr;33(4):307-20 [19108994] PLoS One. 2010;5(2):e9310 [20174579] Expert Opin Drug Metab Toxicol. 2010 Jun;6(6):701-14 [20380483] Chem Biol Drug Des. 2011 Jul;78(1):50-6 [21518262] Trends Microbiol. 2012 Aug;20(8):369-75 [22705107] J Med Chem. 2000 May 18;43(10):1927-39 [10821705] Biochim Biophys Acta. 2002 Jul 18;1587(2-3):258-75 [12084468] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.antiviral.2014.06.019 ER - TY - JOUR T1 - Comparative toxicity and efficacy of engineered anthrax lethal toxin variants with broad anti-tumor activities. AN - 1554459061; 24971906 AB - We have previously designed and characterized versions of anthrax lethal toxin that are selectively cytotoxic in the tumor microenvironment and which display broad and potent anti-tumor activities in vivo. Here, we have performed the first direct comparison of the safety and efficacy of three engineered anthrax lethal toxin variants requiring activation by either matrix-metalloproteinases (MMPs), urokinase plasminogen activator (uPA) or co-localized MMP/uPA activities. C57BL/6J mice were challenged with six doses of engineered toxins via intraperitoneal (I.P.) or intravenous (I.V.) dose routes to determine the maximum tolerated dose for six administrations (MTD6) and dose-limiting toxicities. Efficacy was evaluated using the B16-BL6 syngraft model of melanoma; mice bearing established tumors were treated with six I.P. doses of toxin and tumor measurements and immunohistochemistry, paired with terminal blood work, were used to elaborate upon the anti-tumor mechanism and relative efficacy of each variant. We found that MMP-, uPA- and dual MMP/uPA-activated anthrax lethal toxins exhibited the same dose-limiting toxicity; dose-dependent GI toxicity. In terms of efficacy, all three toxins significantly reduced primary B16-BL6 tumor burden, ranging from 32% to 87% reduction, and they also delayed disease progression as evidenced by dose-dependent normalization of blood work values. While target organ toxicity and effective doses were similar amongst the variants, the dual MMP/uPA-activated anthrax lethal toxin exhibited the highest I.P. MTD6 and was 1.5-3-fold better tolerated than the single MMP- and uPA-activated toxins. Overall, we demonstrate that this dual MMP/uPA-activated anthrax lethal toxin can be administered safely and is highly effective in a preclinical model of melanoma. This modified bacterial cytotoxin is thus a promising candidate for further clinical development and evaluation for use in treating human cancers. Published by Elsevier Inc. JF - Toxicology and applied pharmacology AU - Peters, Diane E AU - Hoover, Benjamin AU - Cloud, Loretta Grey AU - Liu, Shihui AU - Molinolo, Alfredo A AU - Leppla, Stephen H AU - Bugge, Thomas H AD - Proteases and Tissue Remodeling Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA; Program of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Boston, MA, USA. ; Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; Proteases and Tissue Remodeling Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. ; Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. ; Proteases and Tissue Remodeling Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. Electronic address: thomas.bugge@nih.go. Y1 - 2014/09/01/ PY - 2014 DA - 2014 Sep 01 SP - 220 EP - 229 VL - 279 IS - 2 KW - Antigens, Bacterial KW - 0 KW - Antineoplastic Agents KW - Bacterial Toxins KW - Biomarkers, Tumor KW - Prodrugs KW - anthrax toxin KW - Urokinase-Type Plasminogen Activator KW - EC 3.4.21.73 KW - Matrix Metalloproteinases KW - EC 3.4.24.- KW - Index Medicus KW - Bacterial cytotoxin KW - Protease KW - Prodrug KW - Cancer KW - Melanoma KW - Injections, Intraperitoneal KW - Animals KW - Injections, Intravenous KW - Dose-Response Relationship, Drug KW - Mice KW - Urokinase-Type Plasminogen Activator -- metabolism KW - Tumor Burden -- drug effects KW - Mice, Inbred C57BL KW - Matrix Metalloproteinases -- metabolism KW - Maximum Tolerated Dose KW - Biomarkers, Tumor -- blood KW - Time Factors KW - Female KW - Prodrugs -- toxicity KW - Antigens, Bacterial -- pharmacology KW - Antigens, Bacterial -- genetics KW - Skin Neoplasms -- blood KW - Skin Neoplasms -- drug therapy KW - Bacterial Toxins -- genetics KW - Skin Neoplasms -- enzymology KW - Protein Engineering KW - Prodrugs -- pharmacology KW - Antigens, Bacterial -- toxicity KW - Antigens, Bacterial -- metabolism KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Agents -- metabolism KW - Skin Neoplasms -- pathology KW - Bacterial Toxins -- pharmacology KW - Bacterial Toxins -- administration & dosage KW - Melanoma, Experimental -- pathology KW - Prodrugs -- administration & dosage KW - Melanoma, Experimental -- blood KW - Bacterial Toxins -- metabolism KW - Melanoma, Experimental -- enzymology KW - Antineoplastic Agents -- toxicity KW - Melanoma, Experimental -- drug therapy KW - Antigens, Bacterial -- administration & dosage KW - Bacterial Toxins -- toxicity KW - Antineoplastic Agents -- pharmacology KW - Prodrugs -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554459061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparative+toxicity+and+efficacy+of+engineered+anthrax+lethal+toxin+variants+with+broad+anti-tumor+activities.&rft.au=Peters%2C+Diane+E%3BHoover%2C+Benjamin%3BCloud%2C+Loretta+Grey%3BLiu%2C+Shihui%3BMolinolo%2C+Alfredo+A%3BLeppla%2C+Stephen+H%3BBugge%2C+Thomas+H&rft.aulast=Peters&rft.aufirst=Diane&rft.date=2014-09-01&rft.volume=279&rft.issue=2&rft.spage=220&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2014.06.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-12 N1 - Date created - 2014-08-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Science. 1998 May 1;280(5364):734-7 [9563949] Biochem Biophys Res Commun. 1998 Jul 30;248(3):706-11 [9703991] Curr Opin Cell Biol. 1998 Oct;10(5):667-71 [9818179] Nat Biotechnol. 2005 Jun;23(6):725-30 [15895075] Mol Cancer Ther. 2006 Jan;5(1):89-96 [16432166] Clin Cancer Res. 2006 Dec 15;12(24):7437-43 [17189417] Cancer Res. 2007 Apr 1;67(7):3329-36 [17409442] J Biol Chem. 2008 Jan 4;283(1):529-40 [17974567] Cell Cycle. 2008 Mar 15;7(6):745-9 [18245947] Curr Protoc Immunol. 2001 May;Chapter 20:Unit 20.1 [18432774] Front Biosci (Landmark Ed). 2009;14:2335-57 [19273204] Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12424-9 [19617532] J Clin Oncol. 2009 Nov 1;27(31):5287-97 [19738110] Mol Cancer Ther. 2010 Jan;9(1):190-201 [20053778] J Immunol. 2010 Nov 1;185(9):5463-7 [20921524] Infect Immun. 2011 Jan;79(1):118-24 [20974827] Invest New Drugs. 2013 Feb;31(1):206-12 [22843210] Nature. 2013 Sep 5;501(7465):63-8 [23995686] PLoS One. 2011;6(5):e20532 [21655226] PLoS One. 2012;7(3):e33583 [22438953] Clin Chem Lab Med. 2012 Nov;50(11):1877-91 [23093268] Protein Expr Purif. 2000 Apr;18(3):293-302 [10733882] Cancer Res. 2000 Nov 1;60(21):6061-7 [11085528] Biochem J. 2000 Dec 15;352 Pt 3:739-45 [11104681] J Biol Chem. 2001 May 25;276(21):17976-84 [11278833] Nature. 2001 Nov 8;414(6860):225-9 [11700562] Proc Natl Acad Sci U S A. 2002 May 14;99(10):7045-8 [11997437] Proc Natl Acad Sci U S A. 2002 May 14;99(10):7049-53 [11997439] Proc Natl Acad Sci U S A. 2003 Jan 21;100(2):657-62 [12525700] Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5170-4 [12700348] Expert Opin Biol Ther. 2003 Aug;3(5):843-53 [12880383] J Clin Invest. 2003 Sep;112(5):670-82 [12952916] Am J Physiol Regul Integr Comp Physiol. 2004 Apr;286(4):R699-709 [14715494] Cancer Chemother Pharmacol. 1989;24(3):148-54 [2544306] Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10277-81 [1438214] Mol Microbiol. 1994 Sep;13(6):1093-100 [7854123] Int J Cancer. 1997 Jul 3;72(1):1-22 [9212216] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2014.06.010 ER - TY - JOUR T1 - Class II human leucocyte antigen DRB1*11 in hairy cell leukaemia patients with and without haemolytic uraemic syndrome. AN - 1553711783; 24931452 AB - Frequencies of human leucocyte antigens (HLA) were determined in 287 classic hairy cell leukaemia (HCL) patients. With respect to both population (n = 287) and allele (2n = 574) frequency respectively, the most common HLA class I and II antigens expressed were HLA-A*02 (49·1% and 28·6%), HLA-B*07 (21·3% and 11·1%), HLA-C*07 (46·7 and 28·2%), HLA-DQB1*03 (62·7% and 37·3%), HLA-DRB1*11 (30·0% and 16·0%) and HLA-DRB4*01 (45·3% and 29·6%). In comparing 6-14 databases of control Caucasians to 267 Caucasian HCL patients, only HLA-DRB1*11 was consistently over-represented in HCL, 31·1% of patients vs. 17-19·9% of controls (P = 0·0055 to <0·0001) and 16·5% of alleles vs. 6·5-12·3% of control alleles (P = 0·022 to <0·0001). HLA-DRB1*11 is a known risk factor for acquired thrombotic microangiopathy. Anti-CD22 recombinant immunotoxin BL22 in HCL was associated with a 12% incidence of completely reversible grade 3-4 haemolytic uraemic syndrome (HUS), mainly during the second or third retreatment cycle. Of 49 HCL patients receiving ≥2 cycles of BL22, 7 (14%) had HUS and HLA-DRB1*11 was expressed in 71% of 7 with HUS compared with only 21% of 42 without (P = 0·015). These data suggest that DBR1*11 may be a marker for increased susceptibility to HCL and, among HCL patients, could be a risk factor for BL22-induced HUS. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - British journal of haematology AU - Arons, Evgeny AU - Adams, Sharon AU - Venzon, David J AU - Pastan, Ira AU - Kreitman, Robert J AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD, USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 729 EP - 738 VL - 166 IS - 5 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - HLA-DRB1 Chains KW - HLA-DRB1*11 antigen KW - immunotoxin HA22 KW - Index Medicus KW - ADAMTS13 KW - HLA-DQB1*03 KW - thrombotic microangiopathy KW - recombinant immunotoxin KW - moxetumomab pasudotox KW - Young Adult KW - Gene Frequency KW - Humans KW - Aged KW - Tissue Donors KW - Thrombotic Microangiopathies KW - Alleles KW - Aged, 80 and over KW - Risk Factors KW - Adult KW - Bacterial Toxins -- therapeutic use KW - Middle Aged KW - Genetic Predisposition to Disease KW - Exotoxins -- therapeutic use KW - Female KW - Male KW - HLA-DRB1 Chains -- biosynthesis KW - Hemolytic-Uremic Syndrome -- immunology KW - Leukemia, Hairy Cell -- metabolism KW - Hemolytic-Uremic Syndrome -- metabolism KW - Hemolytic-Uremic Syndrome -- genetics KW - HLA-DRB1 Chains -- genetics KW - Leukemia, Hairy Cell -- therapy KW - Leukemia, Hairy Cell -- immunology KW - Leukemia, Hairy Cell -- genetics KW - Hemolytic-Uremic Syndrome -- therapy KW - HLA-DRB1 Chains -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1553711783?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+haematology&rft.atitle=Class+II+human+leucocyte+antigen+DRB1*11+in+hairy+cell+leukaemia+patients+with+and+without+haemolytic+uraemic+syndrome.&rft.au=Arons%2C+Evgeny%3BAdams%2C+Sharon%3BVenzon%2C+David+J%3BPastan%2C+Ira%3BKreitman%2C+Robert+J&rft.aulast=Arons&rft.aufirst=Evgeny&rft.date=2014-09-01&rft.volume=166&rft.issue=5&rft.spage=729&rft.isbn=&rft.btitle=&rft.title=British+journal+of+haematology&rft.issn=1365-2141&rft_id=info:doi/10.1111%2Fbjh.12956 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-08 N1 - Date created - 2014-08-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Blood. 2004 Jun 15;103(12):4514-9 [14976043] Br J Haematol. 2002 Dec;119(3):713-5 [12437649] Blood. 2004 Nov 1;104(9):2879-85 [15217826] Immunol Rev. 1983;70:155-66 [6187661] Tissue Antigens. 1983 Jan;21(1):1-8 [6601312] Stat Med. 1990 Jul;9(7):811-8 [2218183] Hum Immunol. 1991 Mar;30(3):183-9 [1676026] Leuk Lymphoma. 1994;14 Suppl 1:63-5 [7820055] Haematologica. 1998 Aug;83(8):751-2 [9793263] Blood. 1958 Jul;13(7):609-30 [13560561] Leuk Res. 2005 Feb;29(2):153-8 [15607363] Leuk Lymphoma. 2005 Feb;46(2):243-5 [15621808] J Rheumatol Suppl. 2005 Jan;72:10-3 [15660456] J Clin Oncol. 2005 Sep 20;23(27):6719-29 [16061911] Br J Haematol. 2006 Jun;133(5):504-12 [16681637] Hematol Oncol Clin North Am. 2006 Oct;20(5):1051-63 [16990106] Leuk Lymphoma. 2007 Apr;48(4):653-4 [17454620] Leuk Lymphoma. 2007 Apr;48(4):805-7 [17454641] P R Health Sci J. 2007 Jun;26(2):97-101 [17722421] Clin Lymphoma Myeloma. 2007 Nov;7(9):573-9 [18186965] Haematologica. 2008 May;93(5):697-705 [18387977] Br J Haematol. 2008 Jul;142(1):45-51 [18477040] J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673] Blood. 2009 Nov 19;114(21):4687-95 [19745070] Nature. 2010 Jan 7;463(7277):88-92 [20054396] Blood. 2010 Jan 7;115(1):71-7 [19887677] J Thromb Haemost. 2010 Feb;8(2):257-62 [19922436] J Thromb Haemost. 2010 Apr;8(4):856-9 [20141578] Br J Haematol. 2010 Feb;148(4):666-9 [19863540] Blood. 2010 Jun 10;115(23):4820-3 [20385791] Nucleic Acids Res. 2011 Jan;39(Database issue):D913-9 [21062830] Cytometry B Clin Cytom. 2011 Mar;80(2):83-90 [20872890] Blood. 2011 May 5;117(18):4844-51 [21368287] N Engl J Med. 2011 Jun 16;364(24):2305-15 [21663470] Am J Clin Pathol. 2011 Oct;136(4):625-30 [21917686] N Engl J Med. 2011 Oct 27;365(17):1612-23 [22029983] Leuk Lymphoma. 2011 Dec;52(12):2391-2 [21827340] Blood. 2012 Apr 5;119(14):3330-2 [22210875] J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053] Nucleic Acids Res. 2013 Jan;41(Database issue):D1222-7 [23080122] Blood. 2013 Aug 22;122(8):1487-93 [23847193] Int J Cancer. 2001 Apr 15;92(2):203-7 [11291046] N Engl J Med. 2001 Jul 26;345(4):241-7 [11474661] N Engl J Med. 2001 Nov 8;345(19):1426; author reply 1427-8 [11794186] Eur J Haematol. 2001 Sep;67(3):185-8 [11737252] J Virol. 2002 Feb;76(4):1787-9 [11799174] Clin Cancer Res. 2002 Apr;8(4):995-1002 [11948105] Medicine (Baltimore). 2004 Jul;83(4):233-44 [15232311] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/bjh.12956 ER - TY - JOUR T1 - Indices of methylation in sperm DNA from fertile men differ between distinct geographical regions. AN - 1553707290; 25035434 AB - Which are the main determinants, if any, of sperm DNA methylation levels? Geographical region resulted associated with the sperm methylation status assessed on genome-wide repetitive sequences. DNA methylation level, assessed on repetitive sequences from peripheral blood lymphocyte, can vary with age, gender, alcohol consumption and white blood cell counts. A cross-sectional study. Individual data were collected from 269 young healthy men of proven fertility living in three geographical regions: Inuits from Greenland, Caucasians from Warsaw (Poland) and Kharkiv (Ukraine). Semen samples were collected between May 2002 and February 2004 and aliquots were immediately frozen. We estimated sperm DNA global methylation level (DGML) in two ways. First DNA methylation in repetitive DNA sequences (LINE-1, Satα and Alu) was quantified by PCR pyrosequencing after bisulfite conversion and second by flow cytometry (FCM) using fluorescently labeled monoclonal antibodies anti-5-methylcytosine. We analyzed whether personal characteristics and habits, body mass index, semen quality parameters, sperm chromatin integrity, biomarkers of accessory gland function and the plasma concentration of reproductive hormones were associated with sperm DNA methylation levels in men. Associations were evaluated by analysis of variance and linear regression analyses. The geographical location emerged as the main determinant when using the methylation level in repetitive sequences. FCM DGML results were not associated with those from repetitive sequence analysis. No other consistent associations between methylation markers and the assessed variables were identified across countries. The methods used are only surrogates of the actual sperm methylome and the methylation levels at individual specific loci were not explored. Sperm DGML is relatively independent from semen quality parameters and is a new candidate biomarker for epidemiological studies of the impact of environmental contaminants on male fertility. The study is part of the project CLEAR (Climate change, Environmental contaminants and Reproductive health) supported by the European Commission 7th framework program, contract no: FP7-ENV-2008-1-226217. No competing interest is declared. © The Author 2014. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Human reproduction (Oxford, England) AU - Consales, C AU - Leter, G AU - Bonde, J P E AU - Toft, G AU - Eleuteri, P AU - Moccia, T AU - Budillon, A AU - Jönsson, B A G AU - Giwercman, A AU - Pedersen, H S AU - Ludwicki, J K AU - Zviezdai, V AU - Heederik, D AU - Spanò, M AD - Laboratory of Toxicology, Unit of Radiation Biology and Human Health, ENEA Casaccia Research Center, Via Anguillarese 301, 00123 Rome, Italy. ; Department of Occupational and Environmental Medicine, Bispebjerg University Hospital, DK-2400 Copenhagen NV, Denmark. ; Department of Occupational Medicine, Aarhus University Hospital, DK-8000 Aarhus C, Denmark. ; Experimental Pharmacology Unit, Department of Experimental Oncology, National Cancer Institute - G. Pascale, 80131 Naples, Italy. ; Division of Occupational and Environmental Medicine, Department of Laboratory Medicine, Lund University, SE-22185 Lund, Sweden. ; Reproductive Medicine Centre, Skåne University Hospital Malmö, Lund University, Malmö SE-20502, Sweden. ; Centre for Arctic Environmental Medicine, Greenland Institute of Natural Resources, 3900 Nuuk, Greenland. ; Department of Toxicology and Risk Assessment, National Institute of Public Health - National Institute of Hygiene, 00971 Warsaw, Poland. ; Department of Social Medicine and Organization of Public Health, Kharkiv National Medical University, 61022 Kharkiv, Ukraine. ; Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands. ; Laboratory of Toxicology, Unit of Radiation Biology and Human Health, ENEA Casaccia Research Center, Via Anguillarese 301, 00123 Rome, Italy marcello.spano@enea.it. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 2065 EP - 2072 VL - 29 IS - 9 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - human spermatozoa KW - pyrosequencing KW - sperm DNA methylation KW - epidemiology KW - flow cytometry KW - Greenland KW - Cross-Sectional Studies KW - Fertility KW - Genome, Human KW - Semen Analysis KW - Poland KW - Humans KW - Ukraine KW - Geography KW - Male KW - DNA Methylation KW - DNA -- metabolism KW - Spermatozoa -- metabolism KW - Repetitive Sequences, Nucleic Acid -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1553707290?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+reproduction+%28Oxford%2C+England%29&rft.atitle=Indices+of+methylation+in+sperm+DNA+from+fertile+men+differ+between+distinct+geographical+regions.&rft.au=Consales%2C+C%3BLeter%2C+G%3BBonde%2C+J+P+E%3BToft%2C+G%3BEleuteri%2C+P%3BMoccia%2C+T%3BBudillon%2C+A%3BJ%C3%B6nsson%2C+B+A+G%3BGiwercman%2C+A%3BPedersen%2C+H+S%3BLudwicki%2C+J+K%3BZviezdai%2C+V%3BHeederik%2C+D%3BSpan%C3%B2%2C+M&rft.aulast=Consales&rft.aufirst=C&rft.date=2014-09-01&rft.volume=29&rft.issue=9&rft.spage=2065&rft.isbn=&rft.btitle=&rft.title=Human+reproduction+%28Oxford%2C+England%29&rft.issn=1460-2350&rft_id=info:doi/10.1093%2Fhumrep%2Fdeu176 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-23 N1 - Date created - 2014-08-15 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/humrep/deu176 ER - TY - JOUR T1 - Acute and chronic effects of IL-22 on acetaminophen-induced liver injury. AN - 1553705789; 25063867 AB - Acetaminophen (APAP)-induced liver injury (AILI) accounts for half of the acute liver failure cases in the United States. A better understanding of the underlying mechanisms of AILI is necessary for the development of novel antidotes. We found that pretreatment with IL-22 protected mice from APAP-mediated hepatotoxicity. The protection was dependent on STAT3, as IL-22 failed to reduce APAP hepatotoxicity in liver-specific STAT3 knockout mice. In contrast to the acute exposure to IL-22, the endogenous chronic overexpression of IL-22 in IL-22 transgenic (TG) mice or IL-22 adenovirus treatment for 6 wk resulted in a markedly increased susceptibility to AILI. Furthermore, the hepatic expression levels of cytochrome 2E1 (Cyp2E1) and Cyp1A2 were much higher in IL-22TG mice. Ablation of Cyp2E1 but not hepatic STAT3 abolished AILI and protein-adduct formation in IL-22TG mice. Finally, hepatic expression of HNF-1α, a transcriptional factor that is known to control Cyp2E1 expression, was elevated in IL-22TG mice compared with wild-type mice. Upregulation of hepatic Cyp2E1 was only observed in mice with constitutive overexpression of IL-22 but not with short-term treatment with one dose of IL-22 or multiple doses of IL-22 for 2 wk. In conclusion, short-term acute IL-22 exposure protects mice against AILI through STAT3 activation; however, chronic constitutive overexpression of IL-22 exacerbates AILI by increasing Cyp2E1 and toxic reactive APAP metabolite production. These findings may not only enhance our understanding of the effects of chronic inflammation on AILI in patients with liver disease, but are also helpful to identify novel therapeutic targets for the treatment of AILI. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Feng, Dechun AU - Wang, Yan AU - Wang, Hua AU - Weng, Honglei AU - Kong, Xiaoni AU - Martin-Murphy, Brittany V AU - Li, Yongmei AU - Park, Ogyi AU - Dooley, Steven AU - Ju, Cynthia AU - Gao, Bin AD - Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892; ; Medical Clinic, Faculty of Medicine at Mannheim, University of Heidelberg, Mannheim 68167, Germany; ; School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; Med-X Research Institute, Shanghai Jiao Tong University, Shanghai 200030, China; and. ; Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO 80045. ; Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892; bgao@mail.nih.gov. Y1 - 2014/09/01/ PY - 2014 DA - 2014 Sep 01 SP - 2512 EP - 2518 VL - 193 IS - 5 KW - Analgesics, Non-Narcotic KW - 0 KW - Hepatocyte Nuclear Factor 1-alpha KW - Hnf1a protein, mouse KW - Interleukins KW - STAT3 Transcription Factor KW - Stat3 protein, mouse KW - interleukin-22 KW - Acetaminophen KW - 362O9ITL9D KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - Abridged Index Medicus KW - Index Medicus KW - Acute Disease KW - Animals KW - Chemical and Drug Induced Liver Injury -- pathology KW - Hepatocyte Nuclear Factor 1-alpha -- genetics KW - Humans KW - Chemical and Drug Induced Liver Injury -- genetics KW - Mice KW - Gene Expression Regulation, Enzymologic -- immunology KW - Chemical and Drug Induced Liver Injury -- drug therapy KW - Cytochrome P-450 CYP2E1 -- genetics KW - Mice, Knockout KW - Cytochrome P-450 CYP2E1 -- immunology KW - Gene Expression Regulation, Enzymologic -- drug effects KW - STAT3 Transcription Factor -- immunology KW - STAT3 Transcription Factor -- genetics KW - Chronic Disease KW - Hepatocyte Nuclear Factor 1-alpha -- immunology KW - Analgesics, Non-Narcotic -- adverse effects KW - Interleukins -- pharmacology KW - Analgesics, Non-Narcotic -- pharmacology KW - Acetaminophen -- adverse effects KW - Interleukins -- immunology KW - Interleukins -- genetics KW - Acetaminophen -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1553705789?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Acute+and+chronic+effects+of+IL-22+on+acetaminophen-induced+liver+injury.&rft.au=Feng%2C+Dechun%3BWang%2C+Yan%3BWang%2C+Hua%3BWeng%2C+Honglei%3BKong%2C+Xiaoni%3BMartin-Murphy%2C+Brittany+V%3BLi%2C+Yongmei%3BPark%2C+Ogyi%3BDooley%2C+Steven%3BJu%2C+Cynthia%3BGao%2C+Bin&rft.aulast=Feng&rft.aufirst=Dechun&rft.date=2014-09-01&rft.volume=193&rft.issue=5&rft.spage=2512&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.1400588 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-09 N1 - Date created - 2014-08-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hepatology. 2008 Jul;48(1):240-51 [18537186] Gastroenterology. 2008 Apr;134(4):1148-58 [18395093] Curr Drug Metab. 2009 Feb;10(2):164-78 [19275551] J Immunol. 2009 Apr 15;182(8):4521-8 [19342625] Exp Cell Res. 2009 Jul 1;315(11):1975-89 [19331832] Semin Immunopathol. 2010 Mar;32(1):17-31 [20127093] Biochem Pharmacol. 2010 Nov 15;80(10):1592-600 [20723539] Hepatology. 2010 Oct;52(4):1291-300 [20842630] Cytokine Growth Factor Rev. 2010 Oct;21(5):365-79 [20870448] Hepatology. 2011 Jun;53(6):2042-52 [21433044] Hepatology. 2011 Jul;54(1):252-61 [21465510] J Cell Biol. 2011 Oct 17;195(2):263-76 [21987637] Gastroenterology. 2011 Nov;141(5):1897-906 [21708106] Sci Signal. 2012 Jan 17;5(207):ra5 [22253262] J Exp Med. 2012 Feb 13;209(2):307-18 [22291093] Transplantation. 2012 Mar 15;93(5):485-92 [22262131] J Clin Invest. 2012 Apr;122(4):1574-83 [22378043] Gastroenterology. 2012 Jul;143(1):188-98.e7 [22484119] Toxicol Appl Pharmacol. 2013 Jan 15;266(2):224-32 [23200774] Am J Pathol. 2013 Apr;182(4):1107-13 [23375450] Cytokine. 2011 Nov;56(2):174-9 [21843953] Curr Opin Immunol. 2011 Oct;23(5):605-12 [21862302] Hepatology. 2000 Jan;31(1):149-59 [10613740] Hepatology. 2000 Jul;32(1):49-55 [10869288] JAMA. 2002 Jan 16;287(3):337-44 [11790213] Toxicol Sci. 2002 Jun;67(2):322-8 [12011492] J Clin Invest. 2002 Nov;110(10):1503-13 [12438448] Gastroenterology. 2003 Aug;125(2):532-43 [12891556] J Pharmacol Exp Ther. 2003 Dec;307(3):1205-12 [14557382] Hepatology. 2004 May;39(5):1332-42 [15122762] Hepatology. 2004 Nov;40(5):1170-9 [15486922] J Pharmacol Exp Ther. 1973 Oct;187(1):185-94 [4746326] Gastroenterology. 1981 Jan;80(1):140-8 [7192662] Toxicology. 1983;28(3):193-206 [6636205] Toxicol Appl Pharmacol. 1984 Jan;72(1):40-5 [6710483] Res Commun Chem Pathol Pharmacol. 1990 Jul;69(1):115-8 [2218067] Biochem Pharmacol. 1990 Nov 1;40(9):1989-95 [2242029] J Pharmacol Exp Ther. 1990 Dec;255(3):1408-19 [2262910] Mol Pharmacol. 1993 Oct;44(4):707-15 [8232220] DNA Cell Biol. 1995 Apr;14(4):285-93 [7710685] J Biol Chem. 1996 May 17;271(20):12063-7 [8662637] J Pharmacol Exp Ther. 1998 Oct;287(1):352-8 [9765356] Toxicol Appl Pharmacol. 1998 Sep;152(1):193-9 [9772215] J Pharmacol Exp Ther. 1999 Mar;288(3):945-50 [10027830] J Hepatol. 2005 Jan;42(1):110-6 [15629515] J Clin Invest. 2005 Apr;115(4):860-9 [15761498] Hepatology. 2005 Dec;42(6):1364-72 [16317692] Annu Rev Pharmacol Toxicol. 2006;46:123-49 [16402901] Toxicol Appl Pharmacol. 2006 Oct 1;216(1):1-10 [16712892] J Immunol. 2007 Mar 15;178(6):3777-85 [17339476] Hepatology. 2007 Feb;45(2):412-21 [17366662] Am J Physiol Gastrointest Liver Physiol. 2007 Apr;292(4):G1019-28 [17204547] Gut. 2007 Jul;56(7):982-90 [17185352] Immunity. 2007 Oct;27(4):647-59 [17919941] Cytokine. 2008 Mar;41(3):209-16 [18191408] Hepatology. 2008 Oct;48(4):1336-41 [18821593] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4049/jimmunol.1400588 ER - TY - JOUR T1 - Self-renewal and cell lineage differentiation strategies in human embryonic stem cells and induced pluripotent stem cells. AN - 1552374219; 24881868 AB - Since the initial discoveries of human embryonic and induced pluripotent stem cells, many strategies have been developed to utilize the potential of these cells for translational research and disease modeling. The success of these aims and the development of future applications in this area will depend on the ability to generate high-quality and large numbers of differentiated cell types that genetically, epigenetically, and functionally mimic the cells found in the body. In this review, we highlight the current strategies used to maintain stem cell pluripotency (a measure of stem cell quality), as well as provide an overview of the various differentiation strategies being used to generate cells from all three germ lineages. We also discuss the particular considerations that must be addressed when utilizing these cells for translational therapy, and provide an example of a cell type currently used in clinical trials. The major challenge in regenerative medicine and disease modeling will be in generating functional cells of sufficient quality that are physiologically and epigenetically similar to the diverse cells that they are modeled after. By meeting these criteria, these differentiated products can be successfully used in disease modeling, drug/toxicology screens, and cellular replacement therapy. JF - Expert opinion on biological therapy AU - Efthymiou, Anastasia G AU - Chen, Guibin AU - Rao, Mahendra AU - Chen, Guokai AU - Boehm, Manfred AD - National Institutes of Health, Center for Regenerative Medicine , Bethesda, MD , USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 1333 EP - 1344 VL - 14 IS - 9 KW - Index Medicus KW - hiPSC KW - hESC KW - stem cells KW - differentiation KW - self-renewal KW - Animals KW - Humans KW - Cell Culture Techniques KW - Stem Cells -- physiology KW - Regenerative Medicine -- methods KW - Cell- and Tissue-Based Therapy -- methods KW - Cell Lineage -- physiology KW - Embryonic Stem Cells -- cytology KW - Cell Differentiation -- physiology KW - Induced Pluripotent Stem Cells -- physiology KW - Embryonic Stem Cells -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552374219?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+biological+therapy&rft.atitle=Self-renewal+and+cell+lineage+differentiation+strategies+in+human+embryonic+stem+cells+and+induced+pluripotent+stem+cells.&rft.au=Efthymiou%2C+Anastasia+G%3BChen%2C+Guibin%3BRao%2C+Mahendra%3BChen%2C+Guokai%3BBoehm%2C+Manfred&rft.aulast=Efthymiou&rft.aufirst=Anastasia&rft.date=2014-09-01&rft.volume=14&rft.issue=9&rft.spage=1333&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+biological+therapy&rft.issn=1744-7682&rft_id=info:doi/10.1517%2F14712598.2014.922533 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-30 N1 - Date created - 2014-08-08 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1517/14712598.2014.922533 ER - TY - JOUR T1 - Prolonged low intensity EPOCH-rituximab has improved toxicity in Burkitt lymphoma compared with standard short, high intensity therapy. AN - 1552373078; 24919059 AB - Burkitt lymphoma is an aggressive form of non-Hodgkin lymphoma that has a short doubling time, thus intense short-cycle chemotherapy has been thought to be essential. A recent NCI-sponsored clinical trial investigated DA-EPOCH-R given to 19 HIV-negative patients and a short course regimen (SC-EPOCH-RR) given to 11 HIV-positive patients in hopes of maintaining the efficacy of the regimen while decreasing the typical side effects from the intensive short-cycle chemotherapy. Low intensity EPOCH-R based therapy achieved excellent rates of efficacy despite a significant difference in the median cumulative dose between the DA-EPOCH-R and SC-EPOCH-RR cohorts. Furthermore, both cohorts experienced mainly grade 1 and grade 2 toxicities, with SC-EPOCH-RR cohort patients experiencing less adverse events than DA-EPOCH-R cohort patients. This recent clinical investigation suggests the most important therapeutic principle is not the intensity but rather the length of exposure time above an effective threshold concentration. Since short, intense bolus doses are the standard therapy for Burkitt lymphoma, these findings are clinically relevant and significant. JF - Cancer biology & therapy AU - Shahbazi, Shandiz AU - Peer, Cody J AU - Figg, William D AD - Clinical Pharmacology Program; Medical Oncology Branch; National Cancer Institute; Bethesda, MD USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 1117 EP - 1119 VL - 15 IS - 9 KW - Index Medicus KW - EPOCH regimen KW - low-intensity therapy KW - Burkitt lymphoma KW - Humans KW - Male KW - Female KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Burkitt Lymphoma -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552373078?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology+%26+therapy&rft.atitle=Prolonged+low+intensity+EPOCH-rituximab+has+improved+toxicity+in+Burkitt+lymphoma+compared+with+standard+short%2C+high+intensity+therapy.&rft.au=Shahbazi%2C+Shandiz%3BPeer%2C+Cody+J%3BFigg%2C+William+D&rft.aulast=Shahbazi&rft.aufirst=Shandiz&rft.date=2014-09-01&rft.volume=15&rft.issue=9&rft.spage=1117&rft.isbn=&rft.btitle=&rft.title=Cancer+biology+%26+therapy&rft.issn=1555-8576&rft_id=info:doi/10.4161%2Fcbt.29504 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-13 N1 - Date created - 2014-08-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncologist. 2006 Apr;11(4):375-83 [16614233] Curr Opin Oncol. 2004 Sep;16(5):429-35 [15314510] J Clin Oncol. 1996 Mar;14(3):925-34 [8622041] N Engl J Med. 2013 Nov 14;369(20):1915-25 [24224624] J Clin Oncol. 2008 Jun 1;26(16):2717-24 [18378569] Cancer. 2013 May 1;119(9):1660-8 [23361927] Comment On: N Engl J Med. 2013 Nov 14;369(20):1915-25 [24224624] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4161/cbt.29504 ER - TY - JOUR T1 - Hepatotoxicity in a 52-week randomized trial of short-term versus long-term treatment with buprenorphine/naloxone in HIV-negative injection opioid users in China and Thailand. AN - 1552371581; 24999060 AB - Buprenorphine/naloxone (BUP/NX), an effective treatment for opioid dependence, has been implicated in hepatic toxicity. However, as persons taking BUP/NX have multiple hepatic risk factors, comparative data are needed to quantify the risk of hepatoxicity with BUP/NX. We compared rates of alanine aminotransferase (ALT) elevation≥grade 3 (ALT≥5.1 times the upper limit of normal) and graded bilirubin elevations in HIV-negative opioid injectors randomized to long-term (52 weeks) or short-term (18 days) medication assisted treatment (LT-MAT and ST-MAT, respectively) with BUP/NX in a multisite trial conducted in China and Thailand. ALT and bilirubin were measured at baseline, 12, 26, 40 and 52 weeks, times temporally remote from BUP/NX exposure in the ST-MAT participants. Among1036 subjects with at least one laboratory follow-up measurement, 76 (7%) participants experienced ALT elevation≥grade 3. In an intent-to-treat analysis, the risk of ALT events was similar in participants randomized to LT-MAT compared with ST-MAT (adjusted hazard ratio 1.25, 95% confidence interval 0.79 to 1.98). This finding was supported by an as-treated analysis, in which actual exposure to BUP/NX was considered. Hepatitis C seroconversion during follow-up was strongly associated with ALT events. Bilirubin elevations≥grade 2 occurred in 2% of subjects, with no significant difference between arms. Over 52-week follow-up, the risk of hepatotoxicity was similar in opioid injectors receiving brief and prolonged treatment with BUP/NX. These data suggest that most hepatotoxic events observed during treatment with BUP/NX are due to other factors. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Drug and alcohol dependence AU - Lucas, Gregory M AU - Young, Alicia AU - Donnell, Deborah AU - Richardson, Paul AU - Aramrattana, Apinun AU - Shao, Yiming AU - Ruan, Yuhua AU - Liu, Wei AU - Fu, Liping AU - Ma, Jun AU - Celentano, David D AU - Metzger, David AU - Jackson, J Brooks AU - Burns, David AU - HPTN 058 study group AD - Johns Hopkins University School of Medicine, Department of Medicine, 1830 E. Monument St., Room 435A, Baltimore, MD 21287, United States. Electronic address: glucas@jhmi.edu. ; Fred Hutchinson Cancer Research Center, Vaccine and Infectious Disease Division, 1100 Fairview Ave N, Seattle, WA 98109, United States. ; Johns Hopkins School of Medicine, Department of Pathology, 600North Wolfe St., Baltimore, MD 21287, United States. ; Chiang Mai University, Faculty of Medicine, Department of Family Medicine, 110 Intavaroros Road, Chiang Mai, Thailand. ; State Key Laboratory for Infectious Disease Prevention and Control, National Center for AIDS/STD Control and Prevention, Chinese Center for Disease Control and Prevention, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Beijing, China. ; Guangxi Centers for Disease Control and Prevention, Guangxi Center for HIV/AIDS Prevention and Control, No. 18 Jinzhou Road, Nanning 530028, Guangxi, China. ; Xinjiang Autonomous Region Center for Disease Control and Prevention, Jianquanyi Street no. 380, Urumqi 830002, Xinjiang, China. ; Johns Hopkins Bloomberg School of Public Health, Department of Epidemiology, 615 North Wolfe Street, Suite W6041, Baltimore, MD 21205, United States. ; Department of Psychiatry, University of Pennsylvania, 3535 Market Street, Suite 4000, Philadelphia, PA, 19104, United States. ; National Institute of Allergy and Infectious Diseases, Division of AIDS, Prevention Sciences Branch, 6700 B Rockledge Drive, Room 5121, Bethesda, MD 20892, United States. ; HPTN 058 study group Y1 - 2014/09/01/ PY - 2014 DA - 2014 Sep 01 SP - 139 EP - 145 VL - 142 KW - Analgesics, Opioid KW - 0 KW - Narcotic Antagonists KW - Naloxone KW - 36B82AMQ7N KW - Buprenorphine KW - 40D3SCR4GZ KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Bilirubin KW - RFM9X3LJ49 KW - Index Medicus KW - Injection drug use KW - Hepatitis C virus KW - HIV prevention KW - Buprenorphine/naloxone KW - Safety KW - Alanine aminotransferase KW - Opioid dependence KW - Hepatotoxicity KW - Alanine Transaminase -- blood KW - Thailand KW - Humans KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Bilirubin -- blood KW - Male KW - Female KW - China KW - Chemical and Drug Induced Liver Injury -- blood KW - Buprenorphine -- therapeutic use KW - Chemical and Drug Induced Liver Injury -- diagnosis KW - Opioid-Related Disorders -- drug therapy KW - Narcotic Antagonists -- adverse effects KW - Narcotic Antagonists -- therapeutic use KW - Opiate Substitution Treatment -- adverse effects KW - Naloxone -- therapeutic use KW - Analgesics, Opioid -- therapeutic use KW - Buprenorphine -- adverse effects KW - Analgesics, Opioid -- adverse effects KW - Opioid-Related Disorders -- blood KW - Naloxone -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552371581?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Hepatotoxicity+in+a+52-week+randomized+trial+of+short-term+versus+long-term+treatment+with+buprenorphine%2Fnaloxone+in+HIV-negative+injection+opioid+users+in+China+and+Thailand.&rft.au=Lucas%2C+Gregory+M%3BYoung%2C+Alicia%3BDonnell%2C+Deborah%3BRichardson%2C+Paul%3BAramrattana%2C+Apinun%3BShao%2C+Yiming%3BRuan%2C+Yuhua%3BLiu%2C+Wei%3BFu%2C+Liping%3BMa%2C+Jun%3BCelentano%2C+David+D%3BMetzger%2C+David%3BJackson%2C+J+Brooks%3BBurns%2C+David%3BHPTN+058+study+group&rft.aulast=Lucas&rft.aufirst=Gregory&rft.date=2014-09-01&rft.volume=142&rft.issue=&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=1879-0046&rft_id=info:doi/10.1016%2Fj.drugalcdep.2014.06.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-23 N1 - Date created - 2014-08-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biol Psychiatry. 2000 Jun 15;47(12):1072-9 [10862807] Am J Addict. 2000 Summer;9(3):265-9 [11000922] Drug Alcohol Depend. 2001 Jan 1;61(2):173-81 [11137282] J Hepatol. 2001 Feb;34(2):261-9 [11281555] J Hepatol. 2001 Feb;34(2):346-50 [11281569] Eur J Gastroenterol Hepatol. 2004 Oct;16(10):1033-7 [15371928] Drug Alcohol Depend. 2013 Feb 1;128(1-2):71-6 [22921476] Dig Liver Dis. 2005 Sep;37(9):674-80 [15951255] Cochrane Database Syst Rev. 2008;(2):CD002207 [18425880] Ann Intern Med. 2008 May 6;148(9):662-70 [18458279] Dig Liver Dis. 2009 Jul;41(7):e8-e10 [18294936] J Acquir Immune Defic Syndr. 2011 Mar 1;56 Suppl 1:S62-7 [21317596] Int J Drug Policy. 2012 Mar;23(2):162-5 [21852093] Acta Clin Belg Suppl. 1999;1:29-31 [10216978] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.drugalcdep.2014.06.013 ER - TY - JOUR T1 - Influence of lipoic acid on testicular toxicity induced by bi-n-butyl phthalate in rats. AN - 1551020834; 24912129 AB - Bi-n-butyl phthalate (BNBP) is an environmental pollutant. The aim of this study was to evaluate the protective effect of lipoic acid (LA) against testicular dysfunction associated with the intake of to BNBP- intoxicated rats. Adult male Wistar rats were divided into 4 groups of 6 animals each, and received medication orally for 14 days. Group I rats received 0.5 ml corn oil. Group II rats received LA (20 mg/kg B.W./day). Group III rats received BNBP (250 mg/kg B.W./day). Group IV rats received LA 24h prior to BNBP intake. Testes weight, cauda sperm count and sperm motility were decreased significantly by 18.15%, 13.83% and 13.5%, respectively, after BNBP treatment. Significant increase by 12.1%, 10.20% and 11.51%, respectively, was observed in LA-BNBP rats. Significant increase by 1.53%, 1.5% and 1.8%, for serum follicle stimulating hormone, testosterone and total antioxidant status, respectively, were observed in LA-BNBP rats. Testicular lipid peroxides and lactate dehydrogenase enzyme were significantly decreased by 1.5 and 1.6 folds, respectively, in LA-BNBP rats were decreased after BNBP treatment. Testicular superoxide dismutase, catalase and glutathione reductase enzymes were significantly increased in LA-BNBP rats. LA-BNBP rats, decreased the damage to seminiferous tubules produced by BNBP intake. In conclusion, LA mitigated BNBP-induced testicular toxicity through antioxidant mechanism and by direct free radical scavenging activity. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - El-Beshbishy, Hesham A AU - Mariah, Reham A AU - Al-Azhary, Nevin M AU - Aly, Hamdy A A AU - Ozbak, Hani A AU - Baghdadi, Hussam H AD - Medical Laboratories Technology Department, Faculty of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia; Biochemistry Department, Al-Azhar University, Nasr City, Cairo 11751, Egypt. Electronic address: hesham_elbeshbishy@hotmail.com. ; Biochemistry and Molecular Medicine Department, College of Medicine, Taibah University, Saudi Arabia; Medical Biochemistry Department, Faculty of Medicine, Tanta University, Egypt. ; Biochemistry and Molecular Medicine Department, College of Medicine, Taibah University, Saudi Arabia; Clinical Pathology Department, National Cancer Institute, Cairo University, Egypt. ; Medical Biochemistry Department, Faculty of Medicine, Tanta University, Egypt; Pharmacology &Toxicology Department, King AbdulAziz University, Jeddah, Saudi Arabia. ; Medical Laboratories Technology Department, Faculty of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia. ; Biochemistry and Molecular Medicine Department, College of Medicine, Taibah University, Saudi Arabia. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 26 EP - 32 VL - 71 KW - Dibutyl Phthalate KW - 2286E5R2KE KW - Testosterone KW - 3XMK78S47O KW - Thioctic Acid KW - 73Y7P0K73Y KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Catalase KW - EC 1.11.1.6 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Glutathione Reductase KW - EC 1.8.1.7 KW - Index Medicus KW - Testes KW - Oxidative stress KW - Bi-n-butyl phthalate KW - Antioxidant KW - Lipoic acid KW - Rats KW - Catalase -- metabolism KW - Animals KW - Sperm Count KW - Glutathione Reductase -- metabolism KW - Testosterone -- blood KW - Rats, Wistar KW - Lipid Peroxidation -- drug effects KW - Superoxide Dismutase -- metabolism KW - Sperm Motility -- drug effects KW - Male KW - L-Lactate Dehydrogenase -- metabolism KW - Follicle Stimulating Hormone -- blood KW - Testis -- drug effects KW - Thioctic Acid -- pharmacology KW - Testis -- enzymology KW - Dibutyl Phthalate -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551020834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.atitle=Influence+of+lipoic+acid+on+testicular+toxicity+induced+by+bi-n-butyl+phthalate+in+rats.&rft.au=El-Beshbishy%2C+Hesham+A%3BMariah%2C+Reham+A%3BAl-Azhary%2C+Nevin+M%3BAly%2C+Hamdy+A+A%3BOzbak%2C+Hani+A%3BBaghdadi%2C+Hussam+H&rft.aulast=El-Beshbishy&rft.aufirst=Hesham&rft.date=2014-09-01&rft.volume=71&rft.issue=&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.issn=1873-6351&rft_id=info:doi/10.1016%2Fj.fct.2014.05.024 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-06 N1 - Date created - 2014-08-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.fct.2014.05.024 ER - TY - JOUR T1 - The effects of acute alcohol administration on the human brain: insights from neuroimaging. AN - 1548630089; 23978384 AB - Over the last quarter century, researchers have peered into the living human brain to develop and refine mechanistic accounts of alcohol-induced behavior, as well as neurobiological mechanisms for development and maintenance of addiction. These in vivo neuroimaging studies generally show that acute alcohol administration affects brain structures implicated in motivation and behavior control, and that chronic intoxication is correlated with structural and functional abnormalities in these same structures, where some elements of these decrements normalize with extended sobriety. In this review, we will summarize recent findings about acute human brain responses to alcohol using neuroimaging techniques, and how they might explain behavioral effects of alcohol intoxication. We then briefly address how chronic alcohol intoxication (as inferred from cross-sectional differences between various drinking populations and controls) may yield individual brain differences between drinking subjects that may confound interpretation of acute alcohol administration effects. This article is part of the Special Issue Section entitled 'Neuroimaging in Neuropharmacology'. Published by Elsevier Ltd. JF - Neuropharmacology AU - Bjork, James M AU - Gilman, Jodi M AD - Division of Clinical Neuroscience and Behavioral Research, National Institute on Drug Abuse, National Institutes of Health, 6001 Executive Blvd, Room 3163, Bethesda, MD 20892, USA. Electronic address: jbjork@mail.nih.gov. ; Laboratory of Neuroimaging and Genetics, MGH Division of Psychiatric Neuroscience, Martinos Center for Biomedical Imaging, Massachusetts General Hospital, USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 101 EP - 110 VL - 84 KW - Central Nervous System Depressants KW - 0 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Alcohol KW - Neuroimaging KW - Addiction KW - Positron Emission Tomography KW - fMRI KW - Alcohol-Related Disorders -- physiopathology KW - Alcohol-Related Disorders -- diagnostic imaging KW - Cognition Disorders -- diagnostic imaging KW - Humans KW - Cerebrovascular Circulation -- physiology KW - Cerebrovascular Circulation -- drug effects KW - Cognition Disorders -- chemically induced KW - Cognition Disorders -- physiopathology KW - Radionuclide Imaging KW - Brain -- drug effects KW - Ethanol -- administration & dosage KW - Brain -- physiology KW - Brain -- diagnostic imaging KW - Central Nervous System Depressants -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548630089?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropharmacology&rft.atitle=The+effects+of+acute+alcohol+administration+on+the+human+brain%3A+insights+from+neuroimaging.&rft.au=Bjork%2C+James+M%3BGilman%2C+Jodi+M&rft.aulast=Bjork&rft.aufirst=James&rft.date=2014-09-01&rft.volume=84&rft.issue=&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=1873-7064&rft_id=info:doi/10.1016%2Fj.neuropharm.2013.07.039 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-02 N1 - Date created - 2014-06-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Alcohol Clin Exp Res. 1998 Aug;22(5):998-1040 [9726269] Proc Natl Acad Sci U S A. 2012 Feb 21;109(8):3131-6 [22323591] Hum Brain Mapp. 2012 May;33(5):1003-18 [21391283] Biol Psychiatry. 2012 Jun 1;71(11):1015-21 [21907974] AJNR Am J 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Fall;12(3):107-17 [10593699] Alcohol Clin Exp Res. 2000 May;24(5):611-21 [10832902] Alcohol Clin Exp Res. 2000 Jun;24(6):822-9 [10888070] Psychiatry Res. 2000 Jul 10;99(1):1-13 [10891645] J Stud Alcohol. 2000 Sep;61(5):681-7 [11022807] Am J Psychiatry. 2001 Feb;158(2):188-97 [11156800] Am J Psychiatry. 2001 Feb;158(2):198-204 [11156801] J Stud Alcohol. 1993 May;54(3):369-76 [8487546] Int J Addict. 1994 Jan;29(1):1-13 [8144263] Cognition. 1994 Apr-Jun;50(1-3):7-15 [8039375] J Abnorm Psychol. 1995 Feb;104(1):150-5 [7897038] Alcohol Clin Exp Res. 1995 Oct;19(5):1177-91 [8561288] Arch Neurol. 1996 Apr;53(4):359-63 [8929159] Neuron. 1997 Sep;19(3):591-611 [9331351] J Stud Alcohol. 1998 May;59(3):258-69 [9598706] Am J Psychiatry. 1998 Aug;155(8):1009-15 [9699686] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.neuropharm.2013.07.039 ER - TY - JOUR T1 - Phase II trial of pirfenidone in children and young adults with neurofibromatosis type 1 and progressive plexiform neurofibromas. AN - 1547530917; 24753394 AB - Pirfenidone, an oral anti-inflammatory, antifibrotic agent with activity in idiopathic pulmonary fibrosis, may mediate anti-tumor activity in neurofibromatosis type 1 (NF1) and plexiform neurofibromas (PN) by inhibition of fibroblast proliferation and collagen synthesis. The primary objective of this open label, single arm phase II trial was to evaluate the activity of pirfenidone in children and young adults with inoperable PN. Patients (3-21 years) with NF1-related progressive PN received pirfenidone at the previously determined optimal dose (500 mg/m(2) orally, q8h) on a continuous dosing schedule (one cycle = 28 days). Volumetric MRI analysis was used to assess response. Progression was defined as ≥ 20% PN volume increase compared to baseline. Pirfenidone would be considered active if it doubled the median time to progression (TTP) compared to the TTP on the placebo arm of a phase II trial with the farnesyltransferase inhibitor tipifarnib, which used near identical eligibility criteria. Toxicities, objective response rate, and quality of life (QOL) also were evaluated. Thirty-six patients were enrolled and tolerated pirfenidone well with intermittent nausea and vomiting as the most frequent toxicities. A dose reduction was required in only three patients. The median TTP for pirfenidone was 13.2 months compared to 10.6 months for the placebo control group from the tipifarnib trial (two-tailed P = 0.92; one-tailed P = 0.46). No objective responses were observed. Pirfenidone was well tolerated, but did not demonstrate activity as defined in this trial and does not warrant further evaluation in children with NF1 and progressive PN. © 2014 Wiley Periodicals, Inc. JF - Pediatric blood & cancer AU - Widemann, Brigitte C AU - Babovic-Vuksanovic, Dusica AU - Dombi, Eva AU - Wolters, Pamela L AU - Goldman, Stewart AU - Martin, Staci AU - Goodwin, Anne AU - Goodspeed, Wendy AU - Kieran, Mark W AU - Cohen, Bruce AU - Blaney, Susan M AU - King, Allison AU - Solomon, Jeffrey AU - Patronas, Nicholas AU - Balis, Frank M AU - Fox, Elizabeth AU - Steinberg, Seth M AU - Packer, Roger J AD - Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 1598 EP - 1602 VL - 61 IS - 9 KW - Antineoplastic Agents KW - 0 KW - Pyridones KW - Tumor Necrosis Factor-alpha KW - pirfenidone KW - D7NLD2JX7U KW - Index Medicus KW - phase II trial KW - neurofibromatosis type 1 KW - volumetric MRI analysis KW - time to progression KW - progression free survival KW - plexiform neurofibroma KW - Young Adult KW - Neoplasm Staging KW - Humans KW - Disease Progression KW - Prognosis KW - Quality of Life KW - Child KW - Child, Preschool KW - Survival Rate KW - Adult KW - Follow-Up Studies KW - Adolescent KW - Time Factors KW - Female KW - Male KW - Neurofibromatosis 1 -- drug therapy KW - Neurofibroma, Plexiform -- drug therapy KW - Neurofibroma, Plexiform -- pathology KW - Tumor Necrosis Factor-alpha -- antagonists & inhibitors KW - Neurofibroma, Plexiform -- mortality KW - Neurofibromatosis 1 -- mortality KW - Antineoplastic Agents -- therapeutic use KW - Neurofibromatosis 1 -- pathology KW - Pyridones -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547530917?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatric+blood+%26+cancer&rft.atitle=Phase+II+trial+of+pirfenidone+in+children+and+young+adults+with+neurofibromatosis+type+1+and+progressive+plexiform+neurofibromas.&rft.au=Widemann%2C+Brigitte+C%3BBabovic-Vuksanovic%2C+Dusica%3BDombi%2C+Eva%3BWolters%2C+Pamela+L%3BGoldman%2C+Stewart%3BMartin%2C+Staci%3BGoodwin%2C+Anne%3BGoodspeed%2C+Wendy%3BKieran%2C+Mark+W%3BCohen%2C+Bruce%3BBlaney%2C+Susan+M%3BKing%2C+Allison%3BSolomon%2C+Jeffrey%3BPatronas%2C+Nicholas%3BBalis%2C+Frank+M%3BFox%2C+Elizabeth%3BSteinberg%2C+Seth+M%3BPacker%2C+Roger+J&rft.aulast=Widemann&rft.aufirst=Brigitte&rft.date=2014-09-01&rft.volume=61&rft.issue=9&rft.spage=1598&rft.isbn=&rft.btitle=&rft.title=Pediatric+blood+%26+cancer&rft.issn=1545-5017&rft_id=info:doi/10.1002%2Fpbc.25041 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-18 N1 - Date created - 2014-07-21 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/pbc.25041 ER - TY - JOUR T1 - Prefrontal single-unit firing associated with deficient extinction in mice. AN - 1534792411; 24231425 AB - The neural circuitry mediating fear extinction has been increasingly well studied and delineated. The rodent infralimbic subregion (IL) of the ventromedial prefrontal cortex (vmPFC) has been found to promote extinction, whereas the prelimbic cortex (PL) demonstrates an opposing, pro-fear, function. Studies employing in vivo electrophysiological recordings have observed that while increased IL single-unit firing and bursting predicts robust extinction retrieval, increased PL firing can correlate with sustained fear and poor extinction. These relationships between single-unit firing and extinction do not hold under all experimental conditions, however. In the current study, we further investigated the relationship between vmPFC and PL single-unit firing and extinction using inbred mouse models of intact (C57BL/6J, B6) and deficient (129S1/SvImJ, S1) extinction strains. Simultaneous single-unit recordings were made in the PL and vmPFC (encompassing IL) as B6 and S1 mice performed extinction training and retrieval. Impaired extinction retrieval in S1 mice was associated with elevated PL single-unit firing, as compared to firing in extinguishing B6 mice, consistent with the hypothesized pro-fear contribution of PL. Analysis of local field potentials also revealed significantly higher gamma power in the PL of S1 than B6 mice during extinction training and retrieval. In the vmPFC, impaired extinction in S1 mice was also associated with exaggerated single-unit firing, relative to B6 mice. This is in apparent contradiction to evidence that IL activity promotes extinction, but could reflect a (failed) compensatory effort by the vmPFC to mitigate fear-promoting activity in other regions, such as the PL or amygdala. In support of this hypothesis, augmenting IL activity via direct infusion of the GABAA receptor antagonist picrotoxin rescued impaired extinction retrieval in S1 mice. Chronic fluoxetine treatment produced modest reductions in fear during extinction retrieval and increased the number of Zif268-labeled cells in layer II of IL, but failed to increase vmPFC single-unit firing. Collectively, these findings further support the important contribution these cortical regions play in determining the balance between robust extinction on the one hand, and sustained fear on the other. Elucidating the precise nature of these roles could help inform understanding of the pathophysiology of fear-related anxiety disorders. Published by Elsevier Inc. JF - Neurobiology of learning and memory AU - Fitzgerald, Paul J AU - Whittle, Nigel AU - Flynn, Shaun M AU - Graybeal, Carolyn AU - Pinard, Courtney R AU - Gunduz-Cinar, Ozge AU - Kravitz, Alexxai V AU - Singewald, Nicolas AU - Holmes, Andrew AD - Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA. Electronic address: pfitz@mbi.mb.jhu.edu. ; Department of Pharmacology & Toxicology, Institute of Pharmacy and CMBI, University of Innsbruck, Innsbruck, Austria. ; Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA. ; National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA. Y1 - 2014/09// PY - 2014 DA - September 2014 SP - 69 EP - 81 VL - 113 KW - Early Growth Response Protein 1 KW - 0 KW - Egr1 protein, mouse KW - GABA Antagonists KW - Serotonin Uptake Inhibitors KW - Fluoxetine KW - 01K63SUP8D KW - Picrotoxin KW - 124-87-8 KW - Index Medicus KW - Prelimbic cortex KW - C57BL/6J KW - Retrieval KW - Infralimbic cortex KW - 129S1/SvImJ KW - Fear extinction KW - Patch-Clamp Techniques -- methods KW - Mice, 129 Strain KW - Animals KW - Early Growth Response Protein 1 -- metabolism KW - Mice, Inbred C57BL KW - Mice KW - Male KW - Serotonin Uptake Inhibitors -- administration & dosage KW - Fluoxetine -- pharmacology KW - Prefrontal Cortex -- physiopathology KW - Prefrontal Cortex -- physiology KW - Fear -- drug effects KW - GABA Antagonists -- administration & dosage KW - Extinction, Psychological -- physiology KW - GABA Antagonists -- pharmacology KW - Prefrontal Cortex -- drug effects KW - Fluoxetine -- administration & dosage KW - Picrotoxin -- pharmacology KW - Picrotoxin -- administration & dosage KW - Extinction, Psychological -- drug effects KW - Fear -- physiology KW - Serotonin Uptake Inhibitors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534792411?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+learning+and+memory&rft.atitle=Prefrontal+single-unit+firing+associated+with+deficient+extinction+in+mice.&rft.au=Fitzgerald%2C+Paul+J%3BWhittle%2C+Nigel%3BFlynn%2C+Shaun+M%3BGraybeal%2C+Carolyn%3BPinard%2C+Courtney+R%3BGunduz-Cinar%2C+Ozge%3BKravitz%2C+Alexxai+V%3BSingewald%2C+Nicolas%3BHolmes%2C+Andrew&rft.aulast=Fitzgerald&rft.aufirst=Paul&rft.date=2014-09-01&rft.volume=113&rft.issue=&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+learning+and+memory&rft.issn=1095-9564&rft_id=info:doi/10.1016%2Fj.nlm.2013.11.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-09 N1 - Date created - 2014-06-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cereb Cortex. 2001 May;11(5):441-51 [11313296] Proc Natl Acad Sci U S A. 2013 Sep 3;110(36):14783-8 [23959891] Eur J Pharmacol. 2003 Jan 17;459(2-3):221-30 [12524150] Neuron. 2003 Nov 13;40(4):695-701 [14622575] J Neurosci. 2006 May 24;26(21):5733-8 [16723530] Eur J Neurosci. 2006 Jul;24(1):261-9 [16882022] Learn Mem. 2006 Nov-Dec;13(6):728-33 [17142302] Neuron. 2007 Mar 15;53(6):871-80 [17359921] Psychopharmacology (Berl). 2008 Jan;195(4):547-57 [17891380] J Neurosci. 2008 Aug 6;28(32):8074-85 [18685032] Psychopharmacology (Berl). 2008 Oct;200(3):413-24 [18594797] Amino Acids. 2009 Jan;36(1):147-58 [18975044] Science. 2009 Mar 13;323(5920):1492-6 [19286560] Nat Rev Neurosci. 2009 Jun;10(6):423-33 [19469026] J Neurosci. 2009 Jul 1;29(26):8474-82 [19571138] Nat Neurosci. 2009 Jun;12(6):801-7 [19430471] Genes Brain Behav. 2009 Nov;8(8):744-52 [19674120] J Neurosci. 2010 Jan 20;30(3):832-7 [20089891] Trends Pharmacol Sci. 2010 Jan;31(1):2-7 [20036429] Eur J Neurosci. 2010 Feb;31(4):599-612 [20384807] Physiol Rev. 2010 Apr;90(2):419-63 [20393190] Brain Struct Funct. 2010 May;214(4):339-53 [20221886] Cereb Cortex. 2010 Aug;20(8):1955-63 [20032063] PLoS One. 2010;5(8):e11971 [20700483] J Neurosci. 2010 Oct 13;30(41):13586-96 [20943900] Learn Mem. 2010 Nov;17(11):591-9 [21041382] Neuropsychopharmacology. 2011 Jan;36(2):529-38 [20962768] Neuroscience. 2011 Feb 3;174:115-31 [21044660] Epilepsia. 2011 Feb;52(2):337-46 [21054349] Learn Mem. 2011;18(4):221-5 [21430044] Psychopharmacology (Berl). 2011 May;215(2):231-7 [21181120] PLoS Comput Biol. 2011 May;7(5):e1002057 [21625577] PLoS One. 2011;6(6):e21714 [21738775] PLoS One. 2011;6(7):e22600 [21818344] Neuropharmacology. 2012 Jan;62(1):464-73 [21906605] Annu Rev Psychol. 2012;63:129-51 [22129456] Science. 2011 Dec 23;334(6063):1731-4 [22194582] Science. 2012 Mar 23;335(6075):1513-6 [22442487] Neuropsychopharmacology. 2012 May;37(6):1534-47 [22334122] Nature. 2012 Apr 19;484(7394):381-5 [22441246] Annu Rev Neurosci. 2012;35:203-25 [22443509] Genes Brain Behav. 2012 Jul;11(5):503-12 [22530815] Neurosci Biobehav Rev. 2012 Aug;36(7):1773-802 [22230704] Neuropharmacology. 2013 Jan;64:414-23 [22722028] Nat Neurosci. 2012 Oct;15(10):1359-61 [22941108] Proc Natl Acad Sci U S A. 2012 Oct 16;109(42):17093-8 [23027931] Neuron. 2012 Nov 21;76(4):804-12 [23177964] Trends Neurosci. 2013 Jan;36(1):23-31 [23260015] Psychopharmacology (Berl). 2013 Jan;225(1):209-16 [22825580] Learn Mem. 2013 Mar;20(3):156-63 [23422280] J Neurosci. 2013 Apr 24;33(17):7184-93 [23616528] Neuroscience. 2013 Jun 14;240:219-42 [23500092] Mol Psychiatry. 2013 Jul;18(7):813-23 [22688188] Nat Neurosci. 2013 Aug;16(8):1101-10 [23831965] Nature. 2002 Nov 7;420(6911):70-4 [12422216] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.nlm.2013.11.002 ER - TY - JOUR T1 - Multiwalled carbon nanotubes induce altered morphology and loss of barrier function in human bronchial epithelium at noncytotoxic doses AN - 1566848829; 20693554 AB - Multiwalled carbon nanotubes (MWCNTs) have seen increasing application in consumer products over the past decade, resulting in an increasing risk of human exposure. While numerous toxicological studies have been performed using acute high doses of various carbonaceous nanomaterials, the effects of longer-term, low doses of MWCNTs remain relatively unexplored. This study examined bronchoscopy-derived healthy human bronchial epithelial cells exposed in submerged culture to noncytotoxic doses of MWCNTs over 7 days. Under these conditions, doses as low as 3 mu g/mL caused altered cell morphology, superficially resembling fibroblasts. Electrical impedance of the epithelial monolayer was greatly reduced following MWCNT exposure. However, Western blot and polymerase chain reaction showed no elevated expression of the fibroblast markers, vimentin, alpha -smooth muscle actin, or fibronectin, indicating that a mechanism other than epithelial-mesenchymal transition may be responsible for the changes. Phalloidin and tubulin immunostaining showed disruption of the cytoskeleton, and confocal imaging showed a reduction of the tight junction proteins, zona occludens 1 and occludin. We propose that MWCNTs interfere with the cytoskeleton of the lung epithelium, which can result in a harmful reduction in barrier function over time, even at noncytotoxic doses. JF - International Journal of Nanomedicine AU - Snyder, Ryan J AU - Hussain, Salik AU - Rice, Annette B AU - Garantziotis, Stavros AD - Clinical Research Unit, National Institute of Environmental Health Sciences/National Institutes of Health, Research Triangle Park, NC, USA Y1 - 2014/08/25/ PY - 2014 DA - 2014 Aug 25 SP - 4093 EP - 4105 PB - Dove Medical Press Ltd, Beechfield House Macclesfield SK11 0JL United Kingdom VL - 9 SN - 1176-9114, 1176-9114 KW - Biotechnology and Bioengineering Abstracts KW - multiwalled carbon nanotubes KW - bronchial epithelium KW - transepithelial electrical resistance KW - cytoskeleton KW - morphology KW - human KW - Western blotting KW - Epithelial cells KW - Tight junctions KW - Fibronectin KW - Muscles KW - Cell culture KW - Electrical impedance KW - Vimentin KW - Fibroblasts KW - Cytoskeleton KW - Carbon KW - Lung KW - nanotubes KW - Polymerase chain reaction KW - Actin KW - Epithelium KW - Tubulin KW - Toxicity testing KW - nanotechnology KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566848829?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Nanomedicine&rft.atitle=Multiwalled+carbon+nanotubes+induce+altered+morphology+and+loss+of+barrier+function+in+human+bronchial+epithelium+at+noncytotoxic+doses&rft.au=Snyder%2C+Ryan+J%3BHussain%2C+Salik%3BRice%2C+Annette+B%3BGarantziotis%2C+Stavros&rft.aulast=Snyder&rft.aufirst=Ryan&rft.date=2014-08-25&rft.volume=9&rft.issue=&rft.spage=4093&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Nanomedicine&rft.issn=11769114&rft_id=info:doi/10.2147%2FIJN.S65567 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Epithelial cells; Western blotting; Tight junctions; Fibronectin; Muscles; Cell culture; Electrical impedance; Vimentin; Fibroblasts; Cytoskeleton; Carbon; Lung; Polymerase chain reaction; nanotubes; Epithelium; Actin; Tubulin; Toxicity testing; nanotechnology DO - http://dx.doi.org/10.2147/IJN.S65567 ER - TY - JOUR T1 - Autophagic degradation of the inhibitory p53 isoform Δ133p53α as a regulatory mechanism for p53-mediated senescence. AN - 1555620142; 25144556 AB - Δ133p53α, a p53 isoform that can inhibit full-length p53, is downregulated at replicative senescence in a manner independent of mRNA regulation and proteasome-mediated degradation. Here we demonstrate that, unlike full-length p53, Δ133p53α is degraded by autophagy during replicative senescence. Pharmacological inhibition of autophagy restores Δ133p53α expression levels in replicatively senescent fibroblasts, without affecting full-length p53. The siRNA-mediated knockdown of pro-autophagic proteins (ATG5, ATG7 and Beclin-1) also restores Δ133p53α expression. The chaperone-associated E3 ubiquitin ligase STUB1, which is known to regulate autophagy, interacts with Δ133p53α and is downregulated at replicative senescence. The siRNA knockdown of STUB1 in proliferating, early-passage fibroblasts induces the autophagic degradation of Δ133p53α and thereby induces senescence. Upon replicative senescence or STUB1 knockdown, Δ133p53α is recruited to autophagosomes, consistent with its autophagic degradation. This study reveals that STUB1 is an endogenous regulator of Δ133p53α degradation and senescence, and identifies a p53 isoform-specific protein turnover mechanism that orchestrates p53-mediated senescence. JF - Nature communications AU - Horikawa, Izumi AU - Fujita, Kaori AU - Jenkins, Lisa M Miller AU - Hiyoshi, Yukiharu AU - Mondal, Abdul M AU - Vojtesek, Borivoj AU - Lane, David P AU - Appella, Ettore AU - Harris, Curtis C AD - 1] Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892-4258, USA [2]. ; 1] Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892-4258, USA [2] [3]. ; Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892-4258, USA. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, Maryland 20892-4258, USA. ; Regional Centre for Applied and Molecular Oncology, Masaryk Memorial Cancer Institute, Zluty Kopec 7, Brno 65653, Czech Republic. ; Institute of Molecular and Cell Biology, 61 Biopolis Drive, Proteos, Singapore 138673, Singapore. Y1 - 2014/08/21/ PY - 2014 DA - 2014 Aug 21 SP - 4706 VL - 5 KW - Adaptor Proteins, Signal Transducing KW - 0 KW - Androstadienes KW - Apoptosis Regulatory Proteins KW - BECN1 protein, human KW - Beclin-1 KW - MAP1LC3B protein, human KW - Membrane Proteins KW - Microtubule-Associated Proteins KW - Protein Isoforms KW - RNA, Small Interfering KW - SQSTM1 protein, human KW - Sequestosome-1 Protein KW - TP53 protein, human KW - Tumor Suppressor Protein p53 KW - Cycloheximide KW - 98600C0908 KW - STUB1 protein, human KW - EC 2.3.2.27 KW - Ubiquitin-Protein Ligases KW - wortmannin KW - XVA4O219QW KW - Index Medicus KW - Fibroblasts -- drug effects KW - Microtubule-Associated Proteins -- metabolism KW - Apoptosis Regulatory Proteins -- genetics KW - Protein Isoforms -- metabolism KW - Membrane Proteins -- metabolism KW - Humans KW - Androstadienes -- pharmacology KW - Membrane Proteins -- genetics KW - Fibroblasts -- metabolism KW - Adaptor Proteins, Signal Transducing -- metabolism KW - Microtubule-Associated Proteins -- genetics KW - Gene Knockdown Techniques KW - Cells, Cultured KW - Cycloheximide -- pharmacology KW - Ubiquitin-Protein Ligases -- genetics KW - Apoptosis Regulatory Proteins -- metabolism KW - Adaptor Proteins, Signal Transducing -- genetics KW - Ubiquitin-Protein Ligases -- metabolism KW - Autophagy -- drug effects KW - Cell Aging -- physiology KW - Tumor Suppressor Protein p53 -- genetics KW - Tumor Suppressor Protein p53 -- metabolism KW - Autophagy -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1555620142?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=Autophagic+degradation+of+the+inhibitory+p53+isoform+%CE%94133p53%CE%B1+as+a+regulatory+mechanism+for+p53-mediated+senescence.&rft.au=Horikawa%2C+Izumi%3BFujita%2C+Kaori%3BJenkins%2C+Lisa+M+Miller%3BHiyoshi%2C+Yukiharu%3BMondal%2C+Abdul+M%3BVojtesek%2C+Borivoj%3BLane%2C+David+P%3BAppella%2C+Ettore%3BHarris%2C+Curtis+C&rft.aulast=Horikawa&rft.aufirst=Izumi&rft.date=2014-08-21&rft.volume=5&rft.issue=&rft.spage=4706&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms5706 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-02 N1 - Date created - 2014-08-22 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncomms5706 ER - TY - JOUR T1 - Genistein Disrupts Glucocorticoid Receptor Signaling in Human Uterine Endometrial Ishikawa Cells AN - 1654686363; PQ0001052570 AB - Background: The link between environmental estrogen exposure and defects in the female reproductive tract is well established. The phytoestrogen genistein is able to modulate uterine estrogen receptor (ER) activity, and dietary exposure is associated with uterine pathologies. Regulation of stress and immune functions by the glucocorticoid receptor (GR) is also an integral part of maintaining reproductive tract function; disruption of GR signaling by genistein may also have a role in the adverse effects of genistein. Objective: We evaluated the transcriptional response to genistein in Ishikawa cells and investigated the effects of genistein on GR-mediated target genes. Methods: We used Ishikawa cells as a model system to identify novel targets of genistein and the synthetic glucocorticoid dexamethasone through whole genome microarray analysis. Common gene targets were defined and response patterns verified by quantitative real-time reverse-transcription polymerase chain reaction. The mechanism of transcriptional antagonism was determined for select genes. Results: Genistein regulated numerous genes in Ishikawa cells independently of estradiol, and the response to coadministration of genistein and dexamethasone was unique compared with the response to either estradiol or dexamethasone alone. Furthermore, genistein altered glucocorticoid regulation of GR target genes. In a select set of genes, co-regulation by dexamethasone and genistein was found to require both GR and ER alpha signaling, respectively. Conclusions: Using Ishikawa cells, we observed that exposure to genistein resulted in distinct changes in gene expression and unique differences in the GR transcriptome. Citation: Whirledge S, Senbanjo LT, Cidlowski JA. 2015. Genistein disrupts glucocorticoid receptor signaling in human uterine endometrial Ishikawa cells. Environ Health Perspect 123:80-87; http://dx.doi.org/10.1289/ehp.1408437 JF - Environmental Health Perspectives AU - Whirledge, Shannon AU - Senbanjo, Linda T AU - Cidlowski, John A AD - Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA Y1 - 2014/08/19/ PY - 2014 DA - 2014 Aug 19 SP - 80 EP - 87 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 123 IS - 1 SN - 0091-6765, 0091-6765 KW - Environment Abstracts; Health & Safety Science Abstracts KW - Diets KW - Estrogens KW - Pathology KW - Stress KW - Immune response KW - Antagonism KW - Side effects KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654686363?accountid=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=Genistein+Disrupts+Glucocorticoid+Receptor+Signaling+in+Human+Uterine+Endometrial+Ishikawa+Cells&rft.au=Whirledge%2C+Shannon%3BSenbanjo%2C+Linda+T%3BCidlowski%2C+John+A&rft.aulast=Whirledge&rft.aufirst=Shannon&rft.date=2014-08-19&rft.volume=123&rft.issue=1&rft.spage=80&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1408437 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Diets; Estrogens; Pathology; Stress; Antagonism; Immune response; Side effects DO - http://dx.doi.org/10.1289/ehp.1408437 ER - TY - JOUR T1 - Toward a Drug Development Path That Targets Metastatic Progression in Osteosarcoma AN - 1808673722; PQ0003441841 AB - Despite successful primary tumor treatment, the development of pulmonary metastasis continues to be the most common cause of mortality in patients with osteosarcoma. A conventional drug development path requiring drugs to induce regression of established lesions has not led to improvements for patients with osteosarcoma in more than 30 years. On the basis of our growing understanding of metastasis biology, it is now reasonable and essential that we focus on developing therapeutics that target metastatic progression. To advance this agenda, a meeting of key opinion leaders and experts in the metastasis and osteosarcoma communities was convened in Bethesda, Maryland. The goal of this meeting was to provide a "Perspective" that would establish a preclinical translational path that could support the early evaluation of potential therapeutic agents that uniquely target the metastatic phenotype. Although focused on osteosarcoma, the need for this perspective is shared among many cancer types. The consensus achieved from the meeting included the following: the biology of metastatic progression is associated with metastasis-specific targets/processes that may not influence grossly detectable lesions; targeting of metastasis-specific processes is feasible; rigorous preclinical data are needed to support translation of metastasis-specific agents into human trials where regression of measurable disease is not an expected outcome; preclinical data should include an understanding of mechanism of action, validation of pharmacodynamic markers of effective exposure and response, the use of several murine models of effectiveness, and where feasible the inclusion of the dog with naturally occurring osteosarcoma to define the activity of new drugs in the micrometastatic disease setting. Clin Cancer Res; 20(16); 4200-9. copyright 2014 AACR. JF - Clinical Cancer Research AU - Khanna, Chand AU - Fan, Timothy M AU - Gorlick, Richard AU - Helman, Lee J AU - Kleinerman, Eugenie S AU - Adamson, Peter C AU - Houghton, Peter J AU - Tap, William D AU - Welch, Danny R AU - Steeg, Patricia S AU - Merlino, Glenn AU - Sorensen, Poul HB AU - Meltzer, Paul AU - Kirsch, David G AU - Janeway, Katherine A AU - Weigel, Brenda AU - Randall, Lor AU - Withrow, Stephen J AU - Paoloni, Melissa AU - Kaplan, Rosandra AU - Teicher, Beverly A AU - Seibel, Nita L AU - Smith, Malcolm AU - Ueren, Aykut AU - Patel, Shreyaskumar R AU - Trent, Jeffrey AU - Savage, Sharon A AU - Mirabello, Lisa AU - Reinke, Denise AU - Barkaukas, Donald A AU - Krailo, Mark AU - Bernstein, Mark AD - National Cancer Institute, NIH, Bethesda, Maryland; , t-fan@illinois.edu Y1 - 2014/08/15/ PY - 2014 DA - 2014 Aug 15 SP - 4200 EP - 4209 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 20 IS - 16 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Translation KW - Mortality KW - Data processing KW - Animal models KW - Osteosarcoma KW - Drug development KW - Tumors KW - Clinical trials KW - Cancer KW - Metastases KW - Lung KW - Pharmacodynamics KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808673722?accountid=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=Toward+a+Drug+Development+Path+That+Targets+Metastatic+Progression+in+Osteosarcoma&rft.au=Khanna%2C+Chand%3BFan%2C+Timothy+M%3BGorlick%2C+Richard%3BHelman%2C+Lee+J%3BKleinerman%2C+Eugenie+S%3BAdamson%2C+Peter+C%3BHoughton%2C+Peter+J%3BTap%2C+William+D%3BWelch%2C+Danny+R%3BSteeg%2C+Patricia+S%3BMerlino%2C+Glenn%3BSorensen%2C+Poul+HB%3BMeltzer%2C+Paul%3BKirsch%2C+David+G%3BJaneway%2C+Katherine+A%3BWeigel%2C+Brenda%3BRandall%2C+Lor%3BWithrow%2C+Stephen+J%3BPaoloni%2C+Melissa%3BKaplan%2C+Rosandra%3BTeicher%2C+Beverly+A%3BSeibel%2C+Nita+L%3BSmith%2C+Malcolm%3BUeren%2C+Aykut%3BPatel%2C+Shreyaskumar+R%3BTrent%2C+Jeffrey%3BSavage%2C+Sharon+A%3BMirabello%2C+Lisa%3BReinke%2C+Denise%3BBarkaukas%2C+Donald+A%3BKrailo%2C+Mark%3BBernstein%2C+Mark&rft.aulast=Khanna&rft.aufirst=Chand&rft.date=2014-08-15&rft.volume=20&rft.issue=16&rft.spage=4200&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-13-2574 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Metastases; Mortality; Translation; Data processing; Lung; Animal models; Osteosarcoma; Drug development; Tumors; Clinical trials; Pharmacodynamics; Cancer DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-2574 ER - TY - JOUR T1 - Aerosol Vaccination with AERAS-402 Elicits Robust Cellular Immune Responses in the Lungs of Rhesus Macaques but Fails To Protect against High-Dose Mycobacterium tuberculosis Challenge AN - 1808631190; PQ0003441117 AB - Development of a vaccine against pulmonary tuberculosis may require immunization strategies that induce a high frequency of Ag-specific CD4 and CD8 T cells in the lung. The nonhuman primate model is essential for testing such approaches because it has predictive value for how vaccines elicit responses in humans. In this study, we used an aerosol vaccination strategy to administer AERAS-402, a replication-defective recombinant adenovirus (rAd) type 35 expressing Mycobacterium tuberculosis Ags Ag85A, Ag85B, and TB10.4, in bacillus Calmette-Guerin (BCG)-primed or unprimed rhesus macaques. Immunization with BCG generated low purified protein derivative-specific CD4 T cell responses in blood and bronchoalveolar lavage. In contrast, aerosolized AERAS-402 alone or following BCG induced potent and stable Ag85A/b-specific CD4 and CD8 effector T cells in bronchoalveolar lavage that largely produced IFN- gamma , as well as TNF and IL-2. Such responses induced by BCG, AERAS-402, or both failed to confer overall protection following challenge with 275 CFUs M. tuberculosis Erdman, although vaccine-induced responses associated with reduced pathology were observed in some animals. Anamnestic T cell responses to Ag85A/b were not detected in blood of immunized animals after challenge. Overall, our data suggest that a high M. tuberculosis challenge dose may be a critical factor in limiting vaccine efficacy in this model. However, the ability of aerosol rAd immunization to generate potent cellular immunity in the lung suggests that using different or more immunogens, alternative rAd serotypes with enhanced immunogenicity, and a physiological challenge dose may achieve protection against M. tuberculosis. JF - Journal of Immunology AU - Darrah, Patricia A AU - Bolton, Diane L AU - Lackner, Andrew A AU - Kaushal, Deepak AU - Aye, Pyone Pyone AU - Mehra, Smriti AU - Blanchard, James L AU - Didier, Peter J AU - Roy, Chad J AU - Rao, Srinivas S AU - Hokey, David A AU - Scanga, Charles A AU - Sizemore, Donata R AU - Sadoff, Jerald C AU - Roederer, Mario AU - Seder, Robert A AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 Y1 - 2014/08/15/ PY - 2014 DA - 2014 Aug 15 SP - 1799 EP - 1811 PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States VL - 193 IS - 4 SN - 0022-1767, 0022-1767 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - gamma -Interferon KW - Serotypes KW - Interleukin 2 KW - Tumor necrosis factor KW - CD4 antigen KW - Bronchus KW - Lymphocytes T KW - Macaca mulatta KW - Tuberculosis KW - Aerosols KW - Data processing KW - Adenovirus KW - CD8 antigen KW - Alveoli KW - Effector cells KW - Blood KW - Immunity (cell-mediated) KW - BCG KW - Lung KW - Immunogenicity KW - Colony-forming cells KW - Vaccines KW - Immune response KW - Mycobacterium tuberculosis KW - F 06905:Vaccines KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808631190?accountid=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=Aerosol+Vaccination+with+AERAS-402+Elicits+Robust+Cellular+Immune+Responses+in+the+Lungs+of+Rhesus+Macaques+but+Fails+To+Protect+against+High-Dose+Mycobacterium+tuberculosis+Challenge&rft.au=Darrah%2C+Patricia+A%3BBolton%2C+Diane+L%3BLackner%2C+Andrew+A%3BKaushal%2C+Deepak%3BAye%2C+Pyone+Pyone%3BMehra%2C+Smriti%3BBlanchard%2C+James+L%3BDidier%2C+Peter+J%3BRoy%2C+Chad+J%3BRao%2C+Srinivas+S%3BHokey%2C+David+A%3BScanga%2C+Charles+A%3BSizemore%2C+Donata+R%3BSadoff%2C+Jerald+C%3BRoederer%2C+Mario%3BSeder%2C+Robert+A&rft.aulast=Darrah&rft.aufirst=Patricia&rft.date=2014-08-15&rft.volume=193&rft.issue=4&rft.spage=1799&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1400676 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - gamma -Interferon; Aerosols; Data processing; Serotypes; Interleukin 2; Tumor necrosis factor; CD8 antigen; Alveoli; Effector cells; Blood; CD4 antigen; Bronchus; Immunity (cell-mediated); Immunogenicity; Lung; BCG; Colony-forming cells; Lymphocytes T; Tuberculosis; Immune response; Vaccines; Adenovirus; Macaca mulatta; Mycobacterium tuberculosis DO - http://dx.doi.org/10.4049/jimmunol.1400676 ER - TY - JOUR T1 - Perfluorochemicals and Human Semen Quality: The LIFE Study AN - 1654688775; PQ0001052566 AB - Background: The relation between persistent environmental chemicals and semen quality is evolving, although limited data exist for men recruited from general populations. Objectives: We examined the relation between perfluorinated chemicals (PFCs) and semen quality among 501 male partners of couples planning pregnancy. Methods: Using population-based sampling strategies, we recruited 501 couples discontinuing contraception from two U.S. geographic regions from 2005 through 2009. Baseline interviews and anthropometric assessments were conducted, followed by blood collection for the quantification of seven serum PFCs (perfluorosulfonates, perfluorocarboxylates, and perfluorosulfonamides) using tandem mass spectrometry. Men collected a baseline semen sample and another approximately 1 month later. Semen samples were shipped with freezer packs, and analyses were performed on the day after collection. We used linear regression to estimate the difference in each semen parameter associated with a one unit increase in the natural log-transformed PFC concentration after adjusting for confounders and modeling repeated semen samples. Sensitivity analyses included optimal Box-Cox transformation of semen quality end points. Results: Six PFCs [2-(N-methyl-perfluorooctane sulfonamido) acetate (Me-PFOSA-AcOH), perfluorodecanoate (PFDeA), perfluorononanoate (PFNA), perfluorooctane sulfonamide (PFOSA), perfluorooctane sulfonate (PFOS), and perfluorooctanoic acid (PFOA)] were associated with 17 semen quality end points before Box-Cox transformation. PFOSA was associated with smaller sperm head area and perimeter, a lower percentage of DNA stainability, and a higher percentage of bicephalic and immature sperm. PFDeA, PFNA, PFOA, and PFOS were associated with a lower percentage of sperm with coiled tails. Conclusions: Select PFCs were associated with certain semen end points, with the most significant associations observed for PFOSA but with results in varying directions. Citation: Buck Louis GM, Chen Z, Schisterman EF, Kim S, Sweeney AM, Sundaram R, Lynch CD, Gore-Langton RE, Barr DB. 2015. Perfluorochemicals and human semen quality: the LIFE Study. Environ Health Perspect 123:57-63; http://dx.doi.org/10.1289/ehp.1307621 JF - Environmental Health Perspectives AU - Louis, Germaine MBuck AU - Chen, Zhen AU - Schisterman, Enrique F AU - Kim, Sungduk AU - Sweeney, Anne M AU - Sundaram, Rajeshwari AU - Lynch, Courtney D AU - Gore-Langton, Robert E AU - Barr, Dana Boyd AD - Division of Intramural Population Health 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 - 2014/08/15/ PY - 2014 DA - 2014 Aug 15 SP - 57 EP - 63 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 123 IS - 1 SN - 0091-6765, 0091-6765 KW - Environment Abstracts; Health & Safety Science Abstracts KW - Chemicals KW - Sensitivity analysis KW - Sulfonates KW - DNA KW - Mass spectrometry KW - Cadmium KW - Pregnancy KW - ENA 13:Population Planning & Control KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654688775?accountid=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=Perfluorochemicals+and+Human+Semen+Quality%3A+The+LIFE+Study&rft.au=Louis%2C+Germaine+MBuck%3BChen%2C+Zhen%3BSchisterman%2C+Enrique+F%3BKim%2C+Sungduk%3BSweeney%2C+Anne+M%3BSundaram%2C+Rajeshwari%3BLynch%2C+Courtney+D%3BGore-Langton%2C+Robert+E%3BBarr%2C+Dana+Boyd&rft.aulast=Louis&rft.aufirst=Germaine&rft.date=2014-08-15&rft.volume=123&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1307621 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Chemicals; Sensitivity analysis; Sulfonates; DNA; Mass spectrometry; Cadmium; Pregnancy DO - http://dx.doi.org/10.1289/ehp.1307621 ER - TY - JOUR T1 - Mitochondria, Energetics, Epigenetics, and Cellular Responses to Stress AN - 1642628401; 21201989 AB - Background: Cells respond to environmental stressors through several key pathways, including response to reactive oxygen species (ROS), nutrient and ATP sensing, DNA damage response (DDR), and epigenetic alterations. Mitochondria play a central role in these pathways not only through energetics and ATP production but also through metabolites generated in the tricarboxylic acid cycle, as well as mitochondria-nuclear signaling related to mitochondria morphology, biogenesis, fission/fusion, mitophagy, apoptosis, and epigenetic regulation. Objectives: We investigated the concept of bidirectional interactions between mitochondria and cellular pathways in response to environmental stress with a focus on epigenetic regulation, and we examined DNA repair and DDR pathways as examples of biological processes that respond to exogenous insults through changes in homeostasis and altered mitochondrial function. Methods: The National Institute of Environmental Health Sciences sponsored the Workshop on Mitochondria, Energetics, Epigenetics, Environment, and DNA Damage Response on 25-26 March 2013. Here, we summarize key points and ideas emerging from this meeting. Discussion: A more comprehensive understanding of signaling mechanisms (cross-talk) between the mitochondria and nucleus is central to elucidating the integration of mitochondrial functions with other cellular response pathways in modulating the effects of environmental agents. Recent studies have highlighted the importance of mitochondrial functions in epigenetic regulation and DDR with environmental stress. Development and application of novel technologies, enhanced experimental models, and a systems-type research approach will help to discern how environmentally induced mitochondrial dysfunction affects key mechanistic pathways. Conclusions: Understanding mitochondria-cell signaling will provide insight into individual responses to environmental hazards, improving prediction of hazard and susceptibility to environmental stressors. Citation: Shaughnessy DT, McAllister K, Worth L, Haugen AC, Meyer JN, Domann FE, Van Houten B, Mostoslavsky R, Bultman SJ, Baccarelli AA, Begley TJ, Sobol RW, Hirschey MD, Ideker T, Santos JH, Copeland WC, Tice RR, Balshaw DM, Tyson FL. 2014. Mitochondria, energetics, epigenetics, and cellular responses to stress. Environ Health Perspect 122:1271-1278; http://dx.doi.org/10.1289/ehp.1408418 JF - Environmental Health Perspectives AU - Shaughnessy, Daniel T AU - McAllister, Kimberly AU - Worth, Leroy AU - Haugen, Astrid C AU - Meyer, Joel N AU - Domann, Frederick E AU - Van Houten, Bennett AU - Mostoslavsky, Raul AU - Bultman, Scott J AU - Baccarelli, Andrea A AU - Begley, Thomas J AU - Sobol, Robert W AU - Hirschey, Matthew D AU - Ideker, Trey AU - Santos, Janine H AU - Copeland, William C AU - Tice, Raymond R AU - Balshaw, David M AU - Tyson, Frederick L AD - Division of Extramural Research and Training, 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 - 2014/08/15/ PY - 2014 DA - 2014 Aug 15 SP - 1271 EP - 1278 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 122 IS - 12 SN - 0091-6765, 0091-6765 KW - Biochemistry Abstracts 2: Nucleic Acids; Environment Abstracts KW - Prediction KW - Apoptosis KW - Environmental health KW - Mitochondria KW - Nutrients KW - Metabolites KW - Homeostasis KW - Integration KW - Reactive oxygen species KW - Environmental hazards KW - epigenetics KW - Environmental stress KW - Tricarboxylic acid cycle KW - Adenylate cyclase KW - Brazil, Sao Paulo, Santos KW - Conferences KW - ATP KW - DNA repair KW - Oxygen KW - DNA damage KW - Reviews KW - Morphology KW - DNA KW - Technology KW - Signal transduction KW - N 14820:DNA Metabolism & Structure KW - ENA 21:Wildlife UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1642628401?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Mitochondria%2C+Energetics%2C+Epigenetics%2C+and+Cellular+Responses+to+Stress&rft.au=Shaughnessy%2C+Daniel+T%3BMcAllister%2C+Kimberly%3BWorth%2C+Leroy%3BHaugen%2C+Astrid+C%3BMeyer%2C+Joel+N%3BDomann%2C+Frederick+E%3BVan+Houten%2C+Bennett%3BMostoslavsky%2C+Raul%3BBultman%2C+Scott+J%3BBaccarelli%2C+Andrea+A%3BBegley%2C+Thomas+J%3BSobol%2C+Robert+W%3BHirschey%2C+Matthew+D%3BIdeker%2C+Trey%3BSantos%2C+Janine+H%3BCopeland%2C+William+C%3BTice%2C+Raymond+R%3BBalshaw%2C+David+M%3BTyson%2C+Frederick+L&rft.aulast=Shaughnessy&rft.aufirst=Daniel&rft.date=2014-08-15&rft.volume=122&rft.issue=12&rft.spage=1271&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1408418 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Apoptosis; Conferences; Mitochondria; ATP; Metabolites; Nutrients; Homeostasis; DNA repair; Integration; DNA damage; Reactive oxygen species; epigenetics; Reviews; Environmental stress; Tricarboxylic acid cycle; Signal transduction; Adenylate cyclase; Prediction; Oxygen; Environmental hazards; Morphology; DNA; Environmental health; Technology; Brazil, Sao Paulo, Santos DO - http://dx.doi.org/10.1289/ehp.1408418 ER - TY - JOUR T1 - Med25 is required for estrogen receptor alpha (ERα)-mediated regulation of human CYP2C9 expression. AN - 1547542790; 24960263 AB - The CYP2C subfamily of cytochrome P450 enzymes is an important class of drug metabolizing enzymes in human liver. CYP2C9 is the most abundant member of the human CYP2C subfamily in liver and metabolizes ~15% of the therapeutic drugs as well as other xenobiotics and endogenous compounds. A number of nuclear receptors including xenobiotic-sensing receptors such as the constitutive androstane receptor (CAR), pregnane X receptor (PXR), and glucocorticoid receptor (GR) as well as liver enriched receptors hepatic nuclear factor 4α (HNF4α) and the estrogen receptor α (ERα) regulate CYP2C9 expression. Here, we show that Med25, a variable component of Mediator complex, enhanced ligand dependent ERα-mediated transcriptional activation of CYP2C9 promoter and interacts with activated ERα by 17β-estradiol through its C-terminal LXXLL motif. In conclusion, Med25 is identified as a new coactivator of ERα that is required for ERα-mediated regulation of CYP2C9 expression. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Biochemical pharmacology AU - Shi, Zhe AU - Yang, Wenjun AU - Goldstein, Joyce A AU - Zhang, Shu-Yun AD - Department of Preventive Medicine, School of Environmental Science and Public Health, Wenzhou Medical University, Wenzhou, Zhejiang 325035, PR China. ; Department of Hepatobiliary Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325035, PR China. ; Human Metabolism Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Department of Preventive Medicine, School of Environmental Science and Public Health, Wenzhou Medical University, Wenzhou, Zhejiang 325035, PR China. Electronic address: shuyunzh@gmail.com. Y1 - 2014/08/15/ PY - 2014 DA - 2014 Aug 15 SP - 425 EP - 431 VL - 90 IS - 4 KW - Estrogen Receptor alpha KW - 0 KW - MED25 protein, human KW - Mediator Complex KW - CYP2C9 protein, human KW - EC 1.14.13.- KW - Cytochrome P-450 CYP2C9 KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Index Medicus KW - Med25 KW - CYP2C9 KW - Transcription regulation KW - ERα KW - Real-Time Polymerase Chain Reaction KW - Microscopy, Confocal KW - Promoter Regions, Genetic KW - Hep G2 Cells KW - Humans KW - Chromatin Immunoprecipitation KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - Mediator Complex -- physiology KW - Gene Expression Regulation, Enzymologic -- physiology KW - Aryl Hydrocarbon Hydroxylases -- genetics KW - Estrogen Receptor alpha -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547542790?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Med25+is+required+for+estrogen+receptor+alpha+%28ER%CE%B1%29-mediated+regulation+of+human+CYP2C9+expression.&rft.au=Shi%2C+Zhe%3BYang%2C+Wenjun%3BGoldstein%2C+Joyce+A%3BZhang%2C+Shu-Yun&rft.aulast=Shi&rft.aufirst=Zhe&rft.date=2014-08-15&rft.volume=90&rft.issue=4&rft.spage=425&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=1873-2968&rft_id=info:doi/10.1016%2Fj.bcp.2014.06.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-16 N1 - Date created - 2014-07-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Pharmacol Exp Ther. 2011 Jul;338(1):302-9 [21493749] PLoS One. 2011;6(3):e18222 [21479238] PLoS One. 2012;7(8):e44007 [22952853] Biochim Biophys Acta. 2013 Jul;1830(7):3867-75 [22402254] Cell Mol Life Sci. 2013 Aug;70(15):2743-56 [23361037] Annu Rev Biochem. 2000;69:729-49 [10966474] Physiol Rev. 2001 Jul;81(3):1269-304 [11427696] Br J Clin Pharmacol. 2001 Oct;52(4):349-55 [11678778] J Biol Chem. 2002 Jan 4;277(1):209-17 [11679585] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):2642-7 [11867769] Mol Pharmacol. 2002 Sep;62(3):737-46 [12181452] Mol Pharmacol. 2003 Aug;64(2):316-24 [12869636] J Pharmacol Exp Ther. 2004 Feb;308(2):495-501 [14600250] Trends Endocrinol Metab. 2004 Mar;15(2):73-8 [15036253] Cell. 1990 Jun 29;61(7):1209-15 [2163759] Pharmacogenetics. 1994 Dec;4(6):285-99 [7704034] Cell. 1995 Dec 15;83(6):835-9 [8521507] Biochem Pharmacol. 1998 Mar 15;55(6):825-30 [9586955] J Biochem Mol Toxicol. 1999;13(6):289-95 [10487415] Trends Biochem Sci. 2005 May;30(5):235-9 [15896740] J Pharmacol Exp Ther. 2005 Sep;314(3):1125-33 [15919766] Mol Pharmacol. 2005 Sep;68(3):747-57 [15933212] Rev Physiol Biochem Pharmacol. 2006;156:23-43 [16634145] Drug Metab Dispos. 2007 Apr;35(4):682-8 [17220242] EMBO J. 2007 Aug 8;26(15):3545-57 [17641689] Biochimie. 2007 Dec;89(12):1439-46 [17870225] Nat Rev Genet. 2010 Nov;11(11):761-72 [20940737] Mol Cell Biol. 2011 Feb;31(3):466-81 [21135126] FASEB J. 2011 Feb;25(2):703-13 [21059750] Mol Pharmacol. 2012 Sep;82(3):529-40 [22723340] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bcp.2014.06.016 ER - TY - JOUR T1 - Safety of cotrimoxazole in pregnancy: a systematic review and meta-analysis. AN - 1544742922; 24853309 AB - Cotrimoxazole is widely prescribed to treat a range of infections, and for HIV-infected individuals it is administered as prophylaxis to protect against opportunistic infections. Some reports suggest that fetuses exposed to cotrimoxazole during early pregnancy may have an increased risk of congenital anomalies. We carried out this systematic review to update the evidence of cotrimoxazole safety in pregnancy. Three databases and 1 conference abstract site were searched in duplicate up to October 31, 2013, for studies reporting adverse maternal and infant outcomes among women receiving cotrimoxazole during pregnancy. This search was updated in MEDLINE via PubMed to April 28, 2014. Studies were included irrespective of HIV infection status or the presence of other coinfections. Our primary outcome was birth defects of any kind. Secondary outcomes included spontaneous abortions, terminations of pregnancy, stillbirths, preterm deliveries, and drug-associated toxicity. Twenty-four studies were included for review. There were 232 infants with congenital anomalies among 4196 women receiving cotrimoxazole during pregnancy, giving an overall pooled prevalence of 3.5% (95% confidence interval: 1.8% to 5.1%; τ² = 0.03). Three studies reported 31 infants with neural tube defects associated with first trimester exposure to cotrimoxazole, giving a crude prevalence of 0.7% (95% confidence interval: 0.5% to 1.0%) with most data (29 neural tube defects) coming from a single study. The majority of adverse drug reactions were mild. The quality of the evidence was very low. The findings of this review support continued recommendations for cotrimoxazole as a priority intervention for HIV-infected pregnant women. It is critical to improve data collection on maternal and infant outcomes. JF - Journal of acquired immune deficiency syndromes (1999) AU - Ford, Nathan AU - Shubber, Zara AU - Jao, Jennifer AU - Abrams, Elaine J AU - Frigati, Lisa AU - Mofenson, Lynne AD - *Department of HIV/AIDS, World Health Organization, Geneva, Switzerland; †Department of Infectious Disease Epidemiology, Faculty of Medicine, Imperial College, London, United Kingdom; ‡Department of Medicine, Divisions of Infectious Diseases and General Internal Medicine, Icahn School of Medicine at Mount Sinai, New York, NY; §ICAP, Mailman School of Public Health, and College of Physicians and Surgeons, Columbia University, New York, NY; ‖Department of Paediatrics and Child Health, Tygerberg Hospital, University of Stellenbosch, Cape Town South Africa; and ¶Maternal and Pediatric Infectious Disease Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, MD. Y1 - 2014/08/15/ PY - 2014 DA - 2014 Aug 15 SP - 512 EP - 521 VL - 66 IS - 5 KW - Anti-Bacterial Agents KW - 0 KW - Trimethoprim, Sulfamethoxazole Drug Combination KW - 8064-90-2 KW - Index Medicus KW - AIDS/HIV KW - HIV Infections KW - Humans KW - Female KW - Pregnancy KW - Trimethoprim, Sulfamethoxazole Drug Combination -- administration & dosage KW - Abnormalities, Drug-Induced KW - Anti-Bacterial Agents -- adverse effects KW - Anti-Bacterial Agents -- administration & dosage KW - Trimethoprim, Sulfamethoxazole Drug Combination -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544742922?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+acquired+immune+deficiency+syndromes+%281999%29&rft.atitle=Safety+of+cotrimoxazole+in+pregnancy%3A+a+systematic+review+and+meta-analysis.&rft.au=Ford%2C+Nathan%3BShubber%2C+Zara%3BJao%2C+Jennifer%3BAbrams%2C+Elaine+J%3BFrigati%2C+Lisa%3BMofenson%2C+Lynne&rft.aulast=Ford&rft.aufirst=Nathan&rft.date=2014-08-15&rft.volume=66&rft.issue=5&rft.spage=512&rft.isbn=&rft.btitle=&rft.title=Journal+of+acquired+immune+deficiency+syndromes+%281999%29&rft.issn=1944-7884&rft_id=info:doi/10.1097%2FQAI.0000000000000211 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-25 N1 - Date created - 2014-07-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Clin Nutr. 2000 May;71(5 Suppl):1295S-303S [10799405] Clin Infect Dis. 2014 Mar;58(5):651-9 [24336820] Clin Infect Dis. 2001 Apr 15;32(8):1172-7 [11283806] Am J Epidemiol. 2001 May 15;153(10):961-8 [11384952] Sex Transm Infect. 2001 Dec;77(6):441-3 [11714944] Reprod Toxicol. 2001 Nov-Dec;15(6):637-46 [11738517] Ann Hum Biol. 2002 Jul-Aug;29(4):422-31 [12160475] BMJ. 2003 Sep 6;327(7414):557-60 [12958120] Can Fam Physician. 2003 Sep;49:1085-6 [14526858] MMWR Morb Mortal Wkly Rep. 2004 May 7;53(17):362-5 [15129193] J Infect Dis. 1973 Nov;128:Suppl:657-65 p [4585966] Can Med Assoc J. 1975 Jun 14;112(13 Spec No):67-72 [1137830] Aust N Z J Obstet Gynaecol. 1983 Aug;23(3):139-41 [6606421] Control Clin Trials. 1986 Sep;7(3):177-88 [3802833] J Epidemiol Community Health. 1988 Mar;42(1):1-7 [3418278] Lancet. 1991 Jul 20;338(8760):131-7 [1677062] S Afr Med J. 1995 Jan;85(1):15-20 [7784908] Lancet. 1999 May 1;353(9163):1463-8 [10232311] Eur J Contracept Reprod Health Care. 2004 Sep;9(3):141-6 [15697103] Reprod Toxicol. 2005 Jul-Aug;20(2):203-7 [15907654] Arch Dis Child Fetal Neonatal Ed. 2005 Sep;90(5):F374-9 [16113153] AIDS Rev. 2006 Jan-Mar;8(1):24-36 [16736949] J Infect Dis. 2006 Dec 1;194(11):1510-8 [17083035] Birth Defects Res A Clin Mol Teratol. 2007 Feb;79(2):65-186 [17278144] Clin Infect Dis. 2007 Sep 1;45(5):548-55 [17682987] BMJ. 2008 Apr 26;336(7650):924-6 [18436948] CMAJ. 2008 Dec 2;179(12):1263-8 [19047607] AIDS. 2009 Feb 20;23(4):519-24 [19165088] Eur J Clin Microbiol Infect Dis. 2009 Mar;28(3):297-300 [18716804] Br J Clin Pharmacol. 2009 Dec;68(6):956-62 [20002091] PLoS Med. 2011 May;8(5):e1001026 [21559325] Trans R Soc Trop Med Hyg. 2011 Sep;105(9):540-2 [21742362] BJOG. 2011 Oct;118(11):1374-82 [21749628] Bull World Health Organ. 2012 Feb 1;90(2):128C-138C [22423164] Isr Med Assoc J. 2012 Jun;14(6):378-81 [22891400] PLoS One. 2012;7(10):e46638 [23056380] Eur J Clin Microbiol Infect Dis. 2013 Mar;32(3):361-8 [23052984] Epidemiol Infect. 2013 Aug;141(8):1749-55 [23010291] Infect Dis Obstet Gynecol. 2013;2013:340702 [24363547] J Acquir Immune Defic Syndr. 2014 Feb 1;65(2):198-206 [24220287] N Engl J Med. 2000 Nov 30;343(22):1608-14 [11096168] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/QAI.0000000000000211 ER - TY - JOUR T1 - Validation of a hypoxia-inducible factor-1 alpha specimen collection procedure and quantitative enzyme-linked immunosorbent assay in solid tumor tissues. AN - 1542004524; 24799347 AB - Hypoxia-inducible factor-1 alpha (HIF-1α) is an important marker of hypoxia in human tumors and has been implicated in tumor progression. Drugs targeting HIF-1α are being developed, but the ability to measure drug-induced changes in HIF-1α is limited by the lability of the protein in normoxia. Our goal was to devise methods for specimen collection and processing that preserve HIF-1α in solid tumor tissues and to develop and validate a two-site chemiluminescent quantitative enzyme-linked immunosorbent assay (ELISA) for HIF-1α. We tested various strategies for HIF-1α stabilization in solid tumors, including nitrogen gas-purged lysis buffer, the addition of proteasome inhibitors or the prolyl hydroxylase inhibitor 2-hydroxyglutarate, and bead homogenization. Degassing and the addition of 2-hydroxyglutarate to the collection buffer significantly increased HIF-1α recovery, whereas bead homogenization in sealed tubes improved HIF-1α recovery and reduced sample variability. Validation of the ELISA demonstrated intra- and inter-assay variability of less than 15% and accuracy of 99.8±8.3% as assessed by spike recovery. Inter-laboratory reproducibility was also demonstrated (R(2)=0.999). Careful sample handling techniques allow us to quantitatively detect HIF-1α in samples as small as 2.5μg of total protein extract, and this method is currently being applied to analyze tumor biopsy specimens in early-phase clinical trials. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Analytical biochemistry AU - Park, Sook Ryun AU - Kinders, Robert J AU - Khin, Sonny AU - Hollingshead, Melinda AU - Antony, Smitha AU - Parchment, Ralph E AU - Tomaszewski, Joseph E AU - Kummar, Shivaani AU - Doroshow, James H AD - Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD 20892, USA. ; Laboratory of Human Toxicology and Pharmacology, Applied/Developmental Research Directorate, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA. Electronic address: kindersr@mail.nih.gov. ; Laboratory of Human Toxicology and Pharmacology, Applied/Developmental Research Directorate, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA. ; Biological Testing Branch, Developmental Therapeutics Program, Frederick National Laboratory for Cancer Research, Frederick, MD 20892, USA. ; Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD 20892, USA; Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. Y1 - 2014/08/15/ PY - 2014 DA - 2014 Aug 15 SP - 1 EP - 11 VL - 459 KW - Biomarkers, Tumor KW - 0 KW - Hypoxia-Inducible Factor 1, alpha Subunit KW - Index Medicus KW - HIF-1α KW - Solid tumors KW - Hypoxia-inducible factor KW - Quantitative ELISA KW - Pharmacodynamics KW - Biomarkers, Tumor -- metabolism KW - Animals KW - Humans KW - Mice KW - Cell Line, Tumor KW - Female KW - Cell Transformation, Neoplastic KW - Neoplasms -- pathology KW - Enzyme-Linked Immunosorbent Assay KW - Specimen Handling -- methods KW - Hypoxia-Inducible Factor 1, alpha Subunit -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542004524?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+biochemistry&rft.atitle=Validation+of+a+hypoxia-inducible+factor-1+alpha+specimen+collection+procedure+and+quantitative+enzyme-linked+immunosorbent+assay+in+solid+tumor+tissues.&rft.au=Park%2C+Sook+Ryun%3BKinders%2C+Robert+J%3BKhin%2C+Sonny%3BHollingshead%2C+Melinda%3BAntony%2C+Smitha%3BParchment%2C+Ralph+E%3BTomaszewski%2C+Joseph+E%3BKummar%2C+Shivaani%3BDoroshow%2C+James+H&rft.aulast=Park&rft.aufirst=Sook&rft.date=2014-08-15&rft.volume=459&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Analytical+biochemistry&rft.issn=1096-0309&rft_id=info:doi/10.1016%2Fj.ab.2014.04.025 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-04 N1 - Date created - 2014-06-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2011 Mar 1;108(9):3749-54 [21321221] Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5246-50 [9560261] Clin Cancer Res. 2011 Aug 1;17(15):5123-31 [21673063] Proc Natl Acad Sci U S A. 2012 Feb 21;109(8):2784-9 [22308314] Cancer Cell. 2011 Jan 18;19(1):17-30 [21251613] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):7987-92 [9653127] Am J Physiol. 1998 Oct;275(4 Pt 1):L818-26 [9755115] Cancer Res. 2005 Apr 1;65(7):2825-31 [15805283] Cancer Res. 2006 Apr 1;66(7):3639-48 [16585189] J Biol Chem. 2006 Nov 3;281(44):33095-106 [16954218] Nat Rev Cancer. 2007 Feb;7(2):131-9 [17251919] Cancer Metastasis Rev. 2007 Jun;26(2):225-39 [17440684] Blood. 2008 Mar 15;111(6):3131-6 [18174379] Mol Cell. 2008 May 23;30(4):393-402 [18498744] Clin Cancer Res. 2008 Jun 15;14(12):3658-63 [18559579] Clin Cancer Res. 2008 Nov 1;14(21):6877-85 [18980982] Nat Rev Cancer. 2008 Dec;8(12):967-75 [18987634] Mol Cancer Ther. 2009 Jul;8(7):1878-84 [19584232] Clin Cancer Res. 2009 Nov 1;15(21):6619-29 [19843666] J Cell Mol Med. 2009 Sep;13(9A):2780-6 [19674190] Drug Resist Updat. 2011 Jun;14(3):191-201 [21466972] J Biol Chem. 1999 Nov 12;274(46):32631-7 [10551817] Cancer Res. 1999 Nov 15;59(22):5830-5 [10582706] Am J Pathol. 2000 Aug;157(2):411-21 [10934146] Mol Cell Biol. 2001 Jun;21(12):3995-4004 [11359907] Cell Growth Differ. 2001 Jul;12(7):363-9 [11457733] Nat Rev Cancer. 2002 Jan;2(1):38-47 [11902584] Cancer Res. 2002 Aug 1;62(15):4316-24 [12154035] Nat Rev Cancer. 2003 Oct;3(10):721-32 [13130303] Cell Cycle. 2004 Feb;3(2):172-5 [14712084] Cancer Res. 2004 Feb 15;64(4):1475-82 [14983893] Nat Rev Cancer. 2004 Jun;4(6):437-47 [15170446] J Biol Chem. 2004 Sep 24;279(39):40337-44 [15271983] Cancer Res. 2004 Oct 1;64(19):6845-8 [15466170] Wiley Interdiscip Rev Syst Biol Med. 2010 May-Jun;2(3):336-61 [20836033] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ab.2014.04.025 ER - TY - JOUR T1 - Identification by digital immunohistochemistry of intratumoral changes of immune infiltrates after vaccine in the absence of modifications of PBMC immune cell subsets. AN - 1534794068; 24474335 AB - Preclinical studies have demonstrated that the combination of systemic subcutaneous (s.c.) vaccination with intratumoral (i.t.) vaccination was superior in the induction of antitumor activity vs. vaccination with either route alone. A subsequent phase I study employing i.t.-s.c. vaccination was carried out in men with locally recurrent or progressive prostate cancer. rF-PSA-TRICOM (PROSTVAC) vaccine was administered intraprostatically and rV-PSA-TRICOM followed by rF-PSA-TRICOM vaccine was administered systemically. In that study no dose limiting toxicities were observed, 19/21 patients had stable or improved prostate-specific antigen (PSA) values and tumor-infiltrating lymphocytes (TILs) increased in post- vs. pre-treatment tumor biopsies, analyzed employing conventional immunohistochemistry (IHC). In the studies reported here, 31 phenotypes of peripheral blood mononuclear cells (PBMCs) were analyzed prevaccination and postvaccination as well as the functions of PBMC regulatory T cells (Tregs) and natural killer cells. A trend was observed in decreases in serum PSA with the reduction of circulating Tregs postvaccination. Digital IHC was employed prevaccination and postvaccination to measure CD4 and CD8 TILs, as well as Treg TILs by conventional IHC. Few correlations were observed with CD4, CD8 or Treg in TILs vs. PBMCs. However, patients with lower levels of CD4 TILs prevaccination showed the greatest increases in CD4 TILs postvaccine, while Treg TILs decreased postvaccine. There was also a strong correlation between decreases in serum PSA and increases in CD8 TILs postvaccine. These studies provide additional rationale for the use of i.t.-s.c. vaccinations and demonstrate a noncoordinate expression of specific immune subsets in PBMCs vs. tumor. Published 2014. This article is a US Government work and, as such, is in the public domain of the United States of America. JF - International journal of cancer AU - Farsaci, Benedetto AU - Jochems, Caroline AU - Grenga, Italia AU - Donahue, Renee N AU - Tucker, Jo A AU - Pinto, Peter A AU - Merino, Maria J AU - Heery, Christopher R AU - Madan, Ravi A AU - Gulley, James L AU - Schlom, Jeffrey AD - Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 2014/08/15/ PY - 2014 DA - 2014 Aug 15 SP - 862 EP - 870 VL - 135 IS - 4 KW - Cancer Vaccines KW - 0 KW - Vaccines, Synthetic KW - rF-TRICOM vaccine KW - rV-Tricom KW - Prostate-Specific Antigen KW - EC 3.4.21.77 KW - Index Medicus KW - tumor-infiltrating lymphocytes KW - intratumoral vaccine KW - cancer vaccine KW - digital immunohistochemistry KW - PROSTVAC KW - Phenotype KW - Humans KW - Prostate-Specific Antigen -- blood KW - Cohort Studies KW - Biopsy KW - Vaccines, Synthetic -- therapeutic use KW - Neoplasm Recurrence, Local KW - Male KW - Lymphocytes, Tumor-Infiltrating -- cytology KW - Killer Cells, Natural -- immunology KW - Prostatic Neoplasms -- immunology KW - Prostatic Neoplasms -- blood KW - Cancer Vaccines -- therapeutic use KW - Leukocytes, Mononuclear -- immunology KW - Immunohistochemistry -- methods KW - Prostatic Neoplasms -- therapy KW - Leukocytes, Mononuclear -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534794068?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification+by+digital+immunohistochemistry+of+intratumoral+changes+of+immune+infiltrates+after+vaccine+in+the+absence+of+modifications+of+PBMC+immune+cell+subsets.&rft.au=Farsaci%2C+Benedetto%3BJochems%2C+Caroline%3BGrenga%2C+Italia%3BDonahue%2C+Renee+N%3BTucker%2C+Jo+A%3BPinto%2C+Peter+A%3BMerino%2C+Maria+J%3BHeery%2C+Christopher+R%3BMadan%2C+Ravi+A%3BGulley%2C+James+L%3BSchlom%2C+Jeffrey&rft.aulast=Farsaci&rft.aufirst=Benedetto&rft.date=2014-08-15&rft.volume=135&rft.issue=4&rft.spage=862&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.28743 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-08 N1 - Date created - 2014-06-10 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.28743 ER - TY - JOUR T1 - Preconception Maternal and Paternal Exposure to Persistent Organic Pollutants and Birth Size: The LIFE Study AN - 1660066280; PQ0001052575 AB - Background: Persistent organic pollutants (POPs) are developmental toxicants, but the impact of both maternal and paternal exposures on offspring birth size is largely unexplored. Objective: We examined associations between maternal and paternal serum concentrations of 63 POPs, comprising five major classes of pollutants, with birth size measures. Methods: Parental serum concentrations of 9 organochlorine pesticides, 1 polybrominated biphenyl (PBB), 7 perfluoroalkyl chemicals (PFCs), 10 polybrominated diphenyl ethers (PBDEs), and 36 polychlorinated biphenyls (PCBs) were measured before conception for 234 couples. Differences in birth weight, length, head circumference, and ponderal index were estimated using multiple linear regression per 1-SD increase in natural log-transformed (ln-transformed) chemicals. Models were estimated separately for each parent and adjusted for maternal age, maternal prepregnancy body mass index (kilograms per meter squared) and other confounders, and all models included an interaction term between infant sex and each chemical. Results: Among girls (n = 117), birth weight was significantly lower (range, 84-195 g) in association with a 1-SD increase in ln-transformed maternal serum concentrations of DDT, PBDE congeners 28 and 183, and paternal serum concentrations of PBDE-183 and PCB-167. Among boys (n = 113), maternal (PCBs 138, 153, 167, 170, 195, and 209 and perfluorooctane sulfonamide) and paternal (PCBs 172 and 195) serum concentrations of several POPs were statistically associated with lower birth weight (range, 98-170 g), whereas paternal concentrations of PBDEs (66, 99) were associated with higher birth weight. Differences in offspring head circumference, length, and ponderal index were also associated with parental exposures. Conclusions: Preconceptional maternal and paternal concentrations of several POPs were associated with statistically significant differences in birth size among offspring. Citation: Robledo CA, Yeung E, Mendola P, Sundaram R, Maisog J, Sweeney AM, Barr DB, Buck Louis GM. 2015. Preconception maternal and paternal exposure to persistent organic pollutants and birth size: the LIFE Study. Environ Health Perspect 123:88-94; http://dx.doi.org/10.1289/ehp.1308016 JF - Environmental Health Perspectives AU - Robledo, Candace A AU - Yeung, Edwina AU - Mendola, Pauline AU - Sundaram, Rajeshwari AU - Maisog, Jose AU - Sweeney, Anne M AU - Barr, Dana Boyd AU - Louis, Germaine MBuck AD - Division of Intramural Population Health 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 - 2014/08/05/ PY - 2014 DA - 2014 Aug 05 SP - 88 EP - 94 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 123 IS - 1 SN - 0091-6765, 0091-6765 KW - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE) KW - Birth KW - Pollutants KW - Exposure KW - Circumferences KW - Health KW - Serums KW - Perfluoroalkyls KW - Infants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660066280?accountid=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=Preconception+Maternal+and+Paternal+Exposure+to+Persistent+Organic+Pollutants+and+Birth+Size%3A+The+LIFE+Study&rft.au=Robledo%2C+Candace+A%3BYeung%2C+Edwina%3BMendola%2C+Pauline%3BSundaram%2C+Rajeshwari%3BMaisog%2C+Jose%3BSweeney%2C+Anne+M%3BBarr%2C+Dana+Boyd%3BLouis%2C+Germaine+MBuck&rft.aulast=Robledo&rft.aufirst=Candace&rft.date=2014-08-05&rft.volume=123&rft.issue=1&rft.spage=88&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1308016 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-05-04 DO - http://dx.doi.org/10.1289/ehp.1308016 ER - TY - JOUR T1 - Uptake of compounds that selectively kill multidrug-resistant cells: the copper transporter SLC31A1 (CTR1) increases cellular accumulation of the thiosemicarbazone NSC73306. AN - 1551331709; 24800945 AB - Acquired drug resistance in cancer continues to be a challenge in cancer therapy, in part due to overexpression of the drug efflux transporter P-glycoprotein (P-gp, MDR1, ABCB1). NSC73306 is a thiosemicarbazone compound that displays greater toxicity against cells expressing functional P-gp than against other cells. Here, we investigate the cellular uptake of NSC73306, and examine its interaction with P-gp and copper transporter 1 (CTR1, SLC31A1). Overexpression of P-gp sensitizes LLC-PK1 cells to NSC73306. Cisplatin (IC50 = 77 μM), cyclosporin A (IC50 = 500 μM), and verapamil (IC50 = 700 μM) inhibited cellular accumulation of [(3)H]NSC73306. Cellular hypertoxicity of NSC73306 to P-gp-expressing cells was inhibited by cisplatin in a dose-dependent manner. Cells transiently expressing the cisplatin uptake transporter CTR1 (SLC31A1) showed increased [(3)H]NSC73306 accumulation. In contrast, CTR1 knockdown decreased [(3)H]NSC73306 accumulation. The presence of NSC73306 reduced CTR1 levels, similar to the negative feedback of CTR1 levels by copper or cisplatin. Surprisingly, although cisplatin is a substrate of CTR1, we found that CTR1 protein was overexpressed in high-level cisplatin-resistant KB-CP20 and BEL7404-CP20 cell lines. We confirmed that the CTR1 protein was functional, as uptake of NSC73306 was increased in KB-CP20 cells compared to their drug-sensitive parental cells, and downregulation of CTR1 in KB-CP20 cells reduced [(3)H]NSC73306 accumulation. These results suggest that NSC73306 is a transport substrate of CTR1. JF - Molecular pharmaceutics AU - Fung, King Leung AU - Tepede, Abisola K AU - Pluchino, Kristen M AU - Pouliot, Lynn M AU - Pixley, Jessica N AU - Hall, Matthew D AU - Gottesman, Michael M AD - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Bethesda, Maryland 20892, United States. Y1 - 2014/08/04/ PY - 2014 DA - 2014 Aug 04 SP - 2692 EP - 2702 VL - 11 IS - 8 KW - Cation Transport Proteins KW - 0 KW - Indoles KW - NSC73306 KW - P-Glycoprotein KW - RNA, Small Interfering KW - SLC31A1 protein, human KW - Thiosemicarbazones KW - Copper KW - 789U1901C5 KW - Cyclosporine KW - 83HN0GTJ6D KW - Verapamil KW - CJ0O37KU29 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Swine KW - Animals KW - Cisplatin -- chemistry KW - Reproducibility of Results KW - COS Cells KW - HEK293 Cells KW - Humans KW - Thiosemicarbazones -- chemistry KW - Cyclosporine -- chemistry KW - RNA, Small Interfering -- metabolism KW - Copper -- chemistry KW - Cisplatin -- administration & dosage KW - Verapamil -- administration & dosage KW - P-Glycoprotein -- metabolism KW - Cercopithecus aethiops KW - LLC-PK1 Cells KW - Inhibitory Concentration 50 KW - Indoles -- pharmacokinetics KW - Drug Resistance, Multiple -- drug effects KW - Cation Transport Proteins -- metabolism KW - Drug Resistance, Neoplasm -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551331709?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmaceutics&rft.atitle=Uptake+of+compounds+that+selectively+kill+multidrug-resistant+cells%3A+the+copper+transporter+SLC31A1+%28CTR1%29+increases+cellular+accumulation+of+the+thiosemicarbazone+NSC73306.&rft.au=Fung%2C+King+Leung%3BTepede%2C+Abisola+K%3BPluchino%2C+Kristen+M%3BPouliot%2C+Lynn+M%3BPixley%2C+Jessica+N%3BHall%2C+Matthew+D%3BGottesman%2C+Michael+M&rft.aulast=Fung&rft.aufirst=King&rft.date=2014-08-04&rft.volume=11&rft.issue=8&rft.spage=2692&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmaceutics&rft.issn=1543-8392&rft_id=info:doi/10.1021%2Fmp500114e LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-14 N1 - Date created - 2014-08-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2003 Sep 15;63(18):5909-16 [14522917] J Biol Chem. 1994 Oct 14;269(41):25660-7 [7929270] Mol Pharmacol. 2004 Oct;66(4):817-23 [15229296] Clin Cancer Res. 2004 Oct 1;10(19):6744-9 [15475465] J Cell Physiol. 1976 May;88(1):23-31 [57118] Science. 1986 May 2;232(4750):643-5 [3457471] Biochem Pharmacol. 1986 Jul 1;35(13):2257-9 [3827990] Br J Cancer. 1995 Apr;71(4):676-83 [7710928] Proc Natl Acad Sci U S A. 1997 Apr 15;94(8):4028-33 [9108099] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7481-6 [9207117] Mol Cancer Ther. 2004 Dec;3(12):1543-9 [15634647] Nat Rev Drug Discov. 2006 Mar;5(3):219-34 [16518375] Cancer Res. 2006 May 1;66(9):4808-15 [16651436] Curr Drug Targets. 2006 Jul;7(7):861-79 [16842217] Mol Pharmacol. 2006 Oct;70(4):1390-4 [16847145] Cancer Biol Ther. 2006 Aug;5(8):943-9 [16775422] Anticancer Res. 2007 Jul-Aug;27(4B):2209-16 [17695505] Oncol Rep. 2007 Oct;18(4):987-91 [17786364] J Biol Chem. 2007 Sep 14;282(37):26775-85 [17627943] Mol Cancer Ther. 2007 Dec;6(12 Pt 1):3287-96 [18089722] Mol Cancer Ther. 2008 Sep;7(9):3081-91 [18790787] Mol Pharmacol. 2009 Feb;75(2):324-30 [18996970] J Inorg Biochem. 2009 Mar;103(3):333-41 [19124158] Am J Physiol Renal Physiol. 2009 Mar;296(3):F505-11 [19144690] Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4237-42 [19240214] Science. 2009 Mar 27;323(5922):1718-22 [19325113] J Med Chem. 2009 May 28;52(10):3191-204 [19397322] Trends Pharmacol Sci. 2009 Oct;30(10):546-56 [19762091] Biochem Pharmacol. 2010 Apr 15;79(8):1108-17 [20005867] J Trace Elem Med Biol. 2010 Jul;24(3):178-84 [20569931] Metallomics. 2010 Jan;2(1):74-83 [21072377] Anticancer Agents Med Chem. 2010 Oct 1;10(8):601-16 [21194401] J Med Chem. 2011 Jul 28;54(14):4987-97 [21657271] Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6836-41 [11391004] Proc Natl Acad Sci U S A. 2001 Jun 5;98(12):6842-7 [11391005] J Biol Chem. 2002 Feb 8;277(6):4380-7 [11734551] Novartis Found Symp. 2002;243:83-96; discussion 96-102, 180-5 [11990784] J Biol Chem. 2002 Jul 5;277(27):23981-4 [12011036] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14298-302 [12370430] Biochemistry. 2002 Nov 26;41(47):13989-4000 [12437356] J Biol Chem. 2003 Mar 14;278(11):9639-46 [12501239] Cancer Res. 2003 Jun 15;63(12):3084-91 [12810633] J Med Chem. 2011 Aug 25;54(16):5878-89 [21721528] Drug Resist Updat. 2012 Feb-Apr;15(1-2):98-105 [22483810] Metallomics. 2012 Jul;4(7):679-85 [22552365] Curr Cancer Drug Targets. 2012 Oct;12(8):962-86 [22794121] Mol Pharmacol. 2012 Dec;82(6):1008-21 [22826468] Cancer Res. 2014 Jan 15;74(2):598-608 [24305879] Chem Rev. 2014 Jun 11;114(11):5753-74 [24758331] Proc Natl Acad Sci U S A. 1987 Jan;84(1):265-9 [2432605] Proc Natl Acad Sci U S A. 1988 May;85(10):3580-4 [3368466] J Biol Chem. 1989 Sep 5;264(25):14880-4 [2570070] Cell. 1994 Jan 28;76(2):393-402 [8293472] Oncogene. 2003 Oct 20;22(47):7468-85 [14576852] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/mp500114e ER - TY - JOUR T1 - Protective effect of Selenium nanoparticle against cyclophosphamide induced hepatotoxicity and genotoxicity in Swiss albino mice. AN - 1826591683; 24522241 AB - Cyclophosphamide (CP) is the most commonly used chemotherapeutic drug for various types of cancer. However, its use causes severe cytotoxicity to normal cells in human. It is well known that the undesirable side effects are caused due to the formation of reactive oxygen species. Selenium is an essential micronutrient for both animals and humans and has antioxidant and membrane stabilizing property, but selenium is also toxic above certain level. Nano selenium has been well proved to be less toxic than inorganic selenium as well as certain organoselenium compounds. The objective of the study is to evaluate the protective role of Nano-Se against CP-induced hepatotoxicity and genotoxicity in Swiss albino mice. CP was administered intraperitoneally (25 mg/kg b.w.) and Nano-Se was given by oral gavages (2 mg Se/kg b.w.) in concomitant and pretreatment scheme. Intraperitoneal administration of CP induced hepatic damage as indicated by the serum marker enzymes aspartate and alanine transaminases and increased the malonaldehyde level, depleted the glutathione content and antioxidant enzyme activity (glutathione peroxidase, glutathione-s-transferase, superoxide dismutase and catalase), and induced DNA damage and chromosomal aberration. Oral administration of Nano-Se caused a significant reduction in malonaldehyde, ROS level and glutathione levels, restoration of antioxidant enzyme activity, reduction in chromosomal aberration in bone marrow, and DNA damage in lymphocytes and also in bone marrow. Moreover, the chemoprotective efficiency of Nano-Se against CP induced toxicity was confirmed by histopathological evaluation. The results support the protective effect of Nano-Se against CP-induced hepatotoxicity and genotoxicity. © The Author(s) 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav. JF - Journal of biomaterials applications AU - Bhattacharjee, Arin AU - Basu, Abhishek AU - Ghosh, Prosenjit AU - Biswas, Jaydip AU - Bhattacharya, Sudin AD - Chittaranjan National Cancer Institute, Department of Cancer Chemoprevention, Kolkata, West Bengal, India. ; Chittaranjan National Cancer Institute, Department of Translational Research, Kolkata, West Bengal, India. ; Chittaranjan National Cancer Institute, Department of Cancer Chemoprevention, Kolkata, West Bengal, India sudinb19572004@yahoo.co.in. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 303 EP - 317 VL - 29 IS - 2 KW - cyclophosphamide KW - genotoxicity KW - Nano-Se KW - oxidative stress KW - hepatotoxicity KW - antioxidant enzyme UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826591683?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biomaterials+applications&rft.atitle=Protective+effect+of+Selenium+nanoparticle+against+cyclophosphamide+induced+hepatotoxicity+and+genotoxicity+in+Swiss+albino+mice.&rft.au=Bhattacharjee%2C+Arin%3BBasu%2C+Abhishek%3BGhosh%2C+Prosenjit%3BBiswas%2C+Jaydip%3BBhattacharya%2C+Sudin&rft.aulast=Bhattacharjee&rft.aufirst=Arin&rft.date=2014-08-01&rft.volume=29&rft.issue=2&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Journal+of+biomaterials+applications&rft.issn=1530-8022&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2014-07-11 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Short Communication: Serum-Based Assay Accurately Detects Single Nucleotide Polymorphisms of IL28B and SOCS3 in HIV/Hepatitis C Virus-Coinfected Subjects AN - 1768584252; PQ0002687176 AB - Single nucleotide polymorphisms (SNPs) have become important in predicting treatment response to interferon containing anti-hepatitis C virus (HCV) therapy in HCV and HIV/HCV-infected patients. A reliable method for extracting host DNA from serum for genotyping assays would present a practical alternative for clinicians and investigators seeking to perform SNP analyses in HCV-infected patients, particularly in resource-limited settings. Human genomic DNA was extracted from peripheral blood mononuclear cells (PBMCs) and serum of 51 HIV/HCV coinfected patients using the QIAamp DNA Blood Mini Kit and QIAamp Min Elute Virus Spin Kit, respectively. Genotyping assays for the IL28B SNP (rs12979860) and SOCS3 SNP (rs4969170) were performed using the commercially available ABI Taqman allelic discrimination kit and reverse transcriptase-polymerase chain reaction (RT-PCR) was performed using 50 cycles. Results of the genotyping assays using DNA from both PBMCs and cell-free serum were determined separately and then analyzed for concurrence. Genotype analyses performed using DNA isolated from PBMCs or cell-free serum showed a 100% agreement between the IL28B genotyping results from the serum and PBMC isolates and 98% agreement for SOCS3 SNP. This novel serum-based assay to isolate DNA fragments from the serum of HIV/HCV-coinfected subjects can accurately determine a subject's genotype for IL28B (rs12979860) and SOCS3 (rs4969170). This assay could be immediately valuable for detecting clinically relevant SNPs from serum in cases in which PBMCs are not available. JF - AIDS Research and Human Retroviruses AU - Shaffer, Ashton AU - Hubbard, Jon J AU - Townsend, Kerry AU - Kottilil, Shyam AU - Polis, Michael A AU - Masur, Henry AU - Kohli, Anita AD - Critical Care Medicine Department, Clinical Research Center, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 792 EP - 795 PB - Mary Ann Liebert, Inc., 140 Huguenot Street New Rochelle NY 10801 United States VL - 30 IS - 8 SN - 0889-2229, 0889-2229 KW - Biochemistry Abstracts 2: Nucleic Acids; Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Acquired immune deficiency syndrome KW - Genotyping KW - Assays KW - Discrimination KW - Genotypes KW - Interferon KW - Peripheral blood mononuclear cells KW - Retrovirus KW - Communications KW - Hepatitis C virus KW - Human immunodeficiency virus KW - Single-nucleotide polymorphism KW - DNA KW - Polymerase chain reaction KW - genomics KW - Hepatitis C KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22360:AIDS and HIV KW - N 14810:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768584252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Research+and+Human+Retroviruses&rft.atitle=Short+Communication%3A+Serum-Based+Assay+Accurately+Detects+Single+Nucleotide+Polymorphisms+of+IL28B+and+SOCS3+in+HIV%2FHepatitis+C+Virus-Coinfected+Subjects&rft.au=Shaffer%2C+Ashton%3BHubbard%2C+Jon+J%3BTownsend%2C+Kerry%3BKottilil%2C+Shyam%3BPolis%2C+Michael+A%3BMasur%2C+Henry%3BKohli%2C+Anita&rft.aulast=Shaffer&rft.aufirst=Ashton&rft.date=2014-08-01&rft.volume=30&rft.issue=8&rft.spage=792&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/10.1089%2Faid.2014.0028 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 14 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Interferon; Peripheral blood mononuclear cells; Single-nucleotide polymorphism; Genotyping; Polymerase chain reaction; Hepatitis C; genomics; Acquired immune deficiency syndrome; Communications; Human immunodeficiency virus; DNA; Discrimination; Assays; Genotypes; Retrovirus; Hepatitis C virus DO - http://dx.doi.org/10.1089/aid.2014.0028 ER - TY - JOUR T1 - Phagocytosis and Killing of Staphylococcus aureus by Human Neutrophils AN - 1768582624; PQ0002686528 AB - Neutrophils are essential for host defense against Staphylococcus aureus infections. Although significant progress has been made, our understanding of neutrophil interactions with S. aureus remains incomplete. To provide a more comprehensive view of this process, we investigated phagocytosis and killing of S. aureus by human neutrophils using varied assay conditions in vitro. A greater percentage of bacteria were internalized by adherent neutrophils compared to those in suspension, and, unexpectedly, uptake of S. aureus by adherent neutrophils occurred efficiently in the absence of opsonins. An antibody specific for S. aureus promoted uptake of unopsonized bacteria in suspension, but had little or no capacity to enhance phagocytosis of S. aureus opsonized with normal human serum or by adherent neutrophils. Collectively, these results indicate that assay conditions can have a significant influence on the phagocytosis and killing of S. aureus by neutrophils. More importantly, the results suggest a vaccine approach directed to enhance opsonophagocytosis alone is not sufficient to promote increased killing of S. aureus by human neutrophils. With the emergence and reemergence of antibiotic-resistant microorganisms, establishing parameters that are optimal for studying neutrophil-S. aureus interactions will pave the way towards developing immune-directed strategies for anti-staphylococcal therapies. copyright 2014 S. Karger AG, Basel JF - Journal of Innate Immunity AU - Lu, Thea AU - Porter, Adeline R AU - Kennedy, Adam D AU - Kobayashi, Scott D AU - DeLeo, Frank R AD - Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Mont., USA Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 639 EP - 649 PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland VL - 6 IS - 5 SN - 1662-811X, 1662-811X KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Neutrophils KW - Phagocytosis KW - Staphylococcus aureus KW - Antibodies KW - Leukocytes (neutrophilic) KW - opsonophagocytosis KW - Microorganisms KW - Vaccines KW - Infection KW - Opsonins KW - Opsonization KW - F 06905:Vaccines KW - J 02340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768582624?accountid=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+Innate+Immunity&rft.atitle=Phagocytosis+and+Killing+of+Staphylococcus+aureus+by+Human+Neutrophils&rft.au=Lu%2C+Thea%3BPorter%2C+Adeline+R%3BKennedy%2C+Adam+D%3BKobayashi%2C+Scott+D%3BDeLeo%2C+Frank+R&rft.aulast=Lu&rft.aufirst=Thea&rft.date=2014-08-01&rft.volume=6&rft.issue=5&rft.spage=639&rft.isbn=&rft.btitle=&rft.title=Journal+of+Innate+Immunity&rft.issn=1662811X&rft_id=info:doi/10.1159%2F000360478 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Antibodies; Microorganisms; opsonophagocytosis; Leukocytes (neutrophilic); Vaccines; Opsonins; Infection; Phagocytosis; Opsonization; Staphylococcus aureus DO - http://dx.doi.org/10.1159/000360478 ER - TY - JOUR T1 - Interleukin-23 Promotes Interferon- alpha Responsiveness in Hepatitis C Virus/HIV-Coinfected Patients AN - 1768572982; PQ0002687166 AB - Patients coinfected with HIV and hepatitis C virus (HCV) have poor to modest rates of response with interferon-based therapies, which remain a backbone of the treatment in HIV/HCV-coinfected patients. The mechanisms responsible for poor responsiveness to interferon are not well described. In this study a targeted proteomic analysis of plasma from 42 patients infected with both HIV and HCV and undergoing therapy for HCV with peginterferon and ribavirin was performed. Higher baseline plasma levels of interleukin (IL)-23 were associated with sustained virologic response. Further investigation of how IL-23 facilitates interferon (IFN) responsiveness, as evidenced by a >2-fold increase in most interferon-stimulated genes (ISGs), revealed that IL-23 indirectly enhances IFN signaling in peripheral blood mononuclear cells and HCV continuous culture system by preventing the down-regulation of the IFNAR2 receptor after exposure to IFN- alpha . These findings suggest a unique role of the IL-23 pathway in enhancing host response to type I interferons, thereby facilitating eradication of HCV. Low levels of IL-23 present in plasma of nonresponders may reflect an impaired immune state that in the case of HIV/HCV-coinfected subjects could potentially lead to disruption of TH17 CD4+ T cells. This study suggests a major role for HIV-associated immune dysregulation present in HIV-infected subjects that subsequently determines the overall responsiveness to exogenous interferon- alpha -based HCV therapy. JF - AIDS Research and Human Retroviruses AU - Odigie, Madeline AU - Osinusi, Anu AU - Barrett, Lisa AU - Townsend, Kerry AU - Wang, Honghui AU - Suffredini, Anthony F AU - Masur, Henry AU - Polis, Michael A AU - Kottilil, Shyam AD - Immunopathogenesis Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 775 EP - 782 PB - Mary Ann Liebert, Inc., 140 Huguenot Street New Rochelle NY 10801 United States VL - 30 IS - 8 SN - 0889-2229, 0889-2229 KW - Immunology Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Acquired immune deficiency syndrome KW - Helper cells KW - Ribavirin KW - Interferon KW - CD4 antigen KW - Peripheral blood mononuclear cells KW - Plasma levels KW - Retrovirus KW - Interleukin 23 KW - Continuous culture KW - Hepatitis C virus KW - Human immunodeficiency virus KW - alpha -Interferon KW - Lymphocytes T KW - Hepatitis C KW - proteomics KW - Signal transduction KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22360:AIDS and HIV KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768572982?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Research+and+Human+Retroviruses&rft.atitle=Interleukin-23+Promotes+Interferon-+alpha+Responsiveness+in+Hepatitis+C+Virus%2FHIV-Coinfected+Patients&rft.au=Odigie%2C+Madeline%3BOsinusi%2C+Anu%3BBarrett%2C+Lisa%3BTownsend%2C+Kerry%3BWang%2C+Honghui%3BSuffredini%2C+Anthony+F%3BMasur%2C+Henry%3BPolis%2C+Michael+A%3BKottilil%2C+Shyam&rft.aulast=Odigie&rft.aufirst=Madeline&rft.date=2014-08-01&rft.volume=30&rft.issue=8&rft.spage=775&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/10.1089%2Faid.2014.0003 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 22 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Interferon; Plasma levels; Peripheral blood mononuclear cells; CD4 antigen; Continuous culture; Interleukin 23; Helper cells; Ribavirin; alpha -Interferon; Lymphocytes T; proteomics; Signal transduction; Acquired immune deficiency syndrome; Human immunodeficiency virus; Hepatitis C; Retrovirus; Hepatitis C virus DO - http://dx.doi.org/10.1089/aid.2014.0003 ER - TY - JOUR T1 - Chromatin Properties of Regulatory DNA Probed by Manipulation of Transcription Factors AN - 1712777382; PQ0001969343 AB - Transcription factors (TFs) bind to DNA and regulate the transcription of nearby genes. However, only a small fraction of TF binding sites have such regulatory effects. Here we search for the predictors of functional binding sites by carrying out a systematic computational screening of a variety of contextual factors (histone modifications, nuclear lamin-bindings, and cofactor bindings). We used regression analysis to test if contextual factors are associated with upregulation or downregulation of neighboring genes following the induction or knockdown of the 9 TFs in mouse embryonic stem (ES) cells. Functional TF binding sites appeared to be either active (i.e., bound by P300, CHD7, mediator, cohesin, and SWI/SNF) or repressed (i.e., with H3K27me3 histone marks and bound by Polycomb factors). Active binding sites mediated the downregulation of nearby genes upon knocking down the activating TFs or inducing repressors. Repressed TF binding sites mediated the upregulation of nearby genes (e.g., poised developmental regulators) upon inducing TFs. In addition, repressed binding sites mediated repressive effects of TFs, identified by the downregulation of target genes after the induction of TFs or by the upregulation of target genes after the knockdown of TFs. The contextual factors associated with functions of DNA-bound TFs were used to improve the identification of candidate target genes regulated by TFs. JF - Journal of Computational Biology AU - Sharov, Alexei A AU - Nishiyama, Akira AU - Qian, Yong AU - Dudekula, Dawood B AU - Longo, Dan L AU - Schlessinger, David AU - Ko, Minoru SH AD - National Institute on Aging, National Institutes of Health, Baltimore, Maryland. PY - 2014 SP - 569 EP - 577 PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538 United States VL - 21 IS - 8 SN - 1066-5277, 1066-5277 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - chromatin modification KW - cis-regulatory module KW - embryonic stem cells KW - enhancer KW - target genes KW - transcription factor binding site KW - Histones KW - Cofactors KW - Chromatin KW - polycomb group proteins KW - Transcription factors KW - DNA KW - Regression analysis KW - Embryos KW - Computer applications KW - cohesin KW - Repressors KW - N 14820:DNA Metabolism & Structure KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712777382?accountid=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=Chromatin+Properties+of+Regulatory+DNA+Probed+by+Manipulation+of+Transcription+Factors&rft.au=Sharov%2C+Alexei+A%3BNishiyama%2C+Akira%3BQian%2C+Yong%3BDudekula%2C+Dawood+B%3BLongo%2C+Dan+L%3BSchlessinger%2C+David%3BKo%2C+Minoru+SH&rft.aulast=Sharov&rft.aufirst=Alexei&rft.date=2014-08-01&rft.volume=21&rft.issue=8&rft.spage=569&rft.isbn=&rft.btitle=&rft.title=Journal+of+Computational+Biology&rft.issn=10665277&rft_id=info:doi/10.1089%2Fcmb.2013.0126 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 41 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Cofactors; Histones; polycomb group proteins; Chromatin; Transcription factors; Regression analysis; DNA; Embryos; Computer applications; Repressors; cohesin DO - http://dx.doi.org/10.1089/cmb.2013.0126 ER - TY - JOUR T1 - A Symmetrical Fluorous Dendron-Cyanine Dye-Conjugated Bimodal Nanoprobe for Quantitative super(19)F MRI and NIR Fluorescence Bioimaging AN - 1701480790; PQ0001666976 AB - super(19)F MRI and optical imaging are two powerful noninvasive molecular imaging modalities in biomedical applications. super(19)F MRI has great potential for high resolution in vivo imaging, while fluorescent probes enable ultracontrast cellular/tissue imaging with high accuracy and sensitivity. A bimodal nanoprobe is developed, integrating the merits of super(19)F MRI and fluorescence imaging into a single synthetic molecule, which is further engineered into nanoprobe, by addressing shortcomings of conventional contrast agents to explore the quantitative super(19)F MRI and fluorescence imaging and cell tracking. Results show that this bimodal imaging nanoprobe presents high correlation of super(19)F MR signal and NIR fluorescence intensity in vitro and in vivo. Additionally, this nanoprobe enables quantitative super(19)F MR analysis, confirmed by a complementary fluorescence analysis. This unique feature can hardly be obtained by traditional super(19)F MRI contrast agents. It is envisioned that this nanoprobe can hold great potential for quantitative and sensitive multi-modal molecular imaging. super(19)F MRI and optical imaging are two powerful noninvasive molecular imaging modalities in biomedical applications. A bimodal nanoprobe incorporating a symmetrical fluorous dendron-cyanine dye single molecule is developed by addressing shortcomings of conventional contrast agents to explore the quantitative super(19)F MRI and fluorescent imaging. This nanoprobe can hold great potential for quantitative and sensitive multi-modal bioimaging. JF - Advanced Healthcare Materials AU - Wang, Zhe AU - Yue, Xuyi AU - Wang, Yu AU - Qian, Chunqi AU - Huang, Peng AU - Lizak, Marty AU - Niu, Gang AU - Wang, Fu AU - Rong, Pengfei AU - Kiesewetter, Dale O AU - Ma, Ying AU - Chen, Xiaoyuan AD - Laboratory of Molecular Imaging and Nanomedicine, National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health, Bethesda, MD, 20892, USA. Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 1326 EP - 1333 PB - John Wiley & Sons, Ltd., Baffins Lane Chichester W. Sussex PO19 1UD United Kingdom VL - 3 IS - 8 SN - 2192-2640, 2192-2640 KW - Biotechnology and Bioengineering Abstracts KW - Fluorescence KW - Magnetic resonance imaging KW - Computed tomography KW - Contrast media KW - Fluorescent indicators KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701480790?accountid=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=Advanced+Healthcare+Materials&rft.atitle=A+Symmetrical+Fluorous+Dendron-Cyanine+Dye-Conjugated+Bimodal+Nanoprobe+for+Quantitative+super%2819%29F+MRI+and+NIR+Fluorescence+Bioimaging&rft.au=Wang%2C+Zhe%3BYue%2C+Xuyi%3BWang%2C+Yu%3BQian%2C+Chunqi%3BHuang%2C+Peng%3BLizak%2C+Marty%3BNiu%2C+Gang%3BWang%2C+Fu%3BRong%2C+Pengfei%3BKiesewetter%2C+Dale+O%3BMa%2C+Ying%3BChen%2C+Xiaoyuan&rft.aulast=Wang&rft.aufirst=Zhe&rft.date=2014-08-01&rft.volume=3&rft.issue=8&rft.spage=1326&rft.isbn=&rft.btitle=&rft.title=Advanced+Healthcare+Materials&rft.issn=21922640&rft_id=info:doi/10.1002%2Fadhm.201400088 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Fluorescence; Computed tomography; Magnetic resonance imaging; Contrast media; Fluorescent indicators DO - http://dx.doi.org/10.1002/adhm.201400088 ER - TY - JOUR T1 - Teaching Genomic Counseling: Preparing the Genetic Counseling Workforce for the Genomic Era AN - 1665160282 AB - Genetic counselors have a long-standing history of working on the clinical forefront of implementing new genetic technology. Genomic sequencing is no exception. The rapid advancement of genomic sequencing technologies, including but not limited to next generation sequencing approaches, across all subspecialties of genetic counseling mandates attention to genetic counselor training at both the graduate and continuing education levels. The current era provides a tremendous opportunity for counselors to become actively involved in making genomics more accessible, engaging the population in decisions to undergo sequencing and effectively translating genomic information to promote health and well-being. In this commentary, we explore reasons why genomic sequencing warrants particular consideration and put forward strategies for training program curricula and continuing education programs to meet this need. JF - Journal of Genetic Counseling AU - Hooker, Gillian W AU - Ormond, Kelly E AU - Sweet, Kevin AU - Biesecker, Barbara B AD - Social and Behavioral Research Branch, Genetic Counseling Training Program, The Johns Hopkins School of Public Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA, Social and Behavioral Research Branch, National Human Genome Research Institute, 31 Center Dr., Room B1B36K, MSC 2073, Bethesda, MD, 20892, USA ; Department of Genetics, MS Human Genetics and Genetic Counseling Program and Stanford Center for Biomedical Ethics, Stanford University, Stanford, CA, USA ; Division of Human Genetics, Ohio State University Wexner Medical Center, Columbus, OH, USA ; Social and Behavioral Research Branch, Genetic Counseling Training Program, The Johns Hopkins School of Public Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA ; Social and Behavioral Research Branch, Genetic Counseling Training Program, The Johns Hopkins School of Public Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA; Social and Behavioral Research Branch, National Human Genome Research Institute, 31 Center Dr., Room B1B36K, MSC 2073, Bethesda, MD, 20892, USA Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 445 EP - 451 CY - New York PB - Springer Science & Business Media VL - 23 IS - 4 SN - 1059-7700 KW - Psychology KW - Continuing education KW - Counselling KW - Curriculum KW - Educational programmes KW - Genetic counselling KW - Health promotion KW - Labour force KW - Teaching KW - Technology KW - Wellbeing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665160282?accountid=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+Genetic+Counseling&rft.atitle=Teaching+Genomic+Counseling%3A+Preparing+the+Genetic+Counseling+Workforce+for+the+Genomic+Era&rft.au=Hooker%2C+Gillian+W%3BOrmond%2C+Kelly+E%3BSweet%2C+Kevin%3BBiesecker%2C+Barbara+B&rft.aulast=Hooker&rft.aufirst=Gillian&rft.date=2014-08-01&rft.volume=23&rft.issue=4&rft.spage=445&rft.isbn=&rft.btitle=&rft.title=Journal+of+Genetic+Counseling&rft.issn=10597700&rft_id=info:doi/10.1007%2Fs10897-014-9689-4 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-24 DO - http://dx.doi.org/10.1007/s10897-014-9689-4 ER - TY - JOUR T1 - Choice of method for endotoxin detection depends on nanoformulation AN - 1635024782; 21021821 AB - Aims: Many nanoparticles interfere with traditional tests to quantify endotoxin. The aim of this study was to compare the performance of limulus amoebocyte lysate (LAL) formats on clinical-grade nanoformulations, to determine whether there were disparate results among formats and to test the applicability of an alternative bioassay (the macrophage activation test [MAT]) for resolving discrepancies, if observed. Materials & methods: Clinical-grade nanoformulations were tested using turbidimetric, gel-clot and chromogenic LAL. Formulations that cause a discrepancy among LAL tests were also tested by the MAT. Results & conclusion: The gel-clot LAL method cannot be relied upon to resolve discrepancies among LAL tests for certain nanoformulations. No one LAL format was shown to be optimal for all the tested clinical-grade nanoformulations. The tested alternative bioassay (the MAT) was useful for verifying LAL findings, but only for those nanoformulations not carrying/including cytotoxic drugs. Original submitted 1 March 2013; Revised submitted 13 August 2013 JF - Nanomedicine AU - Dobrovolskaia, Marina A AU - Neun, Barry W AU - Clogston, Jeffrey D AU - Grossman, Jennifer H AU - McNeil, Scott E AD - super(1)Nanotechnology Characterization Laboratory, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, 1050 Boyles Street, Frederick, MD 21702, USA., marina@mail.nih.gov Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 1847 EP - 1856 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 9 IS - 12 SN - 1743-5889, 1743-5889 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Biotechnology and Bioengineering Abstracts KW - endotoxin KW - interference KW - in vitro assay KW - limulus amoebocyte lysate KW - lipopolysaccharide nanoparticles KW - rabbit pyrogen test KW - Endotoxins KW - Macrophages KW - Cytotoxicity KW - Limulus KW - nanoparticles KW - Drugs KW - nanotechnology KW - Cell activation KW - A 01490:Miscellaneous KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635024782?accountid=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=Choice+of+method+for+endotoxin+detection+depends+on+nanoformulation&rft.au=Dobrovolskaia%2C+Marina+A%3BNeun%2C+Barry+W%3BClogston%2C+Jeffrey+D%3BGrossman%2C+Jennifer+H%3BMcNeil%2C+Scott+E&rft.aulast=Dobrovolskaia&rft.aufirst=Marina&rft.date=2014-08-01&rft.volume=9&rft.issue=12&rft.spage=1847&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Number of references - 29 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Macrophages; Endotoxins; Cytotoxicity; Drugs; nanoparticles; Cell activation; nanotechnology; Limulus ER - TY - JOUR T1 - Farm residence and lymphohematopoietic cancers in the Iowa Women super(3)s Health Study AN - 1627967146; 20956907 AB - Background Cancer incidence in male farmers has been studied extensively; however, less is known about risk among women residing on farms or in agricultural areas, who may be exposed to pesticides by their proximity to crop fields. We extended a previous follow-up of the Iowa Women super(3)s Health Study cohort to examine farm residence and the incidence of lymphohematopoietic cancers. Further, we investigated crop acreage within 750m of residences, which has been associated with higher herbicide levels in Iowa homes. Methods We analyzed data for a cohort of 37,099 Iowa women aged 55-69 years who reported their residence location (farm, rural (not a farm), town size based on population) at enrollment in 1986. We identified incident lymphohematopoietic cancers (1986-2009) by linkage with the Iowa Cancer Registry. Using a geographic information system, we geocoded addresses and calculated acreage of pasture and row crops within 750m of homes using the 1992 National Land Cover Database. Cox regression was used to estimate hazard ratios (HR) and 95% confidence intervals (CI) in multivariate analyses of cancer risk in relation to both residence location and crop acreage. Results As found in an earlier analysis of residence location, risk of acute myeloid leukemia (AML) was higher among women living on farms (HR=2.23, 95%CI: 1.25-3.99) or rural areas (but not on a farm) (HR=1.95, 95%CI: 0.89-4.29) compared with women living in towns of >10,000 population. We observed no association between farm or rural residence and non-Hodgkin lymphoma (NHL; overall or for major subtypes) or multiple myeloma. In analyses of crop acreage, we observed no association between pasture or row crop acreage within 750m of homes and risk of leukemia overall or for the AML subtype. Chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) risk was nonsignificantly elevated among women with pasture acreage within 750m of their home (HRs for increasing tertiles=1.8, 1.8 and 1.5) and with row crop acreage within 750m (HRs for increasing tertiles of acreage=1.4, 1.5 and 1.6) compared to women with no pasture or row crop acreage, respectively. Conclusions Iowa women living on a farm or in a rural area were at increased risk of developing AML, which was not related to crop acreage near the home. Living near pasture or row crops may confer an increased risk of CLL/SLL regardless of residence location. Further investigation of specific farm-related exposures and these cancers among women living on farms and in agricultural areas is warranted. JF - Environmental Research AU - Jones, Rena R AU - Yu, Chu-Ling AU - Nuckols, John R AU - Cerhan, James R AU - Airola, Matthew AU - Ross, Julie A AU - Robien, Kim 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, Bethesda, MD, USA Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 353 EP - 361 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 133 SN - 0013-9351, 0013-9351 KW - Risk Abstracts; Environment Abstracts KW - Farm residence KW - Pesticides KW - Iowa Women super(3)s Health Study KW - GIS KW - Land use KW - Farms KW - Crop fields KW - Remote sensing KW - Herbicides KW - Pasture KW - Towns KW - Cancer KW - Crops KW - Leukemia KW - Health risks KW - Multiple myeloma KW - USA, Iowa KW - Geographic information systems KW - Lymphoma KW - Rural areas KW - ENA 06:Food & Drugs KW - R2 23050:Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627967146?accountid=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=Farm+residence+and+lymphohematopoietic+cancers+in+the+Iowa+Women+super%283%29s+Health+Study&rft.au=Jones%2C+Rena+R%3BYu%2C+Chu-Ling%3BNuckols%2C+John+R%3BCerhan%2C+James+R%3BAirola%2C+Matthew%3BRoss%2C+Julie+A%3BRobien%2C+Kim%3BWard%2C+Mary+H&rft.aulast=Jones&rft.aufirst=Rena&rft.date=2014-08-01&rft.volume=133&rft.issue=&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2014.05.028 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2015-04-16 N1 - SubjectsTermNotLitGenreText - Farms; Crop fields; Remote sensing; Herbicides; Pasture; Crops; Cancer; Towns; Health risks; Leukemia; Multiple myeloma; Geographic information systems; Lymphoma; Rural areas; USA, Iowa DO - http://dx.doi.org/10.1016/j.envres.2014.05.028 ER - TY - JOUR T1 - Polycyclic aromatic hydrocarbons in residential dust and risk of childhood acute lymphoblastic leukemia AN - 1627961892; 20956908 AB - Several polycyclic aromatic hydrocarbons (PAHs) are known or probable human carcinogens. We evaluated the relationship between PAH exposure and risk of childhood acute lymphoblastic leukemia (ALL) using concentrations in residential dust as an exposure indicator. We conducted a population-based case-control study (251 ALL cases, 306 birth-certificate controls) in Northern and Central California from 2001 to 2007. We collected residential dust using a high volume small surface sampler (HVS3) (n=185 cases, 212 controls) or by sampling from participants' household vacuum cleaners (n=66 cases, 94 controls). We evaluated log-transformed concentrations of 9 individual PAHs, the summed PAHs, and the summed PAHs weighted by their carcinogenic potency (the toxic equivalence). We calculated odds ratios (ORs) and 95% confidence intervals (CI) using logistic regression adjusting for demographic characteristics and duration between diagnosis/reference date and dust collection. Among participants with HVS3 dust, risk of ALL was not associated with increasing concentration of any PAHs based on OR perln(ng/g). Among participants with vacuum dust, we observed positive associations between ALL risk and increasing concentrations of benzo[a]pyrene (OR perln[ng/g]=1.42, 95% CI=0.95, 2.12), dibenzo[a,h]anthracene (OR=1.98, 95% CI=1.11, 3.55), benzo[k]fluoranthene (OR=1.71, 95% CI=0.91, 3.22), indeno[1,2,3-cd]pyrene (OR=1.81, 95% CI=1.04, 3.16), and the toxic equivalence (OR=2.35, 95% CI=1.18, 4.69). The increased ALL risk among participants with vacuum dust suggests that PAH exposure may increase the risk of childhood ALL; however, reasons for the different results based on HVS3 dust samples deserve further study. JF - Environmental Research AU - Deziel, N C AU - Rull, R P AU - Colt, J S AU - Reynolds, P AU - Whitehead, T P AU - Gunier, R B AU - Month AU - Taggart AU - Buffler, P AU - Ward, M H AU - Metayer, C AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 388 EP - 395 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 133 SN - 0013-9351, 0013-9351 KW - Toxicology Abstracts; Risk Abstracts; Environment Abstracts; Meteorological & Geoastrophysical Abstracts KW - ALL acute lymphoblastic leukemia KW - PAHs polycyclic aromatic hydrocarbons KW - HVS3 high volume small surface sampler KW - TEQ toxic equivalence KW - OR odds ratio KW - 95% CI 95% confidence interval KW - Polycyclic aromatic hydrocarbons KW - Childhood leukemia KW - Dust KW - Environmental exposures KW - Environmental epidemiology KW - Statistical analysis KW - Vacuum KW - Environmental research KW - Carcinogens KW - Children KW - Samplers KW - Demography KW - Leukemia KW - Carcinogenicity KW - Households KW - Acute lymphatic leukemia KW - Benzo(a)pyrene KW - USA, California KW - Sampling KW - M2 551.510.42:Air Pollution (551.510.42) 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/1627961892?accountid=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=Polycyclic+aromatic+hydrocarbons+in+residential+dust+and+risk+of+childhood+acute+lymphoblastic+leukemia&rft.au=Deziel%2C+N+C%3BRull%2C+R+P%3BColt%2C+J+S%3BReynolds%2C+P%3BWhitehead%2C+T+P%3BGunier%2C+R+B%3BMonth%3BTaggart%3BBuffler%2C+P%3BWard%2C+M+H%3BMetayer%2C+C&rft.aulast=Deziel&rft.aufirst=N&rft.date=2014-08-01&rft.volume=133&rft.issue=&rft.spage=388&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2014.04.033 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2016-11-23 N1 - SubjectsTermNotLitGenreText - Demography; Polycyclic aromatic hydrocarbons; Acute lymphatic leukemia; Vacuum; Benzo(a)pyrene; Carcinogens; Sampling; Children; Samplers; Dust; Statistical analysis; Environmental research; Leukemia; Carcinogenicity; Households; USA, California DO - http://dx.doi.org/10.1016/j.envres.2014.04.033 ER - TY - JOUR T1 - The root of reduced fertility in aged women and possible therapentic options: current status and future perspects. AN - 1561979190; 23796757 AB - It is well known that maternal ageing not only causes increased spontaneous abortion and reduced fertility, but it is also a high genetic disease risk. Although assisted reproductive technologies (ARTs) have been widely used to treat infertility, the overall success is still low. The main reasons for age-related changes include reduced follicle number, compromised oocyte quality especially aneuploidy, altered reproductive endocrinology, and increased reproductive tract defect. Various approaches for improving or treating infertility in aged women including controlled ovarian hyperstimulation with intrauterine insemination (IUI), IVF/ICSI-ET, ovarian reserve testing, preimplantation genetic diagnosis and screening (PGD/PGS), oocyte selection and donation, oocyte and ovary tissue cryopreservation before ageing, miscarriage prevention, and caloric restriction are summarized in this review. Future potential reproductive techniques for infertile older women including oocyte and zygote micromanipulations, derivation of oocytes from germ stem cells, ES cells, and iPS cells, as well as through bone marrow transplantation are discussed. Copyright © 2013 Elsevier Ltd. All rights reserved. JF - Molecular aspects of medicine AU - Qiao, Jie AU - Wang, Zhen-Bo AU - Feng, Huai-Liang AU - Miao, Yi-Liang AU - Wang, Qiang AU - Yu, Yang AU - Wei, Yan-Chang AU - Yan, Jie AU - Wang, Wei-Hua AU - Shen, Wei AU - Sun, Shao-Chen AU - Schatten, Heide AU - Sun, Qing-Yuan AD - Center of Reproductive Medicine, Department of Obstetrics and Gynecology, Peking University Third Hospital, Beijing 100191, People's Republic of China. ; State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, People's Republic of China. ; Department of Laboratory Medicine, and Obstetrics and Gynecology, New York Hospital Queens, Weill Medical College of Cornell University, New York, NY, USA. ; Reproductive Medicine Group, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Department of Obstetrics and Gynecology, Washington University School of Medicine, 660 South Euclid Ave., St. Louis, MO 63110, USA. ; Houston Fertility Institute, Tomball Regional Hospital, Tomball, TX 77375, USA. ; Laboratory of Germ Cell Biology, Department of Animal Science, Qingdao Agricultural University, Qingdao 266109, People's Republic of China. ; Department of Animal Science, Nanjing Agricultural University, Nanjing 210095, People's Republic of China. ; Department of Veterinary Pathobiology, University of Missouri, Columbia, MO 65211, USA. ; State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, People's Republic of China. Electronic address: sunqy@ioz.ac.cn. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 54 EP - 85 VL - 38 KW - Index Medicus KW - Infertility KW - Maternal age KW - Assited reproductive technology KW - Ovary KW - Oocyte KW - Maternal Age KW - Humans KW - Female KW - Bone Marrow Transplantation KW - Aging -- physiology KW - Infertility, Female -- therapy KW - Reproductive Techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1561979190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+aspects+of+medicine&rft.atitle=The+root+of+reduced+fertility+in+aged+women+and+possible+therapentic+options%3A+current+status+and+future+perspects.&rft.au=Qiao%2C+Jie%3BWang%2C+Zhen-Bo%3BFeng%2C+Huai-Liang%3BMiao%2C+Yi-Liang%3BWang%2C+Qiang%3BYu%2C+Yang%3BWei%2C+Yan-Chang%3BYan%2C+Jie%3BWang%2C+Wei-Hua%3BShen%2C+Wei%3BSun%2C+Shao-Chen%3BSchatten%2C+Heide%3BSun%2C+Qing-Yuan&rft.aulast=Qiao&rft.aufirst=Jie&rft.date=2014-08-01&rft.volume=38&rft.issue=&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=Molecular+aspects+of+medicine&rft.issn=1872-9452&rft_id=info:doi/10.1016%2Fj.mam.2013.06.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-30 N1 - Date created - 2014-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.mam.2013.06.001 ER - TY - JOUR T1 - Identification of Three Noncontiguous Regions on Bacillus anthracis Plasmid pXO1 That Are Important for Its Maintenance AN - 1560139502; 20602765 AB - Bacillus anthracis pXO1 minireplicon (MR) plasmid consisting of open reading frames (ORFs) GBAA_pXO1_0020 to GBAA_pXO1_0023 is not stably maintained in B. anthracis, whereas the full-size parent pXO1 plasmid (having 181,677 bp and 217 ORFs) is extremely stable under the same growth conditions. Two genetic tools developed for DNA manipulation in B. anthracis (Cre-loxP and Flp-FRT systems) were used to identify pXO1 regions important for plasmid stability. We localized a large segment of pXO1 that enables stable plasmid maintenance during vegetative growth. Further genetic analysis identified three genes that are necessary for pXO1 maintenance: amsP (GBAA_pXO1_0069), minP (GBAA_pXO1_0082), and sojP (GBAA_pXO1_0084). Analysis of conserved domains in the corresponding proteins indicated that only AmsP (activator of maintenance system of pXO1) is predicted to bind DNA, due to its strong helix-turn-helix domain. Two conserved domains were found in the MinP protein (Min protein from pXO1): an N-terminal domain having some similarity to the B. anthracis septum site-determining protein MinD and a C-terminal domain that resembles a baculovirus single-stranded-DNA-binding protein. The SojP protein (Soj from pXO1) contains putative Walker box motifs and belongs to the ParA family of ATPases. No sequences encoding other components of type I plasmid partition systems, namely, cis-acting centromere parS and its binding ParB protein, were identified within the pXO1 genome. A model describing the role of the MinP protein in pXO1 distribution between daughter cells is proposed. JF - Journal of Bacteriology AU - Pomerantsev, Andrei P AU - Chang, Zanetta AU - Rappole, Catherine AU - Leppla, Stephen H Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 2921 EP - 2933 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 196 IS - 16 SN - 0021-9193, 0021-9193 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - Genomes KW - Adenosinetriphosphatase KW - Min protein KW - Growth conditions KW - Genetic analysis KW - ParB protein KW - Bacillus anthracis KW - Plasmids KW - Centromeres KW - DNA KW - Septum KW - Baculovirus KW - Open reading frames KW - J 02320:Cell Biology KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560139502?accountid=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=Identification+of+Three+Noncontiguous+Regions+on+Bacillus+anthracis+Plasmid+pXO1+That+Are+Important+for+Its+Maintenance&rft.au=Pomerantsev%2C+Andrei+P%3BChang%2C+Zanetta%3BRappole%2C+Catherine%3BLeppla%2C+Stephen+H&rft.aulast=Pomerantsev&rft.aufirst=Andrei&rft.date=2014-08-01&rft.volume=196&rft.issue=16&rft.spage=2921&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.01747-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 36 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Genomes; Adenosinetriphosphatase; Min protein; Growth conditions; Genetic analysis; DNA; ParB protein; Septum; Plasmids; Open reading frames; Centromeres; Baculovirus; Bacillus anthracis DO - http://dx.doi.org/10.1128/JB.01747-14 ER - TY - JOUR T1 - Lysine ubiquitination and acetylation of human cardiac 20S proteasomes AN - 1560119237; 20584499 AB - Purpose Altered proteasome functions are associated with multiple cardiomyopathies. While the proteasome targets polyubiquitinated proteins for destruction, it itself is modifiable by ubiquitination. We aim to identify the exact ubiquitination sites on cardiac proteasomes and examine whether they are also subject to acetylations. Experimental design Assembled cardiac 20S proteasome complexes were purified from five human hearts with ischemic cardiomyopathy, then analyzed by high-resolution MS to identify ubiquitination and acetylation sites. We developed a library search strategy that may be used to complement database search in identifying PTM in different samples. Results We identified 63 ubiquitinated lysines from intact human cardiac 20S proteasomes. In parallel, 65 acetylated residues were also discovered, 39 of which shared with ubiquitination sites. Conclusion and clinical relevance This is the most comprehensive characterization of cardiac proteasome ubiquitination to date. There are significant overlaps between the discovered ubiquitination and acetylation sites, permitting potential crosstalk in regulating proteasome functions. The information presented here will aid future therapeutic strategies aimed at regulating the functions of cardiac proteasomes. JF - Proteomics Clinical Applications AU - Zong, Nobel AU - Ping, Peipei AU - Lau, Edward AU - Choi, Howard JH AU - Ng, Dominic CM AU - Meyer, David AU - Fang, Caiyun AU - Li, Haomin AU - Wang, Ding AU - Zelaya, Ivette M AU - Yates, John R AU - Lam, Maggie PY AD - The NHLBI Proteomics Center at UCLA, Los Angeles, CA, USA. Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 590 EP - 594 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 8 IS - 7-8 SN - 1862-8346, 1862-8346 KW - Biotechnology and Bioengineering Abstracts KW - Heart KW - ubiquitination KW - Acetylation KW - Cardiomyopathy KW - Databases KW - proteasomes KW - Lysine KW - Therapeutic applications KW - Ischemia KW - proteomics KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560119237?accountid=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=Lysine+ubiquitination+and+acetylation+of+human+cardiac+20S+proteasomes&rft.au=Zong%2C+Nobel%3BPing%2C+Peipei%3BLau%2C+Edward%3BChoi%2C+Howard+JH%3BNg%2C+Dominic+CM%3BMeyer%2C+David%3BFang%2C+Caiyun%3BLi%2C+Haomin%3BWang%2C+Ding%3BZelaya%2C+Ivette+M%3BYates%2C+John+R%3BLam%2C+Maggie+PY&rft.aulast=Zong&rft.aufirst=Nobel&rft.date=2014-08-01&rft.volume=8&rft.issue=7-8&rft.spage=590&rft.isbn=&rft.btitle=&rft.title=Proteomics+Clinical+Applications&rft.issn=18628346&rft_id=info:doi/10.1002%2Fprca.201400029 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-09-05 N1 - SubjectsTermNotLitGenreText - Heart; Databases; Cardiomyopathy; Acetylation; ubiquitination; proteasomes; Therapeutic applications; Lysine; proteomics; Ischemia DO - http://dx.doi.org/10.1002/prca.201400029 ER - TY - JOUR T1 - Characterization of human plasma proteome dynamics using deuterium oxide AN - 1560117667; 20584495 AB - Purpose High-throughput quantification of human protein turnover via in vivo administration of deuterium oxide ( super(2)H sub(2)O) is a powerful new approach to examine potential disease mechanisms. Its immediate clinical translation is contingent upon characterizations of the safety and hemodynamic effects of in vivo administration of super(2)H sub(2)O to human subjects. Experimental design We recruited ten healthy human subjects with a broad demographic variety to evaluate the safety, feasibility, efficacy, and reproducibility of super(2)H sub(2)O intake for studying protein dynamics. We designed a protocol where each subject orally consumed weight-adjusted doses of 70% super(2)H sub(2)O daily for 14 days to enrich body water and proteins with deuterium. Plasma proteome dynamics was measured using a high-resolution MS method we recently developed. Results This protocol was successfully applied in ten human subjects to characterize the endogenous turnover rates of 542 human plasma proteins, the largest such human dataset to-date. Throughout the study, we did not detect physiological effects or signs of discomfort from super(2)H sub(2)O consumption. Conclusions and clinical relevance Our investigation supports the utility of a super(2)H sub(2)O intake protocol that is safe, accessible, and effective for clinical investigations of large-scale human protein turnover dynamics. This workflow shows promising clinical translational value for examining plasma protein dynamics in human diseases. JF - Proteomics Clinical Applications AU - Wang, Ding AU - Liem, David A AU - Lau, Edward AU - Ng, Dominic CM AU - Bleakley, Brian J AU - Cadeiras, Martin AU - Deng, Mario C AU - Lam, Maggie PY AU - Ping, Peipei AD - The NHLBI Proteomics Center at UCLA, Los Angeles, CA, USA. Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 610 EP - 619 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 8 IS - 7-8 SN - 1862-8346, 1862-8346 KW - Biotechnology and Bioengineering Abstracts KW - Plasma proteins KW - Demography KW - Translation KW - Protein turnover KW - oxides KW - Hemodynamics KW - Therapeutic applications KW - Body water KW - proteomics KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560117667?accountid=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=Characterization+of+human+plasma+proteome+dynamics+using+deuterium+oxide&rft.au=Wang%2C+Ding%3BLiem%2C+David+A%3BLau%2C+Edward%3BNg%2C+Dominic+CM%3BBleakley%2C+Brian+J%3BCadeiras%2C+Martin%3BDeng%2C+Mario+C%3BLam%2C+Maggie+PY%3BPing%2C+Peipei&rft.aulast=Wang&rft.aufirst=Ding&rft.date=2014-08-01&rft.volume=8&rft.issue=7-8&rft.spage=610&rft.isbn=&rft.btitle=&rft.title=Proteomics+Clinical+Applications&rft.issn=18628346&rft_id=info:doi/10.1002%2Fprca.201400038 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-09-05 N1 - SubjectsTermNotLitGenreText - Demography; Plasma proteins; Translation; Therapeutic applications; Hemodynamics; oxides; Protein turnover; Body water; proteomics DO - http://dx.doi.org/10.1002/prca.201400038 ER - TY - JOUR T1 - A Rapid Matrix-Assisted Laser Desorption Ionization-Time of Flight Mass Spectrometry-Based Method for Single-Plasmid Tracking in an Outbreak of Carbapenem-Resistant Enterobacteriaceae AN - 1560115334; 20602801 AB - Carbapenem-resistant Enterobacteriaceae (CRE) have spread globally and represent a serious and growing threat to public health. Rapid methods for tracking plasmids carrying carbapenemase genes could greatly benefit infection control efforts. Here, we demonstrate that real-time, direct tracking of a single plasmid in a bacterial strain responsible for an outbreak is possible using a commercial matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) system. In this case, we retrospectively tracked the blaKPC carbapenemase gene-bearing pKpQIL plasmid responsible for a CRE outbreak that occurred at the NIH Clinical Center in 2011. An similar to 11,109-Da MS peak corresponding to a gene product of the blaKPC pKpQIL plasmid was identified and characterized using a combination of proteomics and molecular techniques. This plasmid peak was present in spectra from retrospectively analyzed K. pneumoniae outbreak isolates, concordant with results from whole-genome sequencing, and absent from a diverse control set of blaKPC-negative clinical Enterobacteriaceae isolates. Notably, the gene characterized here is located adjacent to the blaKPC Tn4401 transposon on the pKpQIL plasmid. Sequence analysis demonstrates the presence of this gene in other blaKPC Tn4401-containing plasmids and suggests that this signature MS peak may be useful in tracking other plasmids conferring carbapenem resistance. Plasmid identification using this MALDI-TOF MS method was accomplished in as little as 10 min from isolated colonies and 30 min from positive (spiked) blood cultures, demonstrating the potential clinical utility for real-time plasmid tracking in an outbreak. JF - Journal of Clinical Microbiology AU - Lau, Anna F AU - Wang, Honghui AU - Weingarten, Rebecca A AU - Drake, Steven K AU - Suffredini, Anthony F AU - Garfield, Mark K AU - Chen, Yong AU - Gucek, Marjan AU - Youn, Jung-Ho AU - Stock, Frida AD - Microbiology Service, Department of Laboratory Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland, USA, john.dekker@nih.gov. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 2804 EP - 2812 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 52 IS - 8 SN - 0095-1137, 0095-1137 KW - Health & Safety Science Abstracts; Microbiology Abstracts B: Bacteriology KW - Blood culture KW - Mass spectrometry KW - Carbapenems KW - carbapenemase KW - Plasmids KW - Infection KW - Mass spectroscopy KW - Public health KW - Flight KW - Transposons KW - Colonies KW - Lasers KW - Outbreaks KW - proteomics KW - Enterobacteriaceae KW - Klebsiella pneumoniae KW - H 12000:Epidemiology and Public Health KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560115334?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=A+Rapid+Matrix-Assisted+Laser+Desorption+Ionization-Time+of+Flight+Mass+Spectrometry-Based+Method+for+Single-Plasmid+Tracking+in+an+Outbreak+of+Carbapenem-Resistant+Enterobacteriaceae&rft.au=Lau%2C+Anna+F%3BWang%2C+Honghui%3BWeingarten%2C+Rebecca+A%3BDrake%2C+Steven+K%3BSuffredini%2C+Anthony+F%3BGarfield%2C+Mark+K%3BChen%2C+Yong%3BGucek%2C+Marjan%3BYoun%2C+Jung-Ho%3BStock%2C+Frida&rft.aulast=Lau&rft.aufirst=Anna&rft.date=2014-08-01&rft.volume=52&rft.issue=8&rft.spage=2804&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/10.1128%2FJCM.00694-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 45 N1 - Last updated - 2016-07-20 N1 - SubjectsTermNotLitGenreText - Transposons; Flight; Blood culture; Colonies; Carbapenems; carbapenemase; Lasers; proteomics; Infection; Plasmids; Mass spectroscopy; Public health; Mass spectrometry; Outbreaks; Enterobacteriaceae; Klebsiella pneumoniae DO - http://dx.doi.org/10.1128/JCM.00694-14 ER - TY - JOUR T1 - Plasmodium falciparum Founder Populations in Western Cambodia Have Reduced Artemisinin Sensitivity In Vitro AN - 1560113395; 20602567 AB - Reduced Plasmodium falciparum sensitivity to short-course artemisinin (ART) monotherapy manifests as a long parasite clearance half-life. We recently defined three parasite founder populations with long half-lives in Pursat, western Cambodia, where reduced ART sensitivity is prevalent. Using the ring-stage survival assay, we show that these founder populations have reduced ART sensitivity in vitro at the early ring stage of parasite development and that a genetically admixed population contains subsets of parasites with normal or reduced ART sensitivity. JF - Antimicrobial Agents & Chemotherapy AU - Amaratunga, Chanaki AU - Witkowski, Benoit AU - Dek, Dalin AU - Try, Vorleak AU - Khim, Nimol AU - Miotto, Olivo AU - Menard, Didier AU - Fairhurst, Rick M AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, rfairhurst@niaid.nih.gov. Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 4935 EP - 4937 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 58 IS - 8 SN - 0066-4804, 0066-4804 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Parasites KW - Population genetics KW - Developmental stages KW - Survival KW - artemisinin KW - Plasmodium falciparum KW - K 03340:Effects of Physical & Chemical Factors KW - A 01340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560113395?accountid=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=Plasmodium+falciparum+Founder+Populations+in+Western+Cambodia+Have+Reduced+Artemisinin+Sensitivity+In+Vitro&rft.au=Amaratunga%2C+Chanaki%3BWitkowski%2C+Benoit%3BDek%2C+Dalin%3BTry%2C+Vorleak%3BKhim%2C+Nimol%3BMiotto%2C+Olivo%3BMenard%2C+Didier%3BFairhurst%2C+Rick+M&rft.aulast=Amaratunga&rft.aufirst=Chanaki&rft.date=2014-08-01&rft.volume=58&rft.issue=8&rft.spage=4935&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.03055-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 19 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Population genetics; Parasites; Survival; Developmental stages; artemisinin; Plasmodium falciparum DO - http://dx.doi.org/10.1128/AAC.03055-14 ER - TY - JOUR T1 - Retirement of Hugh A. Tilson AN - 1560113185; 20594452 JF - Environmental Health Perspectives AU - Birnbaum, Linda S AU - Woychik, Rick AD - National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA Y1 - 2014/08/01/ PY - 2014 DA - 2014 Aug 01 SP - A202 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 122 IS - 8 SN - 0091-6765, 0091-6765 KW - Environment Abstracts; Health & Safety Science Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560113185?accountid=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=Retirement+of+Hugh+A.+Tilson&rft.au=Birnbaum%2C+Linda+S%3BWoychik%2C+Rick&rft.aulast=Birnbaum&rft.aufirst=Linda&rft.date=2014-08-01&rft.volume=122&rft.issue=8&rft.spage=A202&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1408939 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-09-05 DO - http://dx.doi.org/10.1289/ehp.1408939 ER - TY - JOUR T1 - Flow Cytometry-Based Analysis of Artemisinin-Resistant Plasmodium falciparum in the Ring-Stage Survival Assay AN - 1560112058; 20602558 AB - The ring-stage survival assay (RSA) is a powerful tool for phenotyping artemisinin-resistant Plasmodium falciparum but requires experienced microscopists to count viable parasites among 10,000 erythrocytes in Giemsa-stained thin blood smears. Here we describe a rapid flow cytometric assay that accurately counts viable parasites among 250,000 erythrocytes in suspension. This method performs as well as light microscopy and can be used to standardize the collection of RSA data between research groups in laboratory and field settings. JF - Antimicrobial Agents & Chemotherapy AU - Amaratunga, Chanaki AU - Neal, Aaron T AU - Fairhurst, Rick M Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 4938 EP - 4940 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 58 IS - 8 SN - 0066-4804, 0066-4804 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Flow cytometry KW - Parasites KW - Blood KW - Phenotyping KW - Data processing KW - Erythrocytes KW - Survival KW - Plasmodium falciparum KW - A 01340:Antibiotics & Antimicrobials KW - K 03420:Plant Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560112058?accountid=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=Flow+Cytometry-Based+Analysis+of+Artemisinin-Resistant+Plasmodium+falciparum+in+the+Ring-Stage+Survival+Assay&rft.au=Amaratunga%2C+Chanaki%3BNeal%2C+Aaron+T%3BFairhurst%2C+Rick+M&rft.aulast=Amaratunga&rft.aufirst=Chanaki&rft.date=2014-08-01&rft.volume=58&rft.issue=8&rft.spage=4938&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.02902-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 14 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Flow cytometry; Phenotyping; Blood; Parasites; Data processing; Erythrocytes; Survival; Plasmodium falciparum DO - http://dx.doi.org/10.1128/AAC.02902-14 ER - TY - JOUR T1 - Repurposing of Clinically Developed Drugs for Treatment of Middle East Respiratory Syndrome Coronavirus Infection AN - 1560106868; 20602565 AB - Outbreaks of emerging infections present health professionals with the unique challenge of trying to select appropriate pharmacologic treatments in the clinic with little time available for drug testing and development. Typically, clinicians are left with general supportive care and often untested convalescent-phase plasma as available treatment options. Repurposing of approved pharmaceutical drugs for new indications presents an attractive alternative to clinicians, researchers, public health agencies, drug developers, and funding agencies. Given the development times and manufacturing requirements for new products, repurposing of existing drugs is likely the only solution for outbreaks due to emerging viruses. In the studies described here, a library of 290 compounds was screened for antiviral activity against Middle East respiratory syndrome coronavirus (MERS-CoV) and severe acute respiratory syndrome coronavirus (SARS-CoV). Selection of compounds for inclusion in the library was dependent on current or previous FDA approval or advanced clinical development. Some drugs that had a well-defined cellular pathway as target were included. In total, 27 compounds with activity against both MERS-CoV and SARS-CoV were identified. The compounds belong to 13 different classes of pharmaceuticals, including inhibitors of estrogen receptors used for cancer treatment and inhibitors of dopamine receptor used as antipsychotics. The drugs identified in these screens provide new targets for in vivo studies as well as incorporation into ongoing clinical studies. JF - Antimicrobial Agents & Chemotherapy AU - Dyall, Julie AU - Coleman, Christopher M AU - Hart, Brit J AU - Venkataraman, Thiagarajan AU - Holbrook, Michael R AU - Kindrachuk, Jason AU - Johnson, Reed F AU - Olinger, Gene G, Jr AU - Jahrling, Peter B AU - Laidlaw, Monique AD - Integrated Research Facility, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, USA, MFrieman@som.umaryland.edu. Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 4885 EP - 4893 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 58 IS - 8 SN - 0066-4804, 0066-4804 KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Severe acute respiratory syndrome KW - Drug development KW - Infection KW - Dopamine receptors KW - Antiviral activity KW - Cancer KW - Public health KW - Antiviral agents KW - Neuroleptics KW - Pharmaceuticals KW - Estrogen receptors KW - SARS coronavirus KW - A 01340:Antibiotics & Antimicrobials KW - V 22410:Animal Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560106868?accountid=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=Repurposing+of+Clinically+Developed+Drugs+for+Treatment+of+Middle+East+Respiratory+Syndrome+Coronavirus+Infection&rft.au=Dyall%2C+Julie%3BColeman%2C+Christopher+M%3BHart%2C+Brit+J%3BVenkataraman%2C+Thiagarajan%3BHolbrook%2C+Michael+R%3BKindrachuk%2C+Jason%3BJohnson%2C+Reed+F%3BOlinger%2C+Gene+G%2C+Jr%3BJahrling%2C+Peter+B%3BLaidlaw%2C+Monique&rft.aulast=Dyall&rft.aufirst=Julie&rft.date=2014-08-01&rft.volume=58&rft.issue=8&rft.spage=4885&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.03036-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 48 N1 - Last updated - 2014-12-11 N1 - SubjectsTermNotLitGenreText - Antiviral agents; Neuroleptics; Severe acute respiratory syndrome; Pharmaceuticals; Drug development; Antiviral activity; Dopamine receptors; Infection; Estrogen receptors; Cancer; Public health; SARS coronavirus DO - http://dx.doi.org/10.1128/AAC.03036-14 ER - TY - JOUR T1 - Threshold and subthreshold generalized anxiety disorder among US adolescents: prevalence, sociodemographic, and clinical characteristics AN - 1558992596; 201428182 AB - Threshold and subthreshold forms of generalized anxiety disorder (GAD) are highly prevalent and impairing conditions among adults. However, there are few general population studies that have examined these conditions during the early life course. The primary objectives of this study were to: (1) examine the prevalence, and sociodemographic and clinical characteristics of threshold and subthreshold forms of GAD in a nationally representative sample of US youth; and (2) test differences in sociodemographic and clinical characteristics between threshold and subthreshold forms of the disorder. The National Comorbidity Survey-Adolescent Supplement is a nationally representative face-to-face survey of 10 123 adolescents 13 to 18 years of age in the continental USA. Approximately 3% of adolescents met criteria for threshold GAD. Reducing the required duration from 6 months to 3 months resulted in a 65.7% increase in prevalence (5.0%); further relaxing the uncontrollability criterion led to an additional 20.7% increase in prevalence (6.1%). Adolescents with all forms of GAD displayed a recurrent clinical course marked by substantial impairment and co-morbidity with other psychiatric disorders. There were few significant differences in sociodemographic and clinical characteristics between threshold and subthreshold cases of GAD. Results also revealed age-related differences in the associated symptoms and clinical course of GAD. Findings demonstrate the clinical significance of subthreshold forms of GAD among adolescent youth, highlighting the continuous nature of the GAD construct. Age-related differences in the associated symptoms and clinical course of GAD provide further support for criteria that capture variation in clinical features across development. Adapted from the source document. JF - Psychological Medicine AU - Burstein, M AU - Beesdo-Baum, K AU - He, J.-P. AU - Merikangas, K R AD - Genetic Epidemiology Research Branch, National Institute of Mental Health, Bethesda, MD, USA Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 2351 EP - 2362 PB - Cambridge University Press, UK VL - 44 IS - 11 SN - 0033-2917, 0033-2917 KW - Generalized anxiety disorders KW - Sociodemographic aspects KW - Comorbidity KW - Adolescents KW - Thresholds KW - Prevalence KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558992596?accountid=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=Threshold+and+subthreshold+generalized+anxiety+disorder+among+US+adolescents%3A+prevalence%2C+sociodemographic%2C+and+clinical+characteristics&rft.au=Burstein%2C+M%3BBeesdo-Baum%2C+K%3BHe%2C+J.-P.%3BMerikangas%2C+K+R&rft.aulast=Burstein&rft.aufirst=M&rft.date=2014-08-01&rft.volume=44&rft.issue=11&rft.spage=2351&rft.isbn=&rft.btitle=&rft.title=Psychological+Medicine&rft.issn=00332917&rft_id=info:doi/10.1017%2FS0033291713002997 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-09-01 N1 - Number of references - 43 N1 - Last updated - 2016-09-27 N1 - CODEN - PSMDCO N1 - SubjectsTermNotLitGenreText - Generalized anxiety disorders; Thresholds; Adolescents; Prevalence; Sociodemographic aspects; Comorbidity DO - http://dx.doi.org/10.1017/S0033291713002997 ER - TY - JOUR T1 - Longitudinal relationship between drinking with peers, descriptive norms, and adolescent alcohol use AN - 1556285609; 4591076 AB - Descriptive norms are consistently found to predict adolescent alcohol use but less is known about the factors that predict descriptive norms. The objective of this study is to test if drinking with peers predicts later alcohol consumption and if this relationship is mediated by a change in the descriptive norms of peer alcohol use. Data are from a nationally representative cohort of high school students surveyed in the 10th and 11th grade ( Italic N = 2,162). Structural equation modeling was used to test a mediation model of the relationship between drinking with peers (T1) on later alcohol use (T2) and mediation of the relationship by descriptive norms (T2). Descriptive norms significantly mediated the relationship between drinking with peers and alcohol use for both males and females with a somewhat larger effect for males compared to females. These results support a continued focus on the development and evaluation of interventions to alter descriptive norms of alcohol use. Reprinted by permission of Springer JF - Prevention science AU - Brooks-Russell, Ashley AU - Simons-Morton, Bruce AU - Haynie, Denise AU - Farhat, Tilda AU - Wang, Jing AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 497 EP - 505 VL - 15 IS - 4 SN - 1389-4986, 1389-4986 KW - Sociology KW - Alcohol KW - Peer groups KW - Structural analysis KW - Adolescents KW - Interventionism KW - Mediation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556285609?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Prevention+science&rft.atitle=Longitudinal+relationship+between+drinking+with+peers%2C+descriptive+norms%2C+and+adolescent+alcohol+use&rft.au=Brooks-Russell%2C+Ashley%3BSimons-Morton%2C+Bruce%3BHaynie%2C+Denise%3BFarhat%2C+Tilda%3BWang%2C+Jing&rft.aulast=Brooks-Russell&rft.aufirst=Ashley&rft.date=2014-08-01&rft.volume=15&rft.issue=4&rft.spage=497&rft.isbn=&rft.btitle=&rft.title=Prevention+science&rft.issn=13894986&rft_id=info:doi/10.1007%2Fs11121-013-0391-9 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-08-26 N1 - Last updated - 2014-08-27 N1 - SubjectsTermNotLitGenreText - 7869 2703 2698; 909; 9347; 12320 971; 6828 7869 2703 2698 5200 5574 10472; 593 DO - http://dx.doi.org/10.1007/s11121-013-0391-9 ER - TY - JOUR T1 - Estimating the burden of pertussis in Mexican adolescents from paired serological data by using a bivariate mixture model AN - 1556285182; 4591115 AB - In recent decades there has been an increase in the reported incidence of clinical pertussis in many countries. Estimation of the true circulation of the bacterium Bordetella pertussis is most reliably made on the basis of studies that measure antibody concentrations against pertussis toxin. Antibody levels decay over time and provide a fading memory of the infection. We develop a discrete bivariate mixture model for paired antibody levels in a cohort of 1002 Mexican adolescents who were followed over the 2008-2009 school year. This model postulates three groups of children based on past pertussis infection; never, prior and new. On the basis of this model we directly estimate incidence and prevalence, and select a diagnostic cut-off for classifying children as recently infected. We also discuss a relatively simple approach that uses only 'discordant' children who test positively on one visit and negatively on the other. The discordant approach provides inferences that are very similar to those of the full model when the data follow the assumed full model. Additionally, the discordant method is much more robust to model misspecification than the full model which has substantial problems with optimization. We estimate the school year incidence of pertussis to be about 3% and the prevalence to be about 8%. A cut-off of 50 was estimated to have about 99.5% specificity and 68% sensitvity. Reprinted by permission of Blackwell Publishers JF - Journal of the Royal Statistical Society AU - Gabrielle Breugelmans, J AU - Rosales Pedraza, Gustave AU - Gessner, Bradford D AU - Ruiz-Palacios, Guillermo M AU - Follmann, Dean AU - Qin, Jing AU - Lourdes Guerrero, M AD - National Institute of Allergy and Infectious Diseases ; Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 621 EP - 637 VL - 63 IS - 4 SN - 0035-9254, 0035-9254 KW - Economics KW - Memory KW - Mexico KW - Schools KW - Estimation KW - Children KW - Serology KW - Adolescents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556285182?accountid=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=Estimating+the+burden+of+pertussis+in+Mexican+adolescents+from+paired+serological+data+by+using+a+bivariate+mixture+model&rft.au=Gabrielle+Breugelmans%2C+J%3BRosales+Pedraza%2C+Gustave%3BGessner%2C+Bradford+D%3BRuiz-Palacios%2C+Guillermo+M%3BFollmann%2C+Dean%3BQin%2C+Jing%3BLourdes+Guerrero%2C+M&rft.aulast=Gabrielle+Breugelmans&rft.aufirst=J&rft.date=2014-08-01&rft.volume=63&rft.issue=4&rft.spage=621&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Royal+Statistical+Society&rft.issn=00359254&rft_id=info:doi/10.1111%2Frssc.12051 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-08-26 N1 - Last updated - 2014-08-27 N1 - SubjectsTermNotLitGenreText - 4403 7854; 2212; 7930; 593; 11324; 11525 9507 1077; 251 293 14 DO - http://dx.doi.org/10.1111/rssc.12051 ER - TY - JOUR T1 - Developing estimates of frequency and intensity of exposure to three types of metalworking fluids in a population-based case-control study of bladder cancer AN - 1554955814; 20446176 AB - Background A systematic, transparent, and data-driven approach was developed to estimate frequency and intensity of exposure to straight, soluble, and synthetic/semi-synthetic metalworking fluids (MWFs) within a case-control study of bladder cancer in New England. Methods We assessed frequency using individual-level information from job-specific questionnaires wherever possible, then derived and applied job group-level patterns to likely exposed jobs with less information. Intensity estimates were calculated using a statistical model developed from measurements and determinants extracted from the published literature. Results For jobs with probabilities of exposure greater than or equal to 0.5, median frequencies were 8-10hr/week, depending on MWF type. Median intensities for these jobs were 2.5, 2.1, and 1.0mg/m super(3) for soluble, straight, and synthetic/semi-synthetic MWFs, respectively. Conclusions Compared to case-by-case assessment, these data-driven decision rules are transparent and reproducible and may result in less biased estimates. These rules can also aid future exposure assessments of MWFs in population-based studies. Am. J. Ind. Med. 57:915-927, 2014. copyright 2014 Wiley Periodicals, Inc. JF - American Journal of Industrial Medicine AU - Friesen, Melissa C AU - Park, Dong-Uk AU - Colt, Joanne S AU - Baris, Dalsu AU - Schwenn, Molly AU - Karagas, Margaret R AU - Armenti, Karla R AU - Johnson, Alison AU - Silverman, Debra T AU - Stewart, Patricia A AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Rockville, Maryland. Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 915 EP - 927 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 57 IS - 8 SN - 0271-3586, 0271-3586 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Inventories KW - Mathematical models KW - USA, New England KW - Urinary bladder KW - Statistical analysis KW - Population studies KW - Metal-working fluids KW - Cancer KW - Models KW - X 24360:Metals KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554955814?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Industrial+Medicine&rft.atitle=Developing+estimates+of+frequency+and+intensity+of+exposure+to+three+types+of+metalworking+fluids+in+a+population-based+case-control+study+of+bladder+cancer&rft.au=Friesen%2C+Melissa+C%3BPark%2C+Dong-Uk%3BColt%2C+Joanne+S%3BBaris%2C+Dalsu%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BArmenti%2C+Karla+R%3BJohnson%2C+Alison%3BSilverman%2C+Debra+T%3BStewart%2C+Patricia+A&rft.aulast=Friesen&rft.aufirst=Melissa&rft.date=2014-08-01&rft.volume=57&rft.issue=8&rft.spage=915&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Industrial+Medicine&rft.issn=02713586&rft_id=info:doi/10.1002%2Fajim.22328 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-11-12 N1 - SubjectsTermNotLitGenreText - Inventories; Mathematical models; Urinary bladder; Statistical analysis; Population studies; Cancer; Models; Metal-working fluids; USA, New England DO - http://dx.doi.org/10.1002/ajim.22328 ER - TY - JOUR T1 - Lung tumors in mice induced by "whole-life" inorganic arsenic exposure at human-relevant doses AN - 1554949668; 20489398 AB - In mice, inorganic arsenic in the drinking water in the parts per million range via the dam during in utero life or with whole-life exposure is a multi-site carcinogen in the offspring. However, human arsenic exposure is typically in the parts per billion (ppb) range. Thus, we studied "whole-life" inorganic arsenic carcinogenesis in mice at levels more relevant to humans. Breeder male and female CD1 mice were exposed to 0, 50, 500 or 5,000 ppb arsenic (as sodium arsenite) in the drinking water for 3 weeks prior to breeding, during pregnancy and lactation, and after weaning (at week 3) groups of male and female offspring (initial n = 40) were exposed for up to 2 years. Tumors were assessed in these offspring. Arsenic exposure had no effect on pregnant dam weights or water consumption, litter size, offspring birthweight or weight at weaning compared to control. In male offspring mice, arsenic exposure increased (p < 0.05) bronchiolo-alveolar tumor (adenoma or carcinoma) incidence at 50-ppb group (51 %) and 500-ppb group (54 %), but not at 5,000-ppb group (28 %) compared to control (22 %). These arsenic-induced bronchiolo-alveolar tumors included increased (p < 0.05) carcinoma at 50-ppb group (27 %) compared to controls (8 %). An increase (p < 0.05) in lung adenoma (25 %) in the 50-ppb group compared to control (11 %) occurred in female offspring. Thus, in CD1 mice whole-life arsenic exposure induced lung tumors at human-relevant doses (i.e., 50 and 500 ppb). JF - Archives of Toxicology AU - Waalkes, Michael P AU - Qu, Wei AU - Tokar, Erik J AU - Kissling, Grace E AU - Dixon, Darlene AD - Inorganic Toxicology Group, National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, 111 Alexander Drive, MD E1-07, P.O. Box 12233, Research Triangle Park, NC, 27709, USA, waalkes@niehs.nih.gov Y1 - 2014/08// PY - 2014 DA - Aug 2014 SP - 1619 EP - 1629 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 88 IS - 8 SN - 0340-5761, 0340-5761 KW - Toxicology Abstracts KW - Birth weight KW - Litter KW - Arsenic KW - Sodium arsenite KW - Weaning KW - Tumors KW - Carcinogens KW - Pregnancy KW - Carcinoma KW - Lactation KW - Breeding KW - Lung KW - Carcinogenesis KW - Progeny KW - Drinking water KW - Adenoma KW - X 24360:Metals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554949668?accountid=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=Lung+tumors+in+mice+induced+by+%22whole-life%22+inorganic+arsenic+exposure+at+human-relevant+doses&rft.au=Waalkes%2C+Michael+P%3BQu%2C+Wei%3BTokar%2C+Erik+J%3BKissling%2C+Grace+E%3BDixon%2C+Darlene&rft.aulast=Waalkes&rft.aufirst=Michael&rft.date=2014-08-01&rft.volume=88&rft.issue=8&rft.spage=1619&rft.isbn=&rft.btitle=&rft.title=Archives+of+Toxicology&rft.issn=03405761&rft_id=info:doi/10.1007%2Fs00204-014-1305-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Number of references - 35 N1 - Last updated - 2015-04-16 N1 - SubjectsTermNotLitGenreText - Birth weight; Arsenic; Litter; Sodium arsenite; Weaning; Carcinogens; Tumors; Lactation; Carcinoma; Pregnancy; Breeding; Lung; Carcinogenesis; Progeny; Drinking water; Adenoma DO - http://dx.doi.org/10.1007/s00204-014-1305-8 ER - TY - JOUR T1 - Strain-specific properties and T cells regulate the susceptibility to papilloma induction by Mus musculus papillomavirus 1. AN - 1553709212; 25121947 AB - The immunocytes that regulate papillomavirus infection and lesion development in humans and animals remain largely undefined. We found that immunocompetent mice with varying H-2 haplotypes displayed asymptomatic skin infection that produced L1 when challenged with 6×1010 MusPV1 virions, the recently identified domestic mouse papillomavirus (also designated "MmuPV1"), but were uniformly resistant to MusPV1-induced papillomatosis. Broad immunosuppression with cyclosporin A resulted in variable induction of papillomas after experimental infection with a similar dose, from robust in Cr:ORL SENCAR to none in C57BL/6 mice, with lesional outgrowth correlating with early viral gene expression and partly with reported strain-specific susceptibility to chemical carcinogens, but not with H-2 haplotype. Challenge with 1×1012 virions in the absence of immunosuppression induced small transient papillomas in Cr:ORL SENCAR but not in C57BL/6 mice. Antibody-induced depletion of CD3+ T cells permitted efficient virus replication and papilloma formation in both strains, providing experimental proof for the crucial role of T cells in controlling papillomavirus infection and associated disease. In Cr:ORL SENCAR mice, immunodepletion of either CD4+ or CD8+ T cells was sufficient for efficient infection and papillomatosis, although deletion of one subset did not inhibit the recruitment of the other subset to the infected epithelium. Thus, the functional cooperation of CD4+ and CD8+ T cells is required to protect this strain. In contrast, C57BL/6 mice required depletion of both CD4+ and CD8+ T cells for infection and papillomatosis, and separate CD4 knock-out and CD8 knock-out C57BL/6 were also resistant. Thus, in C57BL/6 mice, either CD4+ or CD8+ T cell-independent mechanisms exist that can protect this particular strain from MusPV1-associated disease. These findings may help to explain the diversity of pathological outcomes in immunocompetent humans after infection with a specific human papillomavirus genotype. JF - PLoS pathogens AU - Handisurya, Alessandra AU - Day, Patricia M AU - Thompson, Cynthia D AU - Bonelli, Michael AU - Lowy, Douglas R AU - Schiller, John T AD - Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Lymphocyte Cell Biology Section, Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, United States of America; Division of Rheumatology, Internal Medicine III, General Hospital of Vienna, Medical University of Vienna, Vienna, Austria. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1 VL - 10 IS - 8 KW - Index Medicus KW - Animals KW - Mice, Inbred C57BL KW - Papillomaviridae KW - Mice KW - Flow Cytometry KW - Mice, Inbred SENCAR KW - Fluorescent Antibody Technique KW - Mice, Knockout KW - CD8-Positive T-Lymphocytes -- immunology KW - CD4-Positive T-Lymphocytes -- immunology KW - Disease Susceptibility -- immunology KW - Papillomavirus Infections -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1553709212?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+pathogens&rft.atitle=Strain-specific+properties+and+T+cells+regulate+the+susceptibility+to+papilloma+induction+by+Mus+musculus+papillomavirus+1.&rft.au=Handisurya%2C+Alessandra%3BDay%2C+Patricia+M%3BThompson%2C+Cynthia+D%3BBonelli%2C+Michael%3BLowy%2C+Douglas+R%3BSchiller%2C+John+T&rft.aulast=Handisurya&rft.aufirst=Alessandra&rft.date=2014-08-01&rft.volume=10&rft.issue=8&rft.spage=e1004314&rft.isbn=&rft.btitle=&rft.title=PLoS+pathogens&rft.issn=1553-7374&rft_id=info:doi/10.1371%2Fjournal.ppat.1004314 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-21 N1 - Date created - 2014-08-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Virology. 2001 Apr 25;283(1):31-9 [11312659] J Immunol. 2001 Nov 15;167(10):5603-9 [11698431] Nat Protoc. 2009;4(9):1350-62 [19713956] Nature. 2009 Nov 26;462(7272):510-3 [19898495] J Immunol. 2007 Mar 1;178(5):2844-52 [17312128] Annu Rev Immunol. 2007;25:171-92 [17129182] Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6770-5 [17412837] Dis Markers. 2007;23(4):247-59 [17627060] J Transl Med. 2009;7:108 [20021658] J Immunol. 2010 Nov 1;185(9):5405-16 [20870934] J Immunol. 2010 Dec 1;185(11):7107-14 [21037100] Expert Rev Vaccines. 2010 Dec;9(12):1453-63 [21105780] Virology. 2011 Mar 15;411(2):216-28 [21236461] Vet Pathol. 2011 Mar;48(2):500-5 [20685915] Arthritis Rheum. 2011 May;63(5):1281-8 [21321928] Virology. 2011 Jun 5;414(2):153-63 [21492895] Nat Rev Immunol. 2012 Feb;12(2):136-48 [22266691] Med Microbiol Immunol. 2012 May;201(2):117-25 [21792749] J Exp Med. 2012 Jul 30;209(8):1391-5 [22851641] Virology. 2012 Nov 25;433(2):385-94 [22985477] Exp Mol Pathol. 2012 Dec;93(3):416-21 [22796029] J Virol. 2013 Aug;87(16):9391-5 [23785210] J Virol. 2013 Dec;87(24):13214-25 [24067981] J Virol. 2014 Jan;88(1):710-6 [24173230] J Med Virol. 2000 Jul;61(3):289-97 [10861635] J Virol. 2002 Nov;76(22):11291-300 [12388689] Transpl Int. 2003 Mar;16(3):146-53 [12664208] J Gen Virol. 2003 Jul;84(Pt 7):1881-6 [12810883] Drug News Perspect. 2003 Jun;16(5):277-82 [12942158] J Virol. 2004 Jun;78(11):5535-45 [15140950] Br J Dermatol. 1975 Jun;92(6):625-30 [1101940] Cancer Res. 1981 Mar;41(3):773-9 [6780187] Nature. 1987 Jul 2-8;328(6125):77-9 [2955227] J Immunol. 1988 Oct 1;141(7):2216-20 [2459202] Carcinogenesis. 1993 Nov;14(11):2353-8 [8242866] Am J Clin Pathol. 1994 Dec;102(6):768-74 [7801889] Transfus Sci. 1994 Sep;15(3):207-20 [10155542] J Virol. 1996 Dec;70(12):8451-8 [8970967] J Invest Dermatol. 1997 May;108(5):712-5 [9129220] J Virol. 1997 Jul;71(7):5540-8 [9188628] J Virol. 1998 Feb;72(2):959-64 [9444988] Nature. 1998 Jun 4;393(6684):478-80 [9624004] J Exp Med. 1999 Jun 21;189(12):1875-84 [10377183] J Immunol. 2005 Jan 15;174(2):614-8 [15634878] Infect Immun. 2005 Aug;73(8):4913-21 [16041005] Comp Med. 2005 Oct;55(5):431-9 [16270899] Curr Protoc Cell Biol. 2007 Dec;Chapter 26:Unit 26.1 [18228512] Cancer Res. 2008 May 15;68(10):3924-30 [18483278] BJOG. 2008 Dec;115(13):1616-21; discussion 1621-2 [19035938] Immunity. 2009 Feb 20;30(2):218-27 [19200758] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.ppat.1004314 ER - TY - JOUR T1 - Molecular genetics and cellular features of TFE3 and TFEB fusion kidney cancers. AN - 1552804484; 25048860 AB - Despite nearly two decades passing since the discovery of gene fusions involving TFE3 or TFEB in sporadic renal cell carcinoma (RCC), the molecular mechanisms underlying the renal-specific tumorigenesis of these genes remain largely unclear. The recently published findings of The Cancer Genome Atlas Network reported that five of the 416 surveyed clear cell RCC tumours (1.2%) harboured SFPQ-TFE3 fusions, providing further evidence for the importance of gene fusions. A total of five TFE3 gene fusions (PRCC-TFE3, ASPSCR1-TFE3, SFPQ-TFE3, NONO-TFE3, and CLTC-TFE3) and one TFEB gene fusion (MALAT1-TFEB) have been identified in RCC tumours and characterized at the mRNA transcript level. A multitude of molecular pathways well-described in carcinogenesis are regulated in part by TFE3 or TFEB proteins, including activation of TGFβ and ETS transcription factors, E-cadherin expression, CD40L-dependent lymphocyte activation, mTORC1 signalling, insulin-dependent metabolism regulation, folliculin signalling, and retinoblastoma-dependent cell cycle arrest. Determining which pathways are most important to RCC oncogenesis will be critical in discovering the most promising therapeutic targets for this disease. JF - Nature reviews. Urology AU - Kauffman, Eric C AU - Ricketts, Christopher J AU - Rais-Bahrami, Soroush AU - Yang, Youfeng AU - Merino, Maria J AU - Bottaro, Donald P AU - Srinivasan, Ramaprasad AU - Linehan, W Marston AD - Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Building 10, CRC Room 1-5940, Bethesda, MD 20892, USA. ; Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Building 10, CRC Room 1-5940, Bethesda, MD 20892, USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 465 EP - 475 VL - 11 IS - 8 KW - Basic Helix-Loop-Helix Leucine Zipper Transcription Factors KW - 0 KW - Biomarkers, Tumor KW - TFE3 protein, human KW - TFEB protein, human KW - Index Medicus KW - Gene Expression Regulation, Neoplastic KW - Carcinogenesis -- metabolism KW - Carcinogenesis -- genetics KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Kidney Neoplasms -- genetics KW - Biomarkers, Tumor -- metabolism KW - Biomarkers, Tumor -- genetics KW - Carcinoma, Renal Cell -- metabolism KW - Kidney Neoplasms -- metabolism KW - Gene Fusion KW - Carcinoma, Renal Cell -- genetics KW - Basic Helix-Loop-Helix Leucine Zipper Transcription Factors -- metabolism KW - Basic Helix-Loop-Helix Leucine Zipper Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552804484?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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.+Urology&rft.atitle=Molecular+genetics+and+cellular+features+of+TFE3+and+TFEB+fusion+kidney+cancers.&rft.au=Kauffman%2C+Eric+C%3BRicketts%2C+Christopher+J%3BRais-Bahrami%2C+Soroush%3BYang%2C+Youfeng%3BMerino%2C+Maria+J%3BBottaro%2C+Donald+P%3BSrinivasan%2C+Ramaprasad%3BLinehan%2C+W+Marston&rft.aulast=Kauffman&rft.aufirst=Eric&rft.date=2014-08-01&rft.volume=11&rft.issue=8&rft.spage=465&rft.isbn=&rft.btitle=&rft.title=Nature+reviews.+Urology&rft.issn=1759-4820&rft_id=info:doi/10.1038%2Fnrurol.2014.162 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-30 N1 - Date created - 2014-08-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cell Biol. 1996 Mar;16(3):1203-11 [8622664] Hum Genet. 1996 Jul;98(1):16-21 [8682500] Hum Mol 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[11818451] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nrurol.2014.162 ER - TY - JOUR T1 - In vitro and in vivo activity of the low-immunogenic antimesothelin immunotoxin RG7787 in pancreatic cancer. AN - 1552377267; 24928849 AB - Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis, and new therapies are needed. RG7787 is a novel low-immunogenic antimesothelin recombinant immunotoxin (RIT), engineered to overcome the limitations of SS1P, a RIT now in clinical trials. In vitro activity was evaluated on five established PDAC cell lines (KLM-1, AsPC-1, BxPC-3, Panc 3.014, and PK-1) and on PDAC cells directly established from a patient tumor (GUMC108). RG7787 had subnanomolar IC50s in most cell lines, and was significantly more active than SS1P in GUMC108, KLM-1, and Panc 3.014 cells. GUMC108 was most sensitive, with RG7787 killing >99% of the cells. In a subcutaneous KLM-1 xenograft mouse model, two cycles of 3 × 2.5 mg/kg RG7787 QOD combined with two cycles of 1 × 50 mg/kg paclitaxel induced near-complete responses, with all tumors regressing below 5 mm(3) within 30 days after therapy was initiated (>95% decrease) and no significant growth increase for at least another 3 weeks. RG7787 alone gave limited but significant regressions and paclitaxel by itself arrested tumor growth. Quantifying the uptake of Alexa Fluor 647-labeled RG7787 in tumors showed that the RIT reached only 45% of KLM-1 cells, accounting in part for the limited responses. Paclitaxel did not improve RG7787 uptake, which thus cannot explain the beneficial effect of the combination therapy. In conclusion, RG7787 has high cytotoxic activity on PDAC cell lines as well as on primary patient cells. In vivo, this novel RIT gives durable near-complete tumor responses when combined with paclitaxel. RG7787 merits further evaluation for the treatment of PDAC. ©2014 American Association for Cancer Research. JF - Molecular cancer therapeutics AU - Hollevoet, Kevin AU - Mason-Osann, Emily AU - Liu, Xiu-fen AU - Imhof-Jung, Sabine AU - Niederfellner, Gerhard AU - Pastan, Ira AD - Laboratory of Molecular Biology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland; Laboratory for Therapeutic and Diagnostic Antibodies, Department of Pharmaceutical and Pharmacological Sciences, KU Leuven, Leuven, Belgium; and. ; Laboratory of Molecular Biology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland; ; Pharmaceutical Research and Early Development (pRED), Roche Innovation Center Penzberg, Germany. ; Laboratory of Molecular Biology, Center for Cancer Research, NCI, NIH, Bethesda, Maryland; pastani@mail.nih.gov. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 2040 EP - 2049 VL - 13 IS - 8 KW - Antibodies, Monoclonal KW - 0 KW - Antineoplastic Agents KW - GPI-Linked Proteins KW - Immunoconjugates KW - Protein Synthesis Inhibitors KW - RG7787 KW - SS1(dsFv)PE38 KW - mesothelin KW - Index Medicus KW - Animals KW - Apoptosis KW - Antibodies, Monoclonal -- metabolism KW - Humans KW - Cell Line, Tumor KW - Mice, Nude KW - Antibodies, Monoclonal -- pharmacology KW - Cell Proliferation KW - Cell Survival KW - GPI-Linked Proteins -- metabolism KW - Protein Synthesis Inhibitors -- pharmacology KW - Xenograft Model Antitumor Assays KW - Female KW - GPI-Linked Proteins -- immunology KW - Pancreatic Neoplasms -- metabolism KW - Immunoconjugates -- pharmacokinetics KW - Carcinoma, Pancreatic Ductal -- metabolism KW - Carcinoma, Pancreatic Ductal -- drug therapy KW - Antineoplastic Agents -- pharmacokinetics KW - Pancreatic Neoplasms -- drug therapy KW - Immunoconjugates -- pharmacology KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552377267?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+cancer+therapeutics&rft.atitle=In+vitro+and+in+vivo+activity+of+the+low-immunogenic+antimesothelin+immunotoxin+RG7787+in+pancreatic+cancer.&rft.au=Hollevoet%2C+Kevin%3BMason-Osann%2C+Emily%3BLiu%2C+Xiu-fen%3BImhof-Jung%2C+Sabine%3BNiederfellner%2C+Gerhard%3BPastan%2C+Ira&rft.aulast=Hollevoet&rft.aufirst=Kevin&rft.date=2014-08-01&rft.volume=13&rft.issue=8&rft.spage=2040&rft.isbn=&rft.btitle=&rft.title=Molecular+cancer+therapeutics&rft.issn=1538-8514&rft_id=info:doi/10.1158%2F1535-7163.MCT-14-0089-T LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2014-08-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873] Cancer Res. 2014 Jun 1;74(11):2907-12 [24824231] Nat Rev Drug Discov. 2011 Mar;10(3):221-37 [21358741] Mol Cancer Ther. 2011 Aug;10(8):1311-6 [21673092] Lancet. 2011 Aug 13;378(9791):607-20 [21620466] Clin Cancer Res. 2011 Sep 15;17(18):5926-34 [21813632] FEBS J. 2011 Dec;278(23):4683-700 [21585657] J Clin Oncol. 2011 Dec 1;29(34):4548-54 [21969517] Clin Cancer Res. 2012 Jan 1;18(1):152-60 [22068660] Am J Pathol. 2012 Feb;180(2):599-607 [22189618] Am J Pathol. 2012 Feb;180(2):443-5 [22192626] Mol Cancer Ther. 2012 Mar;11(3):517-25 [22351743] Cancer Res. 2010 Feb 1;70(3):1082-9 [20103626] Annu Rev Biomed Eng. 1999;1:241-63 [11701489] Clin Cancer Res. 2001 Dec;7(12):3862-8 [11751476] Am J Surg Pathol. 2003 Nov;27(11):1418-28 [14576474] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):136-40 [8552591] J Mol Graph. 1996 Feb;14(1):33-8, 27-8 [8744570] Semin Cancer Biol. 1996 Apr;7(2):87-95 [8740564] Int J Pancreatol. 1996 Aug;20(1):43-50 [8872523] Clin Cancer Res. 2005 Aug 15;11(16):5840-6 [16115924] Gene Ther. 2005 Sep;12(18):1360-8 [15902276] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638] Clin Cancer Res. 2006 Aug 1;12(15):4695-701 [16899620] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569] Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):17099-104 [17940013] Blood. 2009 Apr 16;113(16):3792-800 [18988862] Science. 2009 Jun 12;324(5933):1457-61 [19460966] J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053] Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11782-7 [22753489] N Engl J Med. 2012 Sep 27;367(13):1220-7 [23013073] Mol Cancer Ther. 2013 Jan;12(1):48-57 [23136186] Sci Transl Med. 2013 Oct 23;5(208):208ra147 [24154601] J Immunother. 2014 Jan;37(1):8-15 [24316551] Erratum In: Mol Cancer Ther. 2015 Jul;14(7):1763 [26018754] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1535-7163.MCT-14-0089-T ER - TY - CONF T1 - Achieving professional success in US government, academia, and industry: an EMGS commentary. AN - 1552373627; 24788591 AB - One of the goals of the EMGS is to help members achieve professional success in the fields they have trained in. Today, there is greater competition for jobs in genetic toxicology, genomics, and basic research than ever before. In addition, job security and the ability to advance in one's career is challenging, regardless of whether one works in a regulatory, academic, or industry environment. At the EMGS Annual Meeting in Monterey, CA (September, 2013), the Women in EMGS Special Interest Group held a workshop to discuss strategies for achieving professional success. Presentations were given by three speakers, each representing a different employment environment: Government (Miriam C. Poirier), Academia (Jeffrey L. Schwartz), and Industry (Marilyn J. Aardema). Although some differences in factors or traits affecting success in the three employment sectors were noted by each of the speakers, common factors considered important for advancement included networking, seeking out mentors, and developing exceptional communication skills. © 2014 Wiley Periodicals, Inc. JF - Environmental and molecular mutagenesis AU - Poirier, Miriam C AU - Schwartz, Jeffrey L AU - Aardema, Marilyn J Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 525 EP - 529 VL - 55 IS - 7 KW - Index Medicus KW - career development KW - Government KW - industry KW - academia KW - United States KW - Humans KW - Career Choice KW - Female KW - Universities -- manpower KW - Women KW - Industry -- manpower KW - Employment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552373627?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Achieving+professional+success+in+US+government%2C+academia%2C+and+industry%3A+an+EMGS+commentary.&rft.au=Poirier%2C+Miriam+C%3BSchwartz%2C+Jeffrey+L%3BAardema%2C+Marilyn+J&rft.aulast=Poirier&rft.aufirst=Miriam&rft.date=2014-08-01&rft.volume=55&rft.issue=7&rft.spage=525&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21871 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-29 N1 - Date created - 2014-08-07 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/em.21871 ER - TY - JOUR T1 - Selective protection of zidovudine-induced DNA-damage by the antioxidants WR-1065 and tempol. AN - 1552373610; 24833597 AB - The cytokinesis-block micronucleus cytome (CBMN) assay, introduced by Fenech, was used to demonstrate different types of DNA damage in MOLT-3 human lymphoblastoid cells exposed to 10 μM zidovudine (AZT). In addition, we explored the cytoprotective potential of two antioxidants, WR-1065 and Tempol, to decrease AZT-induced genotoxicity. Binucleated cells, arrested by Cytochalasin B (Cyt B), were evaluated for micronuclei (MN), caused by DNA damage or chromosomal loss, and chromatin nucleoplasmic bridges (NPBs), caused by telomere attrition. Additionally, nuclear buds (NBUDs), caused by amplified DNA, and apoptotic and necrotic (A/N) cells were scored. We hypothesized that AZT exposure would increase the frequency of genotoxic end points, and that the antioxidants Tempol and WR-1065 would protect against AZT-induced genotoxicity. MOLT-3 cells were exposed to 0 or 10 µM AZT for a total of 76 hr. After the first 24 hr, 0 or 5 µM WR-1065 and/or 0 or 200 µM Tempol were added for the remainder of the experiment. For the last 28 hr (of 76 hr), Cyt B was added to arrest replication after one cell division, leaving a predominance of binucleated cells. The nuclear division index (NDI) was similar for all treatment groups, indicating that the exposures did not alter cell viability. MOLT-3 cells exposed to AZT alone had significant (P < 0.05) increases in MN and NBs, compared to unexposed cells. Both Tempol and WR-1065 protected against AZT-induced MN formation (P < 0.003 for both), and WR-1065, but not Tempol, reduced the levels of A/N (P = 0.041). In cells exposed to AZT/Tempol there were significantly reduced levels of NBUDs, compared to cells exposed to AZT alone (P = 0.015). Cells exposed to AZT/WR-1065 showed reduced levels of NPBs, compared to cells exposed to AZT alone (P = 0.037). Thus WR-1065 and Tempol protected MOLT-3 cells against specific types of AZT-induced DNA damage. © 2014 Wiley Periodicals, Inc. JF - Environmental and molecular mutagenesis AU - Olivero, Ofelia A AU - Ongele, Michael O AU - Braun, Hannan M AU - Marrogi, Ariadna AU - Divi, Kathyiani AU - Mitchell, James B AU - Poirier, Miriam C AD - Carcinogen-DNA Interactions Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 566 EP - 572 VL - 55 IS - 7 KW - Antioxidants KW - 0 KW - Chromatin KW - Cyclic N-Oxides KW - Mercaptoethylamines KW - Mutagens KW - Radiation-Protective Agents KW - Spin Labels KW - WR 1065 KW - 31098-42-7 KW - Cytochalasin B KW - 3CHI920QS7 KW - Zidovudine KW - 4B9XT59T7S KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - nuclear buds KW - chromatin neoplasmic bridges KW - cytome assay KW - apoptosis KW - necrosis KW - MOLT-3 cells KW - CBMN assay KW - micronuclei KW - Apoptosis KW - Radiation-Protective Agents -- chemistry KW - Cell Nucleus -- metabolism KW - Humans KW - Cell Line, Tumor KW - Cell Proliferation KW - Cytochalasin B -- chemistry KW - Cell Survival KW - Necrosis KW - Micronucleus Tests KW - Chromosomes -- ultrastructure KW - Mutagens -- chemistry KW - Mercaptoethylamines -- chemistry KW - DNA Damage KW - Chromatin -- chemistry KW - Zidovudine -- chemistry KW - Cyclic N-Oxides -- chemistry KW - Antioxidants -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552373610?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Selective+protection+of+zidovudine-induced+DNA-damage+by+the+antioxidants+WR-1065+and+tempol.&rft.au=Olivero%2C+Ofelia+A%3BOngele%2C+Michael+O%3BBraun%2C+Hannan+M%3BMarrogi%2C+Ariadna%3BDivi%2C+Kathyiani%3BMitchell%2C+James+B%3BPoirier%2C+Miriam+C&rft.aulast=Olivero&rft.aufirst=Ofelia&rft.date=2014-08-01&rft.volume=55&rft.issue=7&rft.spage=566&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21872 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-29 N1 - Date created - 2014-08-07 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/em.21872 ER - TY - JOUR T1 - Genome-wide interaction study of smoking and bladder cancer risk. AN - 1552370757; 24662972 AB - Bladder cancer is a complex disease with known environmental and genetic risk factors. We performed a genome-wide interaction study (GWAS) of smoking and bladder cancer risk based on primary scan data from 3002 cases and 4411 controls from the National Cancer Institute Bladder Cancer GWAS. Alternative methods were used to evaluate both additive and multiplicative interactions between individual single nucleotide polymorphisms (SNPs) and smoking exposure. SNPs with interaction P values < 5 × 10(-) (5) were evaluated further in an independent dataset of 2422 bladder cancer cases and 5751 controls. We identified 10 SNPs that showed association in a consistent manner with the initial dataset and in the combined dataset, providing evidence of interaction with tobacco use. Further, two of these novel SNPs showed strong evidence of association with bladder cancer in tobacco use subgroups that approached genome-wide significance. Specifically, rs1711973 (FOXF2) on 6p25.3 was a susceptibility SNP for never smokers [combined odds ratio (OR) = 1.34, 95% confidence interval (CI) = 1.20-1.50, P value = 5.18 × 10(-) (7)]; and rs12216499 (RSPH3-TAGAP-EZR) on 6q25.3 was a susceptibility SNP for ever smokers (combined OR = 0.75, 95% CI = 0.67-0.84, P value = 6.35 × 10(-) (7)). In our analysis of smoking and bladder cancer, the tests for multiplicative interaction seemed to more commonly identify susceptibility loci with associations in never smokers, whereas the additive interaction analysis identified more loci with associations among smokers-including the known smoking and NAT2 acetylation interaction. Our findings provide additional evidence of gene-environment interactions for tobacco and bladder cancer. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Figueroa, Jonine D AU - Han, Summer S AU - Garcia-Closas, Montserrat AU - Baris, Dalsu AU - Jacobs, Eric J AU - Kogevinas, Manolis AU - Schwenn, Molly AU - Malats, Nuria AU - Johnson, Alison AU - Purdue, Mark P AU - Caporaso, Neil AU - Landi, Maria Teresa AU - Prokunina-Olsson, Ludmila AU - Wang, Zhaoming AU - Hutchinson, Amy AU - Burdette, Laurie AU - Wheeler, William AU - Vineis, Paolo AU - Siddiq, Afshan AU - Cortessis, Victoria K AU - Kooperberg, Charles AU - Cussenot, Olivier AU - Benhamou, Simone AU - Prescott, Jennifer AU - Porru, Stefano AU - Bueno-de-Mesquita, H Bas AU - Trichopoulos, Dimitrios AU - Ljungberg, Börje AU - Clavel-Chapelon, Françoise AU - Weiderpass, Elisabete AU - Krogh, Vittorio AU - Dorronsoro, Miren AU - Travis, Ruth AU - Tjønneland, Anne AU - Brenan, Paul AU - Chang-Claude, Jenny AU - Riboli, Elio AU - Conti, David AU - Gago-Dominguez, Manuela AU - Stern, Mariana C AU - Pike, Malcolm C AU - Van Den Berg, David AU - Yuan, Jian-Min AU - Hohensee, Chancellor AU - Rodabough, Rebecca AU - Cancel-Tassin, Geraldine AU - Roupret, Morgan AU - Comperat, Eva AU - Chen, Constance AU - De Vivo, Immaculata AU - Giovannucci, Edward AU - Hunter, David J AU - Kraft, Peter AU - Lindstrom, Sara AU - Carta, Angela AU - Pavanello, Sofia AU - Arici, Cecilia AU - Mastrangelo, Giuseppe AU - Karagas, Margaret R AU - Schned, Alan AU - Armenti, Karla R AU - Hosain, G M Monawar AU - Haiman, Chris A AU - Fraumeni, Joseph F AU - Chanock, Stephen J AU - Chatterjee, Nilanjan AU - Rothman, Nathaniel AU - Silverman, Debra T AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA, Institute for Cancer Research, London, UK, Epidemiology Research Program, American Cancer Society, Atlanta, GA, USA, Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain, Municipal Institute of Medical Research, Barcelona, Spain, CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain, National School of Public Health, Athens, Greece, Maine Cancer Registry, Augusta, ME, USA, Spanish National Cancer Research Centre (CNIO), Madrid, Spain, Vermont Cancer Registry, Burlington, VT, USA, Center for Genomics Research, SAIC-Frederick, Inc., National Cancer Institute-Frederick, Frederick, MD, USA, Information Management Services, Inc., Rockville, MD, USA, Imperial College London, London, UK, Department of Preventive Medicine and Department of Obstetrics & Gynecology, Keck School of Medicine of USC, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA, Fred Hutchinson Cancer Research Center, Division of Public Health Sciences, Seattle, WA, USA, Department of Urology, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France, Centre de Recherche sur les Pathologies Prostatiques, Paris, France, Institut national de la sante et de la recherche medicale, U946, Foundation Jean Dausset Centre d'Etude du Polymorphisme Humain (CEPH), Paris, France, Centre National de la Receherche Scientifique, UMR8200, Institut Gustave-Roussy, Villejuif, France, Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA, Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy, National Institute for Public Health and the Environment (RIVM), Biltho ; Institute for Cancer Research, London, UK. ; Epidemiology Research Program, American Cancer Society, Atlanta, GA, USA. ; Maine Cancer Registry, Augusta, ME, USA. ; Spanish National Cancer Research Centre (CNIO), Madrid, Spain. ; Vermont Cancer Registry, Burlington, VT, USA. ; Center for Genomics Research, SAIC-Frederick, Inc., National Cancer Institute-Frederick, Frederick, MD, USA. ; Information Management Services, Inc., Rockville, MD, USA. ; Imperial College London, London, UK. ; Department of Preventive Medicine and Department of Obstetrics & Gynecology, Keck School of Medicine of USC, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA. ; Fred Hutchinson Cancer Research Center, Division of Public Health Sciences, Seattle, WA, USA. ; Department of Urology, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France, Centre de Recherche sur les Pathologies Prostatiques, Paris, France. ; Institut national de la sante et de la recherche medicale, U946, Foundation Jean Dausset Centre d'Etude du Polymorphisme Humain (CEPH), Paris, France, Centre National de la Receherche Scientifique, UMR8200, Institut Gustave-Roussy, Villejuif, France. ; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA, Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. ; Department of Medical and Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, Brescia, Italy. ; Imperial College London, London, UK, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands, Department of Gastroenterology and Hepatology, University Medical Centre, Utrecht, The Netherlands. ; Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden. ; Fondazione IRCCS Istituto Nazionale dei Tumori, Milano, Italy. ; CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain, Public Health Division of Gipuzkoa, BioDonostia Research Institute, Health Department of Basque Region, San Sebastian, Spain. ; Cancer Epidemiology Unit, University of Oxford, Oxford, UK. ; Danish Cancer Society Research Center, Copenhagen, Denmark. ; International Agency for Research on Cancer, Lyon, France. ; DKFZ, Heidelberg, Germany. ; Genomic Medicine Group, Galician Foundation of Genomic Medicine, Complejo Hospitalario Universitario de Santiago, Servicio Galego de Saude (SERGAS), Instituto de Investigación Sanitaria de Santiago (IDIS), Santiago de Compostela, Spain. ; Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA. ; UPMC Univ Paris 06, GRC n°5,ONCOTYPE-URO, Paris, France. ; Department of Urology, Assistance Publique-Hôpitaux de Paris, Tenon Hospital, Paris, France, Centre de Recherche sur les Pathologies Prostatiques, Paris, France, UPMC Univ Paris 06, GRC n°5,ONCOTYPE-URO, Paris, France. ; Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. ; Department of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA. ; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA, Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, Broad Institute of Harvard and MIT, Cambridge, MA, USA. ; Program in Genetic Epidemiology and Statistical Genetics, Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA, Department of Biostatistics, Harvard School of Public Health, Boston, MA, USA. ; Department of Cardiac, Thoracic and Vascular Sciences, University of Padova, Padova, Italy; ; Geisel School of Medicine at Dartmouth, Lebanon, NH, USA. ; New Hampshire Department of Health and Human Services, Concord, NH, USA and. ; Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1737 EP - 1744 VL - 35 IS - 8 KW - Biomarkers, Tumor KW - 0 KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Prognosis KW - Case-Control Studies KW - Genetic Predisposition to Disease KW - Meta-Analysis as Topic KW - Biomarkers, Tumor -- genetics KW - Urinary Bladder Neoplasms -- etiology KW - Genome, Human KW - Smoking -- adverse effects KW - Gene-Environment Interaction KW - Polymorphism, Single Nucleotide -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552370757?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genome-wide+interaction+study+of+smoking+and+bladder+cancer+risk.&rft.au=Figueroa%2C+Jonine+D%3BHan%2C+Summer+S%3BGarcia-Closas%2C+Montserrat%3BBaris%2C+Dalsu%3BJacobs%2C+Eric+J%3BKogevinas%2C+Manolis%3BSchwenn%2C+Molly%3BMalats%2C+Nuria%3BJohnson%2C+Alison%3BPurdue%2C+Mark+P%3BCaporaso%2C+Neil%3BLandi%2C+Maria+Teresa%3BProkunina-Olsson%2C+Ludmila%3BWang%2C+Zhaoming%3BHutchinson%2C+Amy%3BBurdette%2C+Laurie%3BWheeler%2C+William%3BVineis%2C+Paolo%3BSiddiq%2C+Afshan%3BCortessis%2C+Victoria+K%3BKooperberg%2C+Charles%3BCussenot%2C+Olivier%3BBenhamou%2C+Simone%3BPrescott%2C+Jennifer%3BPorru%2C+Stefano%3BBueno-de-Mesquita%2C+H+Bas%3BTrichopoulos%2C+Dimitrios%3BLjungberg%2C+B%C3%B6rje%3BClavel-Chapelon%2C+Fran%C3%A7oise%3BWeiderpass%2C+Elisabete%3BKrogh%2C+Vittorio%3BDorronsoro%2C+Miren%3BTravis%2C+Ruth%3BTj%C3%B8nneland%2C+Anne%3BBrenan%2C+Paul%3BChang-Claude%2C+Jenny%3BRiboli%2C+Elio%3BConti%2C+David%3BGago-Dominguez%2C+Manuela%3BStern%2C+Mariana+C%3BPike%2C+Malcolm+C%3BVan+Den+Berg%2C+David%3BYuan%2C+Jian-Min%3BHohensee%2C+Chancellor%3BRodabough%2C+Rebecca%3BCancel-Tassin%2C+Geraldine%3BRoupret%2C+Morgan%3BComperat%2C+Eva%3BChen%2C+Constance%3BDe+Vivo%2C+Immaculata%3BGiovannucci%2C+Edward%3BHunter%2C+David+J%3BKraft%2C+Peter%3BLindstrom%2C+Sara%3BCarta%2C+Angela%3BPavanello%2C+Sofia%3BArici%2C+Cecilia%3BMastrangelo%2C+Giuseppe%3BKaragas%2C+Margaret+R%3BSchned%2C+Alan%3BArmenti%2C+Karla+R%3BHosain%2C+G+M+Monawar%3BHaiman%2C+Chris+A%3BFraumeni%2C+Joseph+F%3BChanock%2C+Stephen+J%3BChatterjee%2C+Nilanjan%3BRothman%2C+Nathaniel%3BSilverman%2C+Debra+T&rft.aulast=Figueroa&rft.aufirst=Jonine&rft.date=2014-08-01&rft.volume=35&rft.issue=8&rft.spage=1737&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu064 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-18 N1 - Date created - 2014-08-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nucleic Acids Res. 2012 Jan;40(Database issue):D930-4 [22064851] Cancer Res. 2013 Apr 1;73(7):2211-20 [23536561] Proc Natl Acad Sci U S A. 2012 Mar 27;109(13):4974-9 [22416122] Hum Mol Genet. 2011 Nov 1;20(21):4282-9 [21824976] Cancer Causes Control. 2001 Jan;12(1):13-21 [11227921] Am J Epidemiol. 2001 Oct 15;154(8):687-93 [11590080] Stat Med. 1994 Jan 30;13(2):153-62 [8122051] Nature. 1996 Aug 15;382(6592):622-6 [8757131] Stat Med. 1997 Aug 15;16(15):1731-43 [9265696] Lancet. 2005 Aug 20-26;366(9486):649-59 [16112301] Int J Obes (Lond). 2005 Oct;29(10):1267-74 [15997248] Hum Mol Genet. 2014 Mar 1;23(5):1387-98 [24163127] Am J Hum Genet. 2006 Mar;78(3):464-79 [16465622] Development. 2006 Mar;133(5):833-43 [16439479] Cancer Epidemiol Biomarkers Prev. 2006 Jul;15(7):1348-54 [16835335] Chem Res Toxicol. 2006 Oct;19(10):1366-73 [17040106] Int J Epidemiol. 2007 Feb;36(1):23-8 [17510073] Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1214-21 [18483344] Nat Genet. 2008 Nov;40(11):1307-12 [18794855] Nat Genet. 2009 Feb;41(2):221-7 [19151717] Nat Genet. 2009 Sep;41(9):991-5 [19648920] Cancer Res. 2009 Sep 1;69(17):6857-64 [19706757] J Biol Chem. 2009 Oct 23;284(43):29437-45 [19684019] J Natl Cancer Inst. 2009 Nov 18;101(22):1553-61 [19917915] Pharmacogenet Genomics. 2010 Jan;20(1):26-37 [19997042] Nat Genet. 2010 Nov;42(11):978-84 [20972438] Carcinogenesis. 2011 Feb;32(2):182-9 [21037224] Pharmacogenet Genomics. 2011 Apr;21(4):231-6 [20739907] Environ Health Perspect. 2010 Nov;118(11):1545-50 [20675267] Hum Mol Genet. 2011 Nov 1;20(21):4268-81 [21750109] Int J Cancer. 2011 Dec 15;129(12):2894-904 [21678399] Genome Res. 2012 Sep;22(9):1790-7 [22955989] Nature. 2012 Sep 6;489(7414):91-100 [22955619] Am J Epidemiol. 2012 Dec 1;176(11):1060-7 [23118105] Nat Genet. 2012 Dec;44(12):1330-5 [23143601] J Clin Endocrinol Metab. 2013 Mar;98(3):E497-502 [23408570] Hum Mol Genet. 2012 Apr 15;21(8):1918-30 [22228101] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu064 ER - TY - JOUR T1 - Clinical imaging in regenerative medicine. AN - 1552369411; 25093889 AB - In regenerative medicine, clinical imaging is indispensable for characterizing damaged tissue and for measuring the safety and efficacy of therapy. However, the ability to track the fate and function of transplanted cells with current technologies is limited. Exogenous contrast labels such as nanoparticles give a strong signal in the short term but are unreliable long term. Genetically encoded labels are good both short- and long-term in animals, but in the human setting they raise regulatory issues related to the safety of genomic integration and potential immunogenicity of reporter proteins. Imaging studies in brain, heart and islets share a common set of challenges, including developing novel labeling approaches to improve detection thresholds and early delineation of toxicity and function. Key areas for future research include addressing safety concerns associated with genetic labels and developing methods to follow cell survival, differentiation and integration with host tissue. Imaging may bridge the gap between cell therapies and health outcomes by elucidating mechanisms of action through longitudinal monitoring. JF - Nature biotechnology AU - Naumova, Anna V AU - Modo, Michel AU - Moore, Anna AU - Murry, Charles E AU - Frank, Joseph A AD - 1] Department of Radiology, University of Washington, Seattle, Washington, USA. [2] Center for Cardiovascular Biology, University of Washington, Seattle, Washington, USA. [3] Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington, USA. ; 1] McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. [2] Centre for the Neural Basis of Cognition, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. [3] Department of Radiology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. [4] Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. ; Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Charlestown, Massachusetts, USA. ; 1] Center for Cardiovascular Biology, University of Washington, Seattle, Washington, USA. [2] Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington, USA. [3] Department of Pathology, University of Washington, Seattle, Washington, USA. [4] Department of Bioengineering, University of Washington, Seattle, Washington, USA. [5] Department of Medicine/Cardiology, University of Washington, Seattle, Washington, USA. ; 1] Radiology and Imaging Sciences, Clinical, National Institutes of Health, Bethesda, Maryland, USA. [2] National Institutes of Biomedical Imaging and Bioengineering, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 804 EP - 818 VL - 32 IS - 8 KW - Index Medicus KW - Animals KW - Diagnostic Imaging KW - Regenerative Medicine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1552369411?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+biotechnology&rft.atitle=Clinical+imaging+in+regenerative+medicine.&rft.au=Naumova%2C+Anna+V%3BModo%2C+Michel%3BMoore%2C+Anna%3BMurry%2C+Charles+E%3BFrank%2C+Joseph+A&rft.aulast=Naumova&rft.aufirst=Anna&rft.date=2014-08-01&rft.volume=32&rft.issue=8&rft.spage=804&rft.isbn=&rft.btitle=&rft.title=Nature+biotechnology&rft.issn=1546-1696&rft_id=info:doi/10.1038%2Fnbt.2993 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-13 N1 - Date created - 2014-08-08 N1 - Date revised - 2017-01-14 N1 - 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[24136127] Neuroreport. 2013 Dec 18;24(18):1035-40 [24145773] Bioorg Med Chem. 2013 Dec 15;21(24):7816-29 [24183588] Contrast Media Mol Imaging. 2013 Nov-Dec;8(6):439-55 [24375900] JAMA Neurol. 2014 Jan;71(1):83-7 [24217017] ACS Chem Biol. 2014 Jan 17;9(1):134-8 [24138139] J Am Coll Cardiol. 2014 Jan 21;63(2):110-22 [24036024] Cell Stem Cell. 2014 Apr 3;14(4):431-44 [24702995] Circulation. 2014 Apr 29;129(17):1731-41 [24619466] Nature. 2014 Jun 12;510(7504):273-7 [24776797] Stem Cells Dev. 2009 Jun;18(5):683-92 [19099374] Magn Reson Med. 2006 Feb;55(2):242-9 [16416426] Blood. 2006 Mar 15;107(6):2294-302 [16282341] Nephrol Dial Transplant. 2006 Apr;21(4):1104-8 [16431890] Nat Methods. 2006 May;3(5):391-6 [16628210] J Am Soc Echocardiogr. 2006 May;19(5):563-8 [16644442] Blood. 2006 May 15;107(10):3865-7 [16439674] Expert Rev Med Devices. 2006 Jul;3(4):427-39 [16866640] J Nucl Med. 2006 Aug;47(8):1295-301 [16883008] Diabetes. 2006 Sep;55(9):2419-28 [16936189] Diabetes. 2006 Nov;55(11):2931-8 [17065328] N Engl J Med. 2006 Nov 30;355(22):2376-8 [17135597] Nat Protoc. 2006;1(1):429-35 [17406265] Stem Cells. 2008 May;26(5):1366-75 [18276802] Circulation. 2008 Sep 30;118(14):1425-32 [18794392] Circulation. 2008 Sep 30;118(14 Suppl):S121-9 [18824743] Diabetes Obes Metab. 2008 Nov;10 Suppl 4:23-31 [18834430] J Mol Cell Cardiol. 2008 Oct;45(4):567-81 [18466917] Nat Clin Pract Oncol. 2009 Jan;6(1):53-8 [19015650] Transplant Proc. 2008 Dec;40(10):3619-22 [19100453] Curr Pharm Des. 2008;14(36):3835-53 [19128236] Comment In: Nat Biotechnol. 2015 Jun;33(6):587 [26057970] Nat Biotechnol. 2015 Jun;33(6):587 [26057969] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nbt.2993 ER - TY - JOUR T1 - Inhibition of glutathione peroxidase mediates the collateral sensitivity of multidrug-resistant cells to tiopronin. AN - 1551027856; 24930045 AB - Multidrug resistance (MDR) is a major obstacle to the successful chemotherapy of cancer. MDR is often the result of overexpression of ATP-binding cassette transporters following chemotherapy. A common ATP-binding cassette transporter that is overexpressed in MDR cancer cells is P-glycoprotein, which actively effluxes drugs against a concentration gradient, producing an MDR phenotype. Collateral sensitivity (CS), a phenomenon of drug hypersensitivity, is defined as the ability of certain compounds to selectively target MDR cells, but not the drug-sensitive parent cells from which they were derived. The drug tiopronin has been previously shown to elicit CS. However, unlike other CS agents, the mechanism of action was not dependent on the expression of P-glycoprotein in MDR cells. We have determined that the CS activity of tiopronin is mediated by the generation of reactive oxygen species (ROS) and that CS can be reversed by a variety of ROS-scavenging compounds. Specifically, selective toxicity of tiopronin toward MDR cells is achieved by inhibition of glutathione peroxidase (GPx), and the mode of inhibition of GPx1 by tiopronin is shown in this report. Why MDR cells are particularly sensitive to ROS is discussed, as is the difficulty in exploiting this hypersensitivity to tiopronin in the clinic. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Hall, Matthew D AU - Marshall, Travis S AU - Kwit, Alexandra D T AU - Miller Jenkins, Lisa M AU - Dulcey, Andrés E AU - Madigan, James P AU - Pluchino, Kristen M AU - Goldsborough, Andrew S AU - Brimacombe, Kyle R AU - Griffiths, Gary L AU - Gottesman, Michael M AD - From the Laboratory of Cell Biology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892 and. ; the Imaging Probe Development Center, NHLBI, National Institutes of Health, Rockville, Maryland 20850. ; From the Laboratory of Cell Biology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892 and mgottesman@nih.gov. Y1 - 2014/08/01/ PY - 2014 DA - 2014 Aug 01 SP - 21473 EP - 21489 VL - 289 IS - 31 KW - Enzyme Inhibitors KW - 0 KW - Oligodeoxyribonucleotides KW - Reactive Oxygen Species KW - Thiomalates KW - 2-thiomalic acid KW - 94239W5L4H KW - Tiopronin KW - C5W04GO61S KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Index Medicus KW - Oxygen Radicals KW - Enzyme Inhibitor KW - Chemoresistance KW - Reactive Oxygen Species (ROS) KW - Cell Death KW - Thiomalates -- pharmacology KW - Reactive Oxygen Species -- metabolism KW - Base Sequence KW - Humans KW - Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization KW - Molecular Sequence Data KW - Drug Resistance, Neoplasm KW - Cell Line, Tumor KW - Amino Acid Sequence KW - Tandem Mass Spectrometry KW - Drug Resistance, Multiple KW - Glutathione Peroxidase -- chemistry KW - Enzyme Inhibitors -- pharmacology KW - Tiopronin -- pharmacology KW - Glutathione Peroxidase -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551027856?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+glutathione+peroxidase+mediates+the+collateral+sensitivity+of+multidrug-resistant+cells+to+tiopronin.&rft.au=Hall%2C+Matthew+D%3BMarshall%2C+Travis+S%3BKwit%2C+Alexandra+D+T%3BMiller+Jenkins%2C+Lisa+M%3BDulcey%2C+Andr%C3%A9s+E%3BMadigan%2C+James+P%3BPluchino%2C+Kristen+M%3BGoldsborough%2C+Andrew+S%3BBrimacombe%2C+Kyle+R%3BGriffiths%2C+Gary+L%3BGottesman%2C+Michael+M&rft.aulast=Hall&rft.aufirst=Matthew&rft.date=2014-08-01&rft.volume=289&rft.issue=31&rft.spage=21473&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.581702 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-15 N1 - Date created - 2014-08-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2006 May 1;66(9):4808-15 [16651436] J Org Chem. 2006 Mar 31;71(7):2848-53 [16555841] J Biol Chem. 2006 Dec 29;281(52):40485-92 [17088248] Nucleic Acids Res. 2007;35(2):414-23 [17169995] Blood. 2007 Apr 15;109(8):3409-16 [17179223] Biochem Pharmacol. 2007 Jun 1;73(11):1727-37 [17359940] Free Radic Biol Med. 2007 Nov 1;43(9):1271-8 [17893040] Curr Opin Investig Drugs. 2007 Dec;8(12):1022-37 [18058573] Oncologist. 2008 Mar;13(3):277-83 [18378537] Oncogene. 2008 Apr 24;27(19):2754-62 [17998936] Oncol Rep. 2008 Dec;20(6):1299-303 [19020706] J Med Chem. 2009 May 28;52(10):3191-204 [19397322] Assay Drug Dev Technol. 2009 Jun;7(3):233-49 [19548831] Trends Pharmacol Sci. 2009 Oct;30(10):546-56 [19762091] J Nat Prod. 2011 Apr 25;74(4):567-73 [21348461] Nat Rev Drug Discov. 2011 May;10(5):351-64 [21532565] Nature. 2011 Jul 14;475(7355):231-4 [21753854] J Med Chem. 2011 Jul 28;54(14):4987-97 [21657271] Antioxid Redox Signal. 2011 Oct 1;15(7):1957-97 [21087145] Drug Resist Updat. 2012 Feb-Apr;15(1-2):98-105 [22483810] Clin Cancer Res. 2012 Jun 1;18(11):3197-206 [22492981] Arch Biochem Biophys. 2012 Sep 15;525(2):95-101 [22326823] Bioorg Med Chem Lett. 2012 Nov 1;22(21):6712-5 [23031590] Antioxid Redox Signal. 2014 Jan 10;20(2):372-82 [22978713] Cell. 2014 Jan 16;156(1-2):317-31 [24439385] J Med Chem. 2011 Aug 25;54(16):5878-89 [21721528] J Exp Bot. 2000 Dec;51(353):2053-66 [11141179] Cell Mol Life Sci. 2000 Dec;57(13-14):1825-35 [11215509] Toxicol Sci. 2001 Sep;63(1):57-64 [11509744] Hum Cell. 2001 Sep;14(3):237-43 [11774743] Annu Rev Med. 2002;53:615-27 [11818492] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585] Free Radic Res. 2003 Feb;37(2):205-11 [12653209] Science. 2003 May 30;300(5624):1439-43 [12775843] Br J Pharmacol. 2004 May;142(2):231-55 [15155533] J Biol Chem. 1984 Jan 25;259(2):1043-50 [6693375] J Biol Chem. 1986 Jun 15;261(17):7762-70 [3711108] J Biol Chem. 1986 Nov 25;261(33):15544-9 [3782078] Int J Cancer. 1988 Sep 15;42(3):373-81 [3417366] Blood. 1989 Jan;73(1):334-9 [2491951] FEBS Lett. 1990 Jul 30;268(1):69-71 [2384174] Cancer Res. 1991 Jan 15;51(2):521-7 [1845955] Pharmacol Ther. 1990;47(3):359-70 [2290853] Free Radic Res Commun. 1992;16(5):315-23 [1505789] Int J Cancer. 1994 Mar 1;56(5):749-54 [7906257] Immunopharmacology. 1997 Jan;35(3):195-202 [9043932] Clin Chim Acta. 1997 May 6;261(1):35-42 [9187503] Brain Res Brain Res Protoc. 1998 Mar;2(3):223-8 [9507143] J Biomed Sci. 1999 May-Jun;6(3):151-60 [10343164] Free Radic Biol Med. 1999 Jul;27(1-2):146-59 [10443931] Free Radic Biol Med. 1999 Sep;27(5-6):612-6 [10490282] J Neurosci Res. 2005 Jan 1-15;79(1-2):157-65 [15573410] J Biol Chem. 2006 Dec 1;281(48):36501-9 [16956878] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.581702 ER - TY - JOUR T1 - Dual VEGF/VEGFR inhibition in advanced solid malignancies: clinical effects and pharmacodynamic biomarkers. AN - 1551027207; 24842548 AB - Our prior phase I study of the combination of vascular endothelial growth factor (VEGF) antibody, bevacizumab, and VEGF receptor (VEGFR) inhibitor, sunitinib, in advanced solid tumors identified an encouraging response evaluation. An expansion phase of this study was thus undertaken to obtain further safety data, response assessment and characterization of pharmacodynamic biomarkers in melanoma, renal, and adrenal carcinoma patients. Patients with metastatic solid tumors received sunitinib (37.5 mg/d, 4 wk on/2 wk off) and bevacizumab (5 mg/kg intravenously every 2 wk). Responses were assessed every 2 cycles. Serum levels of angiogenic molecules were measured using ELISA assays. Twenty-two patients were enrolled, including 11 melanoma, 5 renal cell carcinoma (RCC), 5 adrenal cancer, and 1 angiosarcoma. Grade 3 or higher adverse events were observed in 15 patients, including hypertension (41%), thrombocytopenia (23%), and fatigue (14%). Three RCC patients, and 1 melanoma patient developed thrombotic microangiopathy (TMA). Partial response (PR) occurred in 21% patients, including melanoma (2), adrenal (1), and renal (1) carcinomas. Overall, 6 patients demonstrated some reduction in their tumor burden. Serum VEGF and several other proangiogenic proteins declined over the first 4 wk of treatment whereas the putative VEGF-resistant protein, prokineticin-2, increased over 10-fold. Occurrence of TMA related to dual VEGF/VEGFR inhibition can result from systemic or nephron specific injury even in non-renal malignancies. While the combination of sunitinib and bevacizumab was clinically efficacious in renal cell carcinoma and melanoma, the observance of microangiopathy, even in non-RCC patients, is a significant toxicity that precludes further clinical development. JF - Cancer biology & therapy AU - Mittal, Kriti AU - Koon, Henry AU - Elson, Paul AU - Triozzi, Pierre AU - Dowlati, Afshin AU - Chen, Helen AU - Borden, Ernest C AU - Rini, Brian I AD - Cleveland Clinic Taussig Cancer Institute; Cleveland, OH USA. ; Case Western University; Cleveland, OH USA. ; National Cancer Institute; Rockville, MD USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 975 EP - 981 VL - 15 IS - 8 KW - Antibodies, Monoclonal, Humanized KW - 0 KW - Biomarkers, Pharmacological KW - Gastrointestinal Hormones KW - Indoles KW - Neuropeptides KW - PROK2 protein, human KW - Pyrroles KW - Vascular Endothelial Growth Factor A KW - Bevacizumab KW - 2S9ZZM9Q9V KW - Receptors, Vascular Endothelial Growth Factor KW - EC 2.7.10.1 KW - sunitinib KW - V99T50803M KW - Index Medicus KW - VEGFR KW - VEGF KW - bevacizumab KW - angiogenesis KW - Neuropeptides -- metabolism KW - Pyrroles -- administration & dosage KW - Biomarkers, Pharmacological -- metabolism KW - Gastrointestinal Hormones -- metabolism KW - Humans KW - Indoles -- administration & dosage KW - Middle Aged KW - Antibodies, Monoclonal, Humanized -- administration & dosage KW - Male KW - Female KW - Vascular Endothelial Growth Factor A -- antagonists & inhibitors KW - Neoplasms -- drug therapy KW - Receptors, Vascular Endothelial Growth Factor -- antagonists & inhibitors KW - Receptors, Vascular Endothelial Growth Factor -- metabolism KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Vascular Endothelial Growth Factor A -- metabolism KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551027207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology+%26+therapy&rft.atitle=Dual+VEGF%2FVEGFR+inhibition+in+advanced+solid+malignancies%3A+clinical+effects+and+pharmacodynamic+biomarkers.&rft.au=Mittal%2C+Kriti%3BKoon%2C+Henry%3BElson%2C+Paul%3BTriozzi%2C+Pierre%3BDowlati%2C+Afshin%3BChen%2C+Helen%3BBorden%2C+Ernest+C%3BRini%2C+Brian+I&rft.aulast=Mittal&rft.aufirst=Kriti&rft.date=2014-08-01&rft.volume=15&rft.issue=8&rft.spage=975&rft.isbn=&rft.btitle=&rft.title=Cancer+biology+%26+therapy&rft.issn=1555-8576&rft_id=info:doi/10.4161%2Fcbt.29187 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-03 N1 - Date created - 2014-08-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Ann Oncol. 2004 Jan;15(1):139-45 [14679134] Clin Cancer Res. 2009 Feb 15;15(4):1384-92 [19228739] J Clin Oncol. 2009 Mar 20;27(9):1432-9 [19224847] J Am Acad Dermatol. 2009 May;60(5):758-66 [19389518] Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6742-7 [19346489] Clin Cancer Res. 2009 Oct 1;15(19):6277-83 [19773375] Expert Rev Anticancer Ther. 2009 Nov;9(11):1583-98 [19895243] Blood. 2010 Jan 28;115(4):846-9 [19965686] J Clin Oncol. 2010 Jun 10;28(17):e284-5; author reply e286-7 [20439632] Cancer Lett. 2010 Oct 28;296(2):144-9 [20633984] BMC Cancer. 2010;10:695 [21194438] Haematologica. 2011 Feb;96(2):333-6 [20952514] Curr Top Med Chem. 2012;12(1):32-49 [22196268] J Clin Oncol. 2012 Feb 1;30(4):362-71 [22184370] J Clin Oncol. 2012 Feb 1;30(4):441-4 [22184396] Arch Dermatol Res. 2012 Jul;304(5):397-400 [22410864] Clin Cancer Res. 2012 Jul 15;18(14):3750-61 [22547772] Clin Cancer Res. 2012 Jul 15;18(14):3961-71 [22573349] Blood. 2012 Sep 13;120(11):2330-9 [22718841] J Transl Med. 2012;10:241 [23217102] Nature. 2007 Dec 6;450(7171):825-31 [18064003] J Clin Oncol. 2001 Jan 15;19(2):577-83 [11208853] Oncol Res. 2000;12(5):241-51 [11417749] Am J Pathol. 2002 Mar;160(3):1009-19 [11891198] J Clin Oncol. 2002 Apr 1;20(7):1826-31 [11919240] J Pathol. 2002 Jul;197(3):355-62 [12115882] Melanoma Res. 2002 Aug;12(4):325-34 [12170181] J Clin Oncol. 2002 Nov 1;20(21):4368-80 [12409337] Semin Oncol. 2002 Dec;29(6 Suppl 16):3-9 [12516032] N Engl J Med. 2003 Jul 31;349(5):427-34 [12890841] Cancer Lett. 2003 Jul 30;198(1):83-8 [12893434] J Exp Med. 1971 Feb 1;133(2):275-88 [4332371] Ann Surg. 1972 Mar;175(3):409-16 [5077799] Science. 1983 Feb 25;219(4587):983-5 [6823562] Science. 1989 Dec 8;246(4935):1306-9 [2479986] Science. 1989 Dec 8;246(4935):1309-12 [2479987] Am J Pathol. 1995 Jan;146(1):197-209 [7531947] Cancer Res. 1996 Jan 1;56(1):172-81 [8548760] Melanoma Res. 1999 Feb;9(1):59-68 [10338335] Anticancer Res. 2004 Nov-Dec;24(6):4255-8 [15736481] Blood. 2005 Apr 15;105(8):3286-94 [15618473] J Cell Mol Med. 2005 Apr-Jun;9(2):267-85 [15963249] Clin Cancer Res. 2005 Jul 15;11(14):5158-66 [16033831] Melanoma Res. 2005 Dec;15(6):515-22 [16314737] Annu Rev Med. 2006;57:1-18 [16409133] J Thromb Haemost. 2006 Mar;4(3):671-7 [16460450] Kidney Int. 2006 Jul;70(1):16-23 [16760911] Cancer Res. 2006 Aug 15;66(16):7833-6 [16912153] Clin Cancer Res. 2007 Apr 15;13(8):2422-8 [17438101] Expert Opin Pharmacother. 2007 Oct;8(14):2359-69 [17927489] Cancer Metastasis Rev. 2007 Dec;26(3-4):443-52 [17786538] Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2640-5 [18268320] N Engl J Med. 2008 Mar 13;358(11):1129-36 [18337603] Annu Rev Pathol. 2008;3:249-77 [18215115] Cancer Res. 2008 Jul 15;68(14):5501-4 [18632597] Med Oncol. 2008;25(4):431-6 [18363112] Cancer Lett. 2004 Sep 30;213(2):241-8 [15327840] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4161/cbt.29187 ER - TY - JOUR T1 - Predicted 25(OH)D score and colorectal cancer risk according to vitamin D receptor expression. AN - 1551027056; 24920642 AB - Despite accumulating evidence for the preventive effect of vitamin D on colorectal carcinogenesis, its precise mechanisms remain unclear. We hypothesized that vitamin D was associated with a lower risk of colorectal cancer with high-level vitamin D receptor (VDR) expression, but not with risk of tumor with low-level VDR expression. Among 140,418 participants followed from 1986 through 2008 in the Nurses' Health Study and the Health Professionals' Follow-up Study, we identified 1,059 incident colorectal cancer cases with tumor molecular data. The predicted 25-hydroxyvitamin D [25(OH)D] score was developed using the known determinants of plasma 25(OH)D. We estimated the HR for cancer subtypes using the duplication method Cox proportional hazards model. A higher predicted 25(OH)D score was associated with a lower risk of colorectal cancer irrespective of VDR expression level (P(heterogeneity) for subtypes = 0.75). Multivariate HRs (95% confidence intervals) comparing the highest with the lowest quintile of predicted 25(OH)D scores were 0.48 (0.30-0.78) for VDR-negative tumor and 0.56 (0.42-0.75) for VDR-positive tumor. Similarly, the significant inverse associations of the predicted 25(OH)D score with colorectal cancer risk did not significantly differ by KRAS, BRAF, or PIK3CA status (P(heterogeneity) for subtypes ≥ 0.22). A higher predicted vitamin D score was significantly associated with a lower colorectal cancer risk, regardless of VDR status and other molecular features examined. The preventive effect of vitamin D on colorectal carcinogenesis may not totally depend on tumor factors. Host factors (such as local and systemic immunity) may need to be considered. ©2014 American Association for Cancer Research. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Jung, Seungyoun AU - Qian, Zhi Rong AU - Yamauchi, Mai AU - Bertrand, Kimberly A AU - Fitzgerald, Kathryn C AU - Inamura, Kentaro AU - Kim, Sun A AU - Mima, Kosuke AU - Sukawa, Yasutaka AU - Zhang, Xuehong AU - Wang, Molin AU - Smith-Warner, Stephanie A AU - Wu, Kana AU - Fuchs, Charles S AU - Chan, Andrew T AU - Giovannucci, Edward L AU - Ng, Kimmie AU - Cho, Eunyoung AU - Ogino, Shuji AU - Nishihara, Reiko AD - Channing Division of Network Medicine, Department of Medicine and. ; Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of. ; Epidemiology. ; Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland; and. ; Epidemiology, Biostatistics, and. ; Epidemiology, Nutrition, Harvard School of Public Health, Boston, Massachusetts; ; Nutrition, Harvard School of Public Health, Boston, Massachusetts; ; Channing Division of Network Medicine, Department of Medicine and Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of. ; Channing Division of Network Medicine, Department of Medicine and Division of Gastroenterology, Massachusetts General Hospital, Harvard Medical School; ; Channing Division of Network Medicine, Department of Medicine and Epidemiology, Nutrition, Harvard School of Public Health, Boston, Massachusetts; ; Channing Division of Network Medicine, Department of Medicine and Department of Dermatology, The Warren Alpert Medical School of Brown University, Providence, Rhode Island. ; Department of Pathology, Brigham and Women's Hospital and Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of Epidemiology, rnishiha@hsph.harvard.edu shuji_ogino@dfci.harvard.edu. ; Department of Medical Oncology, Dana-Farber Cancer Institute; Departments of Nutrition, Harvard School of Public Health, Boston, Massachusetts; rnishiha@hsph.harvard.edu shuji_ogino@dfci.harvard.edu. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1628 EP - 1637 VL - 23 IS - 8 KW - Receptors, Calcitriol KW - 0 KW - Vitamin D KW - 1406-16-2 KW - 25-hydroxyvitamin D KW - 64719-49-9 KW - Index Medicus KW - Polymerase Chain Reaction KW - Risk Factors KW - Humans KW - Adult KW - Incidence KW - Middle Aged KW - Immunohistochemistry KW - Male KW - Female KW - Receptors, Calcitriol -- biosynthesis KW - Colorectal Neoplasms -- metabolism KW - Receptors, Calcitriol -- analysis KW - Vitamin D -- blood KW - Vitamin D -- analogs & derivatives KW - Colorectal Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551027056?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Predicted+25%28OH%29D+score+and+colorectal+cancer+risk+according+to+vitamin+D+receptor+expression.&rft.au=Jung%2C+Seungyoun%3BQian%2C+Zhi+Rong%3BYamauchi%2C+Mai%3BBertrand%2C+Kimberly+A%3BFitzgerald%2C+Kathryn+C%3BInamura%2C+Kentaro%3BKim%2C+Sun+A%3BMima%2C+Kosuke%3BSukawa%2C+Yasutaka%3BZhang%2C+Xuehong%3BWang%2C+Molin%3BSmith-Warner%2C+Stephanie+A%3BWu%2C+Kana%3BFuchs%2C+Charles+S%3BChan%2C+Andrew+T%3BGiovannucci%2C+Edward+L%3BNg%2C+Kimmie%3BCho%2C+Eunyoung%3BOgino%2C+Shuji%3BNishihara%2C+Reiko&rft.aulast=Jung&rft.aufirst=Seungyoun&rft.date=2014-08-01&rft.volume=23&rft.issue=8&rft.spage=1628&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-14-0229 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-18 N1 - Date created - 2014-08-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Rev Cancer. 2003 Aug;3(8):601-14 [12894248] World J Gastroenterol. 2014 Apr 21;20(15):4230-43 [24764661] Am J Epidemiol. 1984 May;119(5):837-9 [6720679] Am J Epidemiol. 1985 Jul;122(1):51-65 [4014201] Control Clin Trials. 1986 Sep;7(3):177-88 [3802833] Pathologe. 1987 May;8(3):138-40 [3303008] Stat Med. 1989 May;8(5):551-61 [2657958] Br J Surg. 1991 Apr;78(4):435-9 [1851650] Am J Epidemiol. 1992 May 15;135(10):1114-26; discussion 1127-36 [1632423] Biometrics. 1995 Jun;51(2):524-32 [7662841] J Biol Chem. 2004 Nov 5;279(45):47298-310 [15331595] J Mol Diagn. 2005 Aug;7(3):413-21 [16049314] J Natl Cancer Inst. 2006 Apr 5;98(7):451-9 [16595781] J Mol Diagn. 2006 Nov;8(5):582-8 [17065427] N Engl J Med. 2007 May 24;356(21):2131-42 [17522398] J Natl Cancer Inst. 2007 Jul 18;99(14):1120-9 [17623801] Cancer Lett. 2007 Aug 28;254(1):75-86 [17412493] Stat Med. 2007 Sep 10;26(20):3735-52 [17538974] Nat Rev Cancer. 2007 Sep;7(9):684-700 [17721433] J Cell Biochem. 2008 Apr 1;103(5):1551-72 [17879954] Mol Aspects Med. 2008 Dec;29(6):388-96 [18755215] Cancer Epidemiol Biomarkers Prev. 2009 Oct;18(10):2765-72 [19789368] N Engl J Med. 2009 Dec 17;361(25):2449-60 [20018966] BMJ. 2010;340:b5500 [20093284] J Natl Cancer Inst. 2010 Mar 17;102(6):365-7 [20208016] Hum Mol Genet. 2010 Jul 1;19(13):2739-45 [20418485] Gut. 2010 Jun;59(6):794-9 [19828464] J Steroid Biochem Mol Biol. 2010 Jul;121(1-2):349-54 [20398758] Mol Nutr Food Res. 2010 Aug;54(8):1114-26 [20486209] Oncogene. 2014 Jun 5;33(23):2949-55 [23792451] Mol Cancer. 2014;13:135 [24885062] Tumour Biol. 2014 Jul;35(7):6195-206 [25051912] Genome Res. 2010 Oct;20(10):1352-60 [20736230] J Steroid Biochem Mol Biol. 2011 Jan;123(1-2):30-6 [20955794] Annu Rev Pharmacol Toxicol. 2011;51:311-36 [20936945] Gut. 2011 Mar;60(3):397-411 [21036793] Oncotarget. 2011 Mar;2(3):135-64 [21411864] J Clin Oncol. 2011 Oct 1;29(28):3775-82 [21876081] Radiat Res. 2001 Jan;155(1 Pt 2):156-162 [11121228] J Clin Endocrinol Metab. 2001 Feb;86(2):888-94 [11158062] Am J Clin Nutr. 2003 Jan;77(1):204-10 [12499343] J Biol Chem. 2003 Jan 24;278(4):2199-205 [12417593] Best Pract Res Clin Gastroenterol. 2011 Aug;25(4-5):485-94 [22122765] PLoS One. 2011;6(12):e28520 [22216097] Cell Cycle. 2012 Mar 15;11(6):1081-9 [22370479] Clin Cancer Res. 2012 Apr 15;18(8):2257-68 [22357840] Endocr Relat Cancer. 2012 Jun;19(3):R51-71 [22383428] Lung Cancer. 2012 Aug;77(2):265-71 [22564539] N Engl J Med. 2012 Oct 25;367(17):1596-606 [23094721] Br J Nutr. 2012 Nov 28;108(10):1889-96 [22264926] Mod Pathol. 2013 Apr;26(4):465-84 [23307060] Int J Mol Sci. 2013;14(8):16365-85 [23965959] J Bone Miner Res. 2004 Jan;19(1):133-46 [14753745] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1055-9965.EPI-14-0229 ER - TY - JOUR T1 - Vanadium as a chemoprotectant: effect of vanadium(III)-L-cysteine complex against cyclophosphamide-induced hepatotoxicity and genotoxicity in Swiss albino mice. AN - 1551025005; 24777843 AB - Vanadium is an essential micronutrient for living systems and has antioxidant and genoprotective property. In the present study, the protective role of an organovanadium compound vanadium(III)-L-cysteine (VC-III) was evaluated against hepatotoxicity and genotoxicity induced by cyclophosphamide (CP) (25 mg/kg b.w., i.p.) in Swiss albino mice. Treatment with VC-III (1 mg/kg b.w., p.o.) mitigated CP-induced hepatic injury as indicated by reduction in activities of alanine transaminase, aspartate transaminase, alkaline phosphatase by 1.57-, 1.58- and 1.32-fold in concomitant treatment schedule and by 1.83-, 1.77- and 1.45-fold in pretreatment schedule, respectively, and confirmed by histopathological evidences. Parallel to these changes, VC-III ameliorated CP-induced oxidative stress in liver by 1.46-, 1.26-, 1.32- and 1.42-fold in concomitant treatment group and by 1.95-, 1.40-, 1.46- and 1.73-fold in pretreatment group at the level of H2O2, superoxide, nitric oxide and lipid peroxidation, respectively. VC-III also enhanced activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase and glutathione (reduced) level in mice liver by 1.46-, 1.37-, 1.29-, 1.44- and 1.45-fold in concomitant treatment schedule and by 1.64-, 1.65-, 1.42-, 1.49- and 1.57-fold in pretreatment schedule, respectively. In addition, the organovanadium compound could efficiently attenuate CP-induced chromosomal aberrations, DNA fragmentation and apoptosis in bone marrow cells and DNA damage in lymphocytes by 1.49-, 1.43-, 1.48- and 1.59-fold in concomitant treatment group and by 1.76-, 1.92-, 1.99- and 2.15-fold in pretreatment group, respectively. Thus, the present study showed that VC-III could exert protection against CP-induced hepatotoxicity and genotoxicity. JF - Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry AU - Basu, Abhishek AU - Bhattacharjee, Arin AU - Roy, Somnath Singha AU - Ghosh, Prosenjit AU - Chakraborty, Pramita AU - Das, Ila AU - Bhattacharya, Sudin AD - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata, 700 026, West Bengal, India. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 981 EP - 996 VL - 19 IS - 6 KW - Mutagens KW - 0 KW - Organometallic Compounds KW - Vanadium KW - 00J9J9XKDE KW - Cyclophosphamide KW - 8N3DW7272P KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Animals KW - DNA Damage KW - Mutagens -- toxicity KW - Mice KW - Cytoprotection -- drug effects KW - Mutagens -- administration & dosage KW - Female KW - Cyclophosphamide -- administration & dosage KW - Organometallic Compounds -- pharmacology KW - Liver -- injuries KW - Cyclophosphamide -- antagonists & inhibitors KW - Liver -- metabolism KW - Cyclophosphamide -- toxicity KW - Vanadium -- chemistry KW - Organometallic Compounds -- chemistry KW - Chromosome Aberrations -- chemically induced KW - Chromosome Aberrations -- drug effects KW - Cysteine -- chemistry KW - Liver -- drug effects KW - Organometallic Compounds -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551025005?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biological+inorganic+chemistry+%3A+JBIC+%3A+a+publication+of+the+Society+of+Biological+Inorganic+Chemistry&rft.atitle=Vanadium+as+a+chemoprotectant%3A+effect+of+vanadium%28III%29-L-cysteine+complex+against+cyclophosphamide-induced+hepatotoxicity+and+genotoxicity+in+Swiss+albino+mice.&rft.au=Basu%2C+Abhishek%3BBhattacharjee%2C+Arin%3BRoy%2C+Somnath+Singha%3BGhosh%2C+Prosenjit%3BChakraborty%2C+Pramita%3BDas%2C+Ila%3BBhattacharya%2C+Sudin&rft.aulast=Basu&rft.aufirst=Abhishek&rft.date=2014-08-01&rft.volume=19&rft.issue=6&rft.spage=981&rft.isbn=&rft.btitle=&rft.title=Journal+of+biological+inorganic+chemistry+%3A+JBIC+%3A+a+publication+of+the+Society+of+Biological+Inorganic+Chemistry&rft.issn=1432-1327&rft_id=info:doi/10.1007%2Fs00775-014-1141-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-30 N1 - Date created - 2014-08-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00775-014-1141-6 ER - TY - JOUR T1 - Analysis of polychlorinated biphenyls and organochlorine pesticides in archived dried blood spots and its application to track temporal trends of environmental chemicals in newborns. AN - 1551023706; 24968082 AB - Dried blood spots (DBS) collected from infants shortly after birth for the newborn screening program (NSP) in the United States are valuable resources for the assessment of exposure to environmental chemicals in newborns. The NSP was debuted as a public health program in the United States in the 1960s; and the DBS samples collected over a period of time can be used in tracking temporal trends in exposure to environmental chemicals by newborns. In this study, polychlorinated biphenyls (PCBs) and organochlorine pesticides (OCPs) were measured in DBS samples collected from newborns in Upstate New York from 1997 to 2011 by gas chromatography-high resolution mass spectrometry (GC-HRMS). Twelve PCBs and two OCPs were found in DBS samples at a detection rate above 50% (n=51). The mean whole blood concentration of ΣPCBs (sum of 12 congeners) over the 15-year period was 1.06 ng/mL, followed by p,p'-DDE (0.421 ng/mL) and HCB (0.065 ng/mL). The measured concentrations of PCBs and p,p'-DDE in infants'blood were comparable to those reported in cord blood, suggesting maternal/trans-placental transfer of these compounds from mothers to fetuses. The concentrations of ΣPCBs and p,p'-DDE in blood samples of infants decreased significantly between 1997 and 2001, and no significant reduction was found thereafter. This observation is consistent with the trends reported for these chemicals in other human tissues in the United States. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Environmental research AU - Ma, Wan-Li AU - Gao, Chongjing AU - Bell, Erin M AU - Druschel, Charlotte M AU - Caggana, Michele AU - Aldous, Kenneth M AU - Louis, Germaine M Buck AU - Kannan, Kurunthachalam AD - Wadsworth Center, New York State Department of Health, and Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, Empire State Plaza, P.O. Box 509, Albany, NY 12201-0509, USA; International Joint Research Center for Persistent Toxic Substances, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin 150090, China. ; Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, Albany, NY, USA. ; New York State Department of Health, Bureau of Environmental & Occupational Epidemiology, Empire State Plaza-Corning Tower, Room 1203, Albany, NY 12237, USA; Department of Epidemiology and Biostatistics, School of Public Health, State University of New York at Albany, Albany, NY, USA. ; Wadsworth Center, New York State Department of Health, and Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, Empire State Plaza, P.O. Box 509, Albany, NY 12201-0509, USA. ; Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, the National Institutes of Health, 6100 Executive Blvd. Room 7B03, Rockville, MD 20852, USA. ; Wadsworth Center, New York State Department of Health, and Department of Environmental Health Sciences, School of Public Health, State University of New York at Albany, Empire State Plaza, P.O. Box 509, Albany, NY 12201-0509, USA; International Joint Research Center for Persistent Toxic Substances, State Key Laboratory of Urban Water Resource and Environment, Harbin Institute of Technology, Harbin 150090, China; Experimental Biochemistry Unit, King Fahd Medical Research Center, King Abdulaziz University, PO Box 80216, Jeddah 21589, Saudi Arabia. Electronic address: kkannan@wadsworth.org. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 204 EP - 210 VL - 133 KW - Environmental Pollutants KW - 0 KW - Hydrocarbons, Chlorinated KW - Pesticides KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - PCBs KW - OCPs KW - Temporal trend KW - Dried blood spot KW - Infants KW - New York KW - Humans KW - Reference Standards KW - Infant, Newborn KW - Time Factors KW - Quality Control KW - Neonatal Screening -- trends KW - Hydrocarbons, Chlorinated -- blood KW - Polychlorinated Biphenyls -- blood KW - Hydrocarbons, Chlorinated -- adverse effects KW - Environmental Pollutants -- blood KW - Pesticides -- adverse effects KW - Environmental Pollutants -- adverse effects KW - Polychlorinated Biphenyls -- adverse effects KW - Pesticides -- blood KW - Neonatal Screening -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551023706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+research&rft.atitle=Analysis+of+polychlorinated+biphenyls+and+organochlorine+pesticides+in+archived+dried+blood+spots+and+its+application+to+track+temporal+trends+of+environmental+chemicals+in+newborns.&rft.au=Ma%2C+Wan-Li%3BGao%2C+Chongjing%3BBell%2C+Erin+M%3BDruschel%2C+Charlotte+M%3BCaggana%2C+Michele%3BAldous%2C+Kenneth+M%3BLouis%2C+Germaine+M+Buck%3BKannan%2C+Kurunthachalam&rft.aulast=Ma&rft.aufirst=Wan-Li&rft.date=2014-08-01&rft.volume=133&rft.issue=&rft.spage=204&rft.isbn=&rft.btitle=&rft.title=Environmental+research&rft.issn=1096-0953&rft_id=info:doi/10.1016%2Fj.envres.2014.05.029 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-03 N1 - Date created - 2014-08-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Arch Environ Health. 1999 Jan-Feb;54(1):40-7 [10025415] Biochem Mol Med. 1997 Aug;61(2):236-9 [9259989] Environ Sci Technol. 2006 Nov 1;40(21):6587-93 [17144282] Environ Sci Technol. 2006 Dec 1;40(23):7157-66 [17180962] Environ Res. 2007 Jun;104(2):296-304 [17189629] Environ Health Perspect. 2007 Aug;115(8):1204-9 [17687448] Environ Health Perspect. 2007 Dec;115(12):1767-79 [18087597] Environ Sci Technol. 2008 Jul 15;42(14):5361-7 [18754394] Environ Sci Technol. 2008 Sep 15;42(18):6991-6 [18853821] Anal Chim Acta. 2009 Dec 10;656(1-2):51-5 [19932814] Anal Bioanal Chem. 2010 May;397(2):687-93 [20229277] Anal Chem. 2009 Mar 1;81(5):1931-6 [19199567] Environ Sci Technol. 2010 Aug 15;44(16):6488-95 [20666461] Environ Sci Technol. 2010 Nov 1;44(21):8050-5 [20932001] Chemosphere. 2011 Jan;82(5):687-91 [21111447] Environ Health Perspect. 2012 Mar;120(3):451-7 [22027556] J Chromatogr B Analyt Technol Biomed Life Sci. 2012 Apr 1;891-892:36-43 [22406104] J Chromatogr B Analyt Technol Biomed Life Sci. 2012 May 15;897:72-9 [22552005] J Pharm Biomed Anal. 2012 Aug-Sep;67-68:86-91 [22559989] Environ Health Perspect. 2013 Feb;121(2):153-61 [23131992] Environ Health Perspect. 2013 Feb;121(2):231-6 [23151773] Anal Bioanal Chem. 2013 May;405(12):4127-38 [23404131] Chemosphere. 2013 Jun;91(10):1426-33 [23453434] Environ Int. 2013 Jul;57-58:34-41 [23651836] Placenta. 2013 Jul;34(7):619-23 [23623486] Environ Health. 2013;12:44 [23724965] Environ Health Perspect. 2013 Jul;121(7):774-83 [23651634] Environ Sci Technol. 2013 Jul 16;47(14):8015-21 [23755886] Environ Sci Technol. 2014;48(1):753-60 [24298999] Paediatr Perinat Epidemiol. 2014 May;28(3):191-202 [24665916] Clin Chem. 2000 Jan;46(1):126-8 [10620584] Sci Total Environ. 2002 Oct 21;298(1-3):45-53 [12449328] Environ Health Perspect. 2004 May;112(6):654-8 [15121506] Bull Environ Contam Toxicol. 1996 Jan;56(1):50-7 [9026157] Sci Total Environ. 2006 Dec 15;372(1):20-31 [16650462] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.envres.2014.05.029 ER - TY - JOUR T1 - Research resource: comparison of gene profiles from wild-type ERα and ERα hinge region mutants. AN - 1551019542; 24947674 AB - We showed previously that the hinge region of estrogen receptor (ER) α is involved in mediating its actions. The hinge 1 (H1) ERα mutant has disrupted nuclear localization and has lost interaction with c-JUN, but retains estrogen response element (ERE)-mediated functions. The hinge 2 + nuclear export sequence (H2NES) ERα mutant does not maintain nuclear translocation with hormone and no longer activates ERE target genes but does retain a nongenomic, nonnuclear, rapid-action response. Herein, we used the human endometrial cancer Ishikawa stable cell lines (Ishikawa/vector, Ishikawa/wild-type [WT] ERα, Ishikawa/H1 ERα, or Ishikawa/H2NES ERα) to characterize the biological activities of these 2 ERα hinge region mutants. We confirmed by confocal microscopy increased cytoplasmic ERα in the H1 ERα cell line and full cytoplasmic ERα localization in the H2NES ERα cell line. Luciferase assays using the 3xERE reporter showed activation of H1 ERα and H2NES ERα by estradiol (E2) treatment, but using the endogenous pS2 reporter, luciferase activity was only seen with the H1 ERα cell line. Examining cell proliferation revealed that only the WT ERα and H1 ERα cell lines increased proliferation after treatment. Using microarrays, we found that WT ERα and H1 ERα cluster together, whereas vector and H2NES ERα are most similar and cluster independently of E2 treatment. These studies revealed that the nongenomic activities of ERα are unable to mediate proliferative changes or the transcriptional profile after treatment and demonstrate the importance of genomic action for ERα/E2-mediated responses with the nongenomic actions of ERα being complementary to elicit the full biological actions of ERα. JF - Molecular endocrinology (Baltimore, Md.) AU - Burns, Katherine A AU - Li, Yin AU - Liu, Liwen AU - Korach, Kenneth S AD - Receptor Biology (K.A.B., Y.L., K.S.K.), Laboratory of Reproductive and Developmental Toxicology and Molecular Genomics Core Facility (L.L.), National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1352 EP - 1361 VL - 28 IS - 8 KW - Estrogen Receptor alpha KW - 0 KW - estrogen receptor alpha, human KW - Estradiol KW - 4TI98Z838E KW - Index Medicus KW - Oligonucleotide Array Sequence Analysis KW - HeLa Cells KW - Cell Nucleus -- metabolism KW - Humans KW - Estradiol -- physiology KW - Gene Expression Regulation KW - Protein Structure, Tertiary KW - Cell Proliferation KW - Protein Transport KW - Estrogen Receptor alpha -- genetics KW - Transcriptome KW - Estrogen Receptor alpha -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551019542?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Research+resource%3A+comparison+of+gene+profiles+from+wild-type+ER%CE%B1+and+ER%CE%B1+hinge+region+mutants.&rft.au=Burns%2C+Katherine+A%3BLi%2C+Yin%3BLiu%2C+Liwen%3BKorach%2C+Kenneth+S&rft.aulast=Burns&rft.aufirst=Katherine&rft.date=2014-08-01&rft.volume=28&rft.issue=8&rft.spage=1352&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=1944-9917&rft_id=info:doi/10.1210%2Fme.2014-1122 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-30 N1 - Date created - 2014-08-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Vitam Horm. 2001;62:231-52 [11345900] Hum Cell. 2002 Sep;15(3):104-17 [12703541] J Biol Chem. 2001 Sep 28;276(39):36361-9 [11477071] J Steroid Biochem Mol Biol. 2000 Nov 30;74(5):311-7 [11162939] J Biol Chem. 2001 Apr 27;276(17):13615-21 [11278408] Mol Endocrinol. 2001 Nov;15(11):1953-70 [11682626] Mol Endocrinol. 2002 Aug;16(8):1810-27 [12145336] Mol Endocrinol. 2002 Oct;16(10):2188-201 [12351685] Endocr Rev. 2002 Oct;23(5):665-86 [12372846] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886] Nat Rev Drug Discov. 2004 Jan;3(1):27-41 [14708019] Nucleic Acids Res. 1982 Dec 20;10(24):7895-903 [6897676] Nucleic Acids Res. 1993 Mar 11;21(5):1125-32 [8385312] Mol Endocrinol. 1993 Aug;7(8):992-8 [8232319] Endocr Rev. 1994 Jun;15(3):391-407 [8076589] J Biol Chem. 1995 May 12;270(19):11502-13 [7744790] Genes Chromosomes Cancer. 1995 May;13(1):18-24 [7541639] Cell. 1995 Dec 15;83(6):835-9 [8521507] Mol Endocrinol. 1997 Mar;11(3):353-65 [9058381] Steroids. 1999 May;64(5):310-9 [10406480] Mol Endocrinol. 1999 Oct;13(10):1672-85 [10517669] Trends Endocrinol Metab. 2005 Oct;16(8):347-53 [16126407] Mol Interv. 2005 Dec;5(6):343-57 [16394250] Endocr Rev. 2007 Dec;28(7):726-41 [17916740] Mol Endocrinol. 2008 Jul;22(7):1535-51 [18388150] Mol Cell Endocrinol. 2008 Aug 13;290(1-2):24-30 [18534740] Mol Endocrinol. 2008 Sep;22(9):2116-27 [18617595] J Biol Chem. 2009 Feb 6;284(6):3488-95 [19054762] Environ Health Perspect. 2009 Jul;117(7):1155-61 [19654927] Mol Endocrinol. 2009 Dec;23(12):2111-6 [19812388] J Biol Chem. 2010 Jan 22;285(4):2676-85 [19920132] J Cell Sci. 2010 Apr 15;123(Pt 8):1253-61 [20332105] J Clin Invest. 2010 Jul;120(7):2319-30 [20577047] Mol Cell Biol. 2011 Jan;31(1):226-36 [20956553] J Biol Chem. 2011 Apr 8;286(14):12640-9 [21285458] Environ Health Perspect. 2012 Jul;120(7):1029-35 [22494775] Mol Cancer Res. 2012 Aug;10(8):1120-32 [22669764] Gynecol Oncol. 2012 Oct;127(1):241-8 [22710073] Mol Endocrinol. 2013 Jan;27(1):2-11 [23242705] Proc Natl Acad Sci U S A. 2013 Oct 22;110(43):17284-9 [24101509] Proc Natl Acad Sci U S A. 2014 Jan 14;111(2):E283-90 [24371309] Steroids. 2014 Mar;81:64-9 [24252382] J Biol Chem. 2003 Apr 4;278(14):12255-62 [12547836] J Biol Chem. 2001 May 25;276(21):18375-83 [11279135] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/me.2014-1122 ER - TY - JOUR T1 - Whole-exome and targeted gene sequencing of gallbladder carcinoma identifies recurrent mutations in the ErbB pathway. AN - 1549632568; 24997986 AB - Individuals with gallbladder carcinoma (GBC), the most aggressive malignancy of the biliary tract, have a poor prognosis. Here we report the identification of somatic mutations for GBC in 57 tumor-normal pairs through a combination of exome sequencing and ultra-deep sequencing of cancer-related genes. The mutation pattern is defined by a dominant prevalence of C>T mutations at TCN sites. Genes with a significant frequency (false discovery rate (FDR)<0.05) of non-silent mutations include TP53 (47.1%), KRAS (7.8%) and ERBB3 (11.8%). Moreover, ErbB signaling (including EGFR, ERBB2, ERBB3, ERBB4 and their downstream genes) is the most extensively mutated pathway, affecting 36.8% (21/57) of the GBC samples. Multivariate analyses further show that cases with ErbB pathway mutations have a worse outcome (P=0.001). These findings provide insight into the somatic mutational landscape in GBC and highlight the key role of the ErbB signaling pathway in GBC pathogenesis. JF - Nature genetics AU - Li, Maolan AU - Zhang, Zhou AU - Li, Xiaoguang AU - Ye, Junyi AU - Wu, Xiangsong AU - Tan, Zhujun AU - Liu, Chang AU - Shen, Baiyong AU - Wang, Xu-An AU - Wu, Wenguang AU - Zhou, Daizhan AU - Zhang, Di AU - Wang, Ting AU - Liu, Bingya AU - Qu, Kai AU - Ding, Qichen AU - Weng, Hao AU - Ding, Qian AU - Mu, Jiasheng AU - Shu, Yijun AU - Bao, Runfa AU - Cao, Yang AU - Chen, Peizhan AU - Liu, Tianyu AU - Jiang, Lin AU - Hu, Yunping AU - Dong, Ping AU - Gu, Jun AU - Lu, Wei AU - Shi, Weibin AU - Lu, Jianhua AU - Gong, Wei AU - Tang, Zhaohui AU - Zhang, Yong AU - Wang, Xuefeng AU - Chin, Y Eugene AU - Weng, Xiaoling AU - Zhang, Hong AU - Tang, Wei AU - Zheng, Yonglan AU - He, Lin AU - Wang, Hui AU - Liu, Yun AU - Liu, Yingbin AD - 1] Department of General Surgery, Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. [2] Institute of Biliary Tract Disease, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [3]. ; 1] Department of General Surgery, Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. [2] Institute of Biliary Tract Disease, Shanghai Jiao Tong University School of Medicine, Shanghai, China. [3] Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Center, Shanghai Jiao Tong University, Shanghai, China. [4]. ; 1] Key Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China. [2]. ; Institutes of Biomedical Sciences, Fudan University, Shanghai, China. ; 1] Department of General Surgery, Xinhua Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. [2] Institute of Biliary Tract Disease, Shanghai Jiao Tong University School of Medicine, Shanghai, China. ; Department of Hepatobiliary Surgery, The First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, China. ; Department of General Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. ; Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Center, Shanghai Jiao Tong University, Shanghai, China. ; Key Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China. ; Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, US National Institutes of Health, Bethesda, Maryland, USA. ; Department of Medicine, The University of Chicago, Chicago, Illinois, USA. ; 1] Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Center, Shanghai Jiao Tong University, Shanghai, China. [2] Institutes of Biomedical Sciences, Fudan University, Shanghai, China. [3] Women's Hospital, Zhejiang University School of Medicine, Hangzhou, China. ; 1] Key Laboratory of Food Safety Research, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China. [2] Key Laboratory of Food Safety Risk Assessment, Ministry of Health, Beijing, China. [3]. ; 1] Institutes of Biomedical Sciences, Fudan University, Shanghai, China. [2]. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 872 EP - 876 VL - 46 IS - 8 KW - EGFR protein, human KW - EC 2.7.10.1 KW - Receptor, Epidermal Growth Factor KW - Index Medicus KW - High-Throughput Nucleotide Sequencing -- methods KW - Aged, 80 and over KW - Humans KW - HEK293 Cells KW - Adult KW - Signal Transduction -- genetics KW - Aged KW - Middle Aged KW - Cell Line, Tumor KW - Male KW - Female KW - Cell Line KW - Gallbladder Neoplasms -- enzymology KW - Receptor, Epidermal Growth Factor -- genetics KW - Exome KW - Neoplasm Recurrence, Local -- enzymology KW - Carcinoma -- enzymology KW - Gallbladder Neoplasms -- genetics KW - Mutation KW - Neoplasm Recurrence, Local -- genetics KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549632568?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+genetics&rft.atitle=Whole-exome+and+targeted+gene+sequencing+of+gallbladder+carcinoma+identifies+recurrent+mutations+in+the+ErbB+pathway.&rft.au=Li%2C+Maolan%3BZhang%2C+Zhou%3BLi%2C+Xiaoguang%3BYe%2C+Junyi%3BWu%2C+Xiangsong%3BTan%2C+Zhujun%3BLiu%2C+Chang%3BShen%2C+Baiyong%3BWang%2C+Xu-An%3BWu%2C+Wenguang%3BZhou%2C+Daizhan%3BZhang%2C+Di%3BWang%2C+Ting%3BLiu%2C+Bingya%3BQu%2C+Kai%3BDing%2C+Qichen%3BWeng%2C+Hao%3BDing%2C+Qian%3BMu%2C+Jiasheng%3BShu%2C+Yijun%3BBao%2C+Runfa%3BCao%2C+Yang%3BChen%2C+Peizhan%3BLiu%2C+Tianyu%3BJiang%2C+Lin%3BHu%2C+Yunping%3BDong%2C+Ping%3BGu%2C+Jun%3BLu%2C+Wei%3BShi%2C+Weibin%3BLu%2C+Jianhua%3BGong%2C+Wei%3BTang%2C+Zhaohui%3BZhang%2C+Yong%3BWang%2C+Xuefeng%3BChin%2C+Y+Eugene%3BWeng%2C+Xiaoling%3BZhang%2C+Hong%3BTang%2C+Wei%3BZheng%2C+Yonglan%3BHe%2C+Lin%3BWang%2C+Hui%3BLiu%2C+Yun%3BLiu%2C+Yingbin&rft.aulast=Li&rft.aufirst=Maolan&rft.date=2014-08-01&rft.volume=46&rft.issue=8&rft.spage=872&rft.isbn=&rft.btitle=&rft.title=Nature+genetics&rft.issn=1546-1718&rft_id=info:doi/10.1038%2Fng.3030 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-12 N1 - Date created - 2014-07-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: Cancer Discov. 2014 Sep;4(9):OF12 [25185194] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ng.3030 ER - TY - JOUR T1 - Inducible nitric oxide synthase is key to peroxynitrite-mediated, LPS-induced protein radical formation in murine microglial BV2 cells. AN - 1549199269; 24746617 AB - Microglia are the resident immune cells in the brain. Microglial activation is characteristic of several inflammatory and neurodegenerative diseases including Alzheimer's disease, multiple sclerosis, and Parkinson's disease. Though lipopolysaccharide (LPS)-induced microglial activation in models of Parkinson's disease is well documented, the free radical-mediated protein radical formation and its underlying mechanism during LPS-induced microglial activation are not known. Here we have used immuno-spin trapping and RNA interference to investigate the role of inducible nitric oxide synthase (iNOS) in peroxynitrite-mediated protein radical formation in murine microglial BV2 cells treated with LPS. Treatment of BV2 cells with LPS resulted in morphological changes, induction of iNOS, and increased protein radical formation. Pretreatments with FeTPPS (a peroxynitrite decomposition catalyst), L-NAME (total NOS inhibitor), 1400W (iNOS inhibitor), and apocynin significantly attenuated LPS-induced protein radical formation and tyrosine nitration. Results obtained with coumarin-7-boronic acid, a highly specific probe for peroxynitrite detection, correlated with LPS-induced tyrosine nitration, which demonstrated involvement of peroxynitrite in protein radical formation. A similar degree of protection conferred by 1400W and L-NAME led us to conclude that only iNOS, and no other forms of NOS, is involved in LPS-induced peroxynitrite formation. Subsequently, siRNA for iNOS, the iNOS-specific inhibitor 1400W, the NF-κB inhibitor PDTC, and the p38 MAPK inhibitor SB202190 was used to inhibit iNOS directly or indirectly. Inhibition of iNOS precisely correlated with decreased protein radical formation in LPS-treated BV2 cells. The time course of protein radical formation also matched the time course of iNOS expression. Taken together, these results prove the role of iNOS in peroxynitrite-mediated protein radical formation in LPS-treated microglial BV2 cells. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Free radical biology & medicine AU - Kumar, Ashutosh AU - Chen, Shih-Heng AU - Kadiiska, Maria B AU - Hong, Jau-Shyong AU - Zielonka, Jacek AU - Kalyanaraman, Balaraman AU - Mason, Ronald P AD - Free Radical Metabolism Group, Laboratory of Toxicology & Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: kumara10@niehs.nih.gov. ; Neuropharmacology Group, Laboratory of Toxicology & Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Free Radical Metabolism Group, Laboratory of Toxicology & Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Department of Biophysics and Free Radical Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 51 EP - 59 VL - 73 KW - 5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinato iron(III) chloride KW - 0 KW - Acetophenones KW - Amidines KW - Antioxidants KW - Benzylamines KW - Boronic Acids KW - Coumarins KW - Enzyme Inhibitors KW - Free Radicals KW - Imidazoles KW - Lipopolysaccharides KW - Metalloporphyrins KW - N-(3-(aminomethyl)benzyl)acetamidine KW - NF-kappa B KW - Pyridines KW - RNA, Small Interfering KW - Thiocarbamates KW - prolinedithiocarbamate KW - 135467-92-4 KW - Peroxynitrous Acid KW - 14691-52-2 KW - Proline KW - 9DLQ4CIU6V KW - acetovanillone KW - B6J7B9UDTR KW - Nitric Oxide Synthase Type II KW - EC 1.14.13.39 KW - p38 Mitogen-Activated Protein Kinases KW - EC 2.7.11.24 KW - 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole KW - PVX798P8GI KW - NG-Nitroarginine Methyl Ester KW - V55S2QJN2X KW - Index Medicus KW - Nitrone adducts KW - Parkinson disease KW - Peroxynitrite KW - Inducible nitric oxide synthase KW - Free radicals KW - Microglia KW - Protein radical KW - Lipopolysaccharide KW - Boronic Acids -- pharmacology KW - Benzylamines -- pharmacology KW - Animals KW - NG-Nitroarginine Methyl Ester -- pharmacology KW - Imidazoles -- pharmacology KW - Metalloporphyrins -- pharmacology KW - Spin Trapping KW - Coumarins -- pharmacology KW - Antioxidants -- pharmacology KW - Cell Line, Transformed KW - RNA Interference KW - Microglia -- metabolism KW - NF-kappa B -- antagonists & inhibitors KW - Proline -- pharmacology KW - Acetophenones -- pharmacology KW - Mice KW - Amidines -- pharmacology KW - p38 Mitogen-Activated Protein Kinases -- antagonists & inhibitors KW - Microglia -- cytology KW - Enzyme Inhibitors -- pharmacology KW - Thiocarbamates -- pharmacology KW - Pyridines -- pharmacology KW - Proline -- analogs & derivatives KW - Peroxynitrous Acid -- metabolism KW - Nitric Oxide Synthase Type II -- antagonists & inhibitors KW - Neurodegenerative Diseases -- metabolism KW - Nitric Oxide Synthase Type II -- metabolism KW - Nitric Oxide Synthase Type II -- genetics KW - Free Radicals -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549199269?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inducible+nitric+oxide+synthase+is+key+to+peroxynitrite-mediated%2C+LPS-induced+protein+radical+formation+in+murine+microglial+BV2+cells.&rft.au=Kumar%2C+Ashutosh%3BChen%2C+Shih-Heng%3BKadiiska%2C+Maria+B%3BHong%2C+Jau-Shyong%3BZielonka%2C+Jacek%3BKalyanaraman%2C+Balaraman%3BMason%2C+Ronald+P&rft.aulast=Kumar&rft.aufirst=Ashutosh&rft.date=2014-08-01&rft.volume=73&rft.issue=&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2014.04.014 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2014-07-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Mol Med. 2013 May;31(5):1030-6 [23546639] Glia. 2013 Jun;61(6):855-68 [23536230] J Immunol. 2013 May 1;190(9):4786-94 [23530143] Proc Natl Acad Sci U S A. 2013 Oct 8;110(41):E3945-54 [23983262] Neuropharmacology. 2014 Jul;82:108-20 [23973292] Free Radic Biol Med. 2013 Aug;61:265-72 [23624303] Brain Res. 2000 Jan 31;854(1-2):224-9 [10784126] Biochem Biophys Res Commun. 2000 Jun 24;273(1):5-9 [10873554] Free Radic Biol Med. 2000 Aug;29(3-4):222-30 [11035250] J Biol Chem. 2001 Sep 7;276(36):34051-8 [11425852] J Neurosci. 2002 May 1;22(9):3484-92 [11978825] Toxicology. 2002 Aug 1;177(1):1-9 [12126791] Eur J Neurosci. 2002 Dec;16(11):2103-12 [12473078] Neurology. 2004 Feb 24;62(4):635-6 [14981185] Nat Rev Immunol. 2004 Mar;4(3):181-9 [15039755] Free Radic Biol Med. 2004 May 15;36(10):1214-23 [15110386] Free Radic Biol Med. 2004 Nov 15;37(10):1591-603 [15477010] J Neurosci. 1986 Aug;6(8):2163-78 [3018187] J Neuroimmunol. 1990 May;27(2-3):229-37 [2110186] Free Radic Res Commun. 1991;15(2):111-27 [1661698] Arch Biochem Biophys. 1992 Nov 1;298(2):446-51 [1329657] Trends Neurosci. 1996 Aug;19(8):312-8 [8843599] Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):6954-8 [9192673] Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7659-63 [9636206] Nat Rev Neurosci. 2013 Jan;14(1):38-48 [23254192] Brain Res. 2013 Jan 25;1492:108-21 [23174417] Acc Chem Res. 2013 Feb 19;46(2):550-9 [23157446] Proc Natl Acad Sci U S A. 2013 Mar 19;110(12):E1102-11 [23487751] J Neurosci. 1998 Oct 15;18(20):8126-32 [9763459] Biochim Biophys Acta. 2005 Jan 17;1703(2):93-109 [15680218] Free Radic Biol Med. 2005 Oct 15;39(8):1050-8 [16198232] J Am Chem Soc. 2005 Nov 30;127(47):16652-9 [16305254] Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1391-418 [16986999] Neurobiol Dis. 2007 Feb;25(2):392-400 [17166727] Brain Res Rev. 2007 Apr;54(1):205-18 [17500094] Biochemistry. 2007 Jun 26;46(25):7536-48 [17530864] J Am Chem Soc. 2007 Nov 7;129(44):13493-501 [17939657] Immunology. 2008 May;124(1):58-67 [18028373] Nat Chem Biol. 2008 May;4(5):278-86 [18421291] Free Radic Biol Med. 2009 Nov 15;47(10):1401-7 [19686842] J Neural Transm (Vienna). 2010 Jan;117(1):13-22 [19866338] J Biol Chem. 2010 May 7;285(19):14210-6 [20194496] Neurosci Lett. 2010 Jun 14;477(1):6-10 [20399833] Mov Disord. 2011 May;26(6):993-1002 [21626544] J Biol Chem. 2012 Jan 27;287(5):2984-95 [22139901] Arch Pharm Res. 2012 Mar;35(4):709-15 [22553064] Free Radic Biol Med. 2012 Jul 1;53(1):172-81 [22580125] Clin Exp Pharmacol Physiol. 2012 Jul;39(7):599-607 [22519637] J Mol Neurosci. 2012 Sep;48(1):225-33 [22638860] Chem Res Toxicol. 2012 Sep 17;25(9):1793-9 [22731669] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2014.04.014 ER - TY - JOUR T1 - LC-MS-based metabolomics: an update. AN - 1548640885; 24710571 AB - Liquid chromatography-mass spectrometry (LC-MS)-based metabolomics can have a major impact in multiple research fields, especially when combined with other technologies, such as stable isotope tracers and genetically modified mice. This review highlights recent applications of metabolomic technology in the study of xenobiotic metabolism and toxicity, and the understanding of disease pathogenesis and therapeutics. Metabolomics has been employed to study metabolism of noscapine, an aryl hydrocarbon receptor antagonist, and to determine the mechanisms of liver toxicities of rifampicin and isoniazid, trichloroethylene, and gemfibrozil. Metabolomics-based insights into the pathogenesis of inflammatory bowel disease, alcohol-induced liver diseases, non-alcoholic steatohepatitis, and farnesoid X receptor signaling pathway-based therapeutic target discovery will also be discussed. Limitations in metabolomics technology such as sample preparation and lack of LC-MS databases and metabolite standards, need to be resolved in order to improve and broaden the application of metabolomic studies. JF - Archives of toxicology AU - Fang, Zhong-Ze AU - Gonzalez, Frank J AD - Laboratory of Metabolism, Center for Cancer Research, National Institutes of Health, Bethesda, MD, 20892, USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1491 EP - 1502 VL - 88 IS - 8 KW - Pharmaceutical Preparations KW - 0 KW - Xenobiotics KW - Index Medicus KW - Animals KW - Pharmaceutical Preparations -- metabolism KW - Disease -- etiology KW - Pharmaceutical Preparations -- chemistry KW - Biotransformation KW - Xenobiotics -- metabolism KW - Humans KW - Xenobiotics -- toxicity KW - Metabolomics -- methods KW - Mass Spectrometry KW - Chromatography, Liquid KW - Metabolomics -- instrumentation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548640885?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+toxicology&rft.atitle=LC-MS-based+metabolomics%3A+an+update.&rft.au=Fang%2C+Zhong-Ze%3BGonzalez%2C+Frank+J&rft.aulast=Fang&rft.aufirst=Zhong-Ze&rft.date=2014-08-01&rft.volume=88&rft.issue=8&rft.spage=1491&rft.isbn=&rft.btitle=&rft.title=Archives+of+toxicology&rft.issn=1432-0738&rft_id=info:doi/10.1007%2Fs00204-014-1234-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-30 N1 - Date created - 2014-07-25 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00204-014-1234-6 ER - TY - JOUR T1 - Inactivation of Wnt signaling by a human antibody that recognizes the heparan sulfate chains of glypican-3 for liver cancer therapy. AN - 1548194944; 24492943 AB - Wnt signaling is important for cancer pathogenesis and is often up-regulated in hepatocellular carcinoma (HCC). Heparan sulfate proteoglycans (HSPGs) function as coreceptors or modulators of Wnt activation. Glypican-3 (GPC3) is an HSPG that is highly expressed in HCC, where it can attract Wnt proteins to the cell surface and promote cell proliferation. Thus, GPC3 has emerged as a candidate therapeutic target in liver cancer. While monoclonal antibodies to GPC3 are currently being evaluated in preclinical and clinical studies, none have shown an effect on Wnt signaling. Here, we first document the expression of Wnt3a, multiple Wnt receptors, and GPC3 in several HCC cell lines, and demonstrate that GPC3 enhanced the activity of Wnt3a/β-catenin signaling in these cells. Then we report the identification of HS20, a human monoclonal antibody against GPC3, which preferentially recognized the heparan sulfate chains of GPC3, both the sulfated and nonsulfated portions. HS20 disrupted the interaction of Wnt3a and GPC3 and blocked Wnt3a/β-catenin signaling. Moreover, HS20 inhibited Wnt3a-dependent cell proliferation in vitro and HCC xenograft growth in nude mice. In addition, HS20 had no detectable undesired toxicity in mice. Taken together, our results show that a monoclonal antibody primarily targeting the heparin sulfate chains of GPC3 inhibited Wnt/β-catenin signaling in HCC cells and had potent antitumor activity in vivo. An antibody directed against the heparan sulfate of a proteoglycan shows efficacy in blocking Wnt signaling and HCC growth, suggesting a novel strategy for liver cancer therapy. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - Hepatology (Baltimore, Md.) AU - Gao, Wei AU - Kim, Heungnam AU - Feng, Mingqian AU - Phung, Yen AU - Xavier, Charles P AU - Rubin, Jeffrey S AU - Ho, Mitchell AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 576 EP - 587 VL - 60 IS - 2 KW - Antibodies, Monoclonal KW - 0 KW - CTNNB1 protein, human KW - GPC3 protein, human KW - Glypicans KW - beta Catenin KW - Heparitin Sulfate KW - 9050-30-0 KW - Index Medicus KW - Animals KW - Hep G2 Cells KW - Humans KW - Xenograft Model Antitumor Assays KW - Cell Surface Display Techniques KW - Mice, Nude KW - Mice KW - beta Catenin -- immunology KW - Mice, Inbred BALB C KW - Female KW - Heparitin Sulfate -- immunology KW - Carcinoma, Hepatocellular -- drug therapy KW - Liver Neoplasms -- drug therapy KW - Wnt Signaling Pathway -- immunology KW - Wnt Signaling Pathway -- drug effects KW - Glypicans -- immunology KW - Antibodies, Monoclonal -- pharmacology KW - Carcinoma, Hepatocellular -- immunology KW - Liver Neoplasms -- immunology KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548194944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inactivation+of+Wnt+signaling+by+a+human+antibody+that+recognizes+the+heparan+sulfate+chains+of+glypican-3+for+liver+cancer+therapy.&rft.au=Gao%2C+Wei%3BKim%2C+Heungnam%3BFeng%2C+Mingqian%3BPhung%2C+Yen%3BXavier%2C+Charles+P%3BRubin%2C+Jeffrey+S%3BHo%2C+Mitchell&rft.aulast=Gao&rft.aufirst=Wei&rft.date=2014-08-01&rft.volume=60&rft.issue=2&rft.spage=576&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.26996 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-22 N1 - Date created - 2014-07-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Genome Biol. 2008;9(5):224 [18505598] Oncol Rep. 2007 Sep;18(3):691-4 [17671721] Expert Opin Investig Drugs. 2008 Nov;17(11):1769-76 [18922112] Cancer Res. 2008 Dec 1;68(23):9832-8 [19047163] Int Rev Cell Mol Biol. 2009;276:105-59 [19584012] Cancer Sci. 2009 Aug;100(8):1403-7 [19496787] Mol Cancer. 2009;8:76 [19778454] J Biol Chem. 2009 Nov 20;284(47):32959-67 [19783663] Dev Dyn. 2010 Jan;239(1):184-90 [19705435] Acta Neuropathol. 2010 Feb;119(2):211-20 [19636575] Int J Cancer. 2010 Mar 15;126(6):1291-301 [19816934] Proc Natl Acad Sci U S A. 2010 Aug 31;107(35):15473-8 [20713706] Eur J Cancer. 2011 Feb;47(3):333-8 [21112773] Clin Cancer Res. 2011 Mar 1;17(5):1024-32 [21343375] Int J Cancer. 2011 May 1;128(9):2246-7 [20617511] Int J Cancer. 2011 May 1;128(9):2020-30 [20635390] Mol Cancer. 2011;10:16 [21314951] Anticancer Agents Med Chem. 2011 Jul;11(6):549-59 [21554202] PLoS One. 2011;6(6):e21106 [21698156] Int J Mol Med. 2011 Oct;28(4):497-503 [21617840] Proc Natl Acad Sci U S A. 2011 Aug 9;108(32):13112-7 [21828006] Neoplasia. 2011 Aug;13(8):735-47 [21847365] Eur J Immunol. 2000 Jan;30(1):254-61 [10602048] Annu Rev Biochem. 1999;68:729-77 [10872465] Electrophoresis. 2001 Jan;22(1):3-11 [11197174] Br J Cancer. 2008 Jul 8;99(1):143-50 [18577996] Biochem Biophys Res Commun. 2012 Mar 23;419(4):656-61 [22382024] FEBS Lett. 2012 Mar 23;586(6):884-91 [22449976] J Biol Chem. 2012 Apr 20;287(17):14040-51 [22351761] Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11717-22 [22753465] MAbs. 2012 Sep-Oct;4(5):592-9 [22820551] Clin Cancer Res. 2013 Feb 15;19(4):920-8 [23362325] Proc Natl Acad Sci U S A. 2013 Mar 19;110(12):E1083-91 [23471984] Nat Rev Cancer. 2002 Jul;2(7):521-8 [12094238] Cell. 2004 Mar 19;116(6):883-95 [15035989] Cancer Res. 1997 Nov 15;57(22):5179-84 [9371521] Cancer Res. 1999 Jul 15;59(14):3433-41 [10416607] J Biol Chem. 2005 Jan 7;280(1):777-86 [15509575] J Biol Chem. 2005 May 27;280(21):20516-23 [15778504] Cancer Res. 2005 Jul 15;65(14):6245-54 [16024626] Front Biosci. 2006;11:1901-15 [16368566] Nature. 2007 Apr 26;446(7139):1030-7 [17460664] Cancer Res. 2007 Jun 1;67(11):5371-9 [17545618] Semin Thromb Hemost. 2007 Jul;33(5):557-68 [17629854] Comment In: Hepatology. 2014 Aug;60(2):452-4 [24644061] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/hep.26996 ER - TY - JOUR T1 - In vitro anti-proliferative and anti-angiogenic activities of thalidomide dithiocarbamate analogs. AN - 1547832584; 24859059 AB - Inhibition of angiogenesis is currently perceived as a promising strategy in the treatment of cancer. The anti-angiogenicity of thalidomide has inspired a second wave of research on this teratogenic drug. The present study aimed to investigate the anti-proliferative and anti-angiogenic activities of two thalidomide dithiocarbamate analogs by studying their anti-proliferative effects on human umbilical vein endothelial cells (HUVECs) and MDA-MB-231 human breast cancer cell lines. Their action on the expression levels of IL-6, IL-8, TNF-α, VEGF165, and MMP-2 was also assessed. Furthermore, their effect on angiogenesis was evaluated through wound healing, migration, tube formation, and nitric oxide (NO) assays. Results illustrated that the proliferation of HUVECs and MDA-MB-231 cells was not significantly affected by thalidomide at 6.25-100μM. Thalidomide failed to block angiogenesis at similar concentrations. By contrast, thalidomide dithiocarbamate analogs exhibited significant anti-proliferative action on HUVECs and MDA-MB-231 cells without causing cytotoxicity and also showed powerful anti-angiogenicity in wound healing, migration, tube formation, and NO assays. Thalidomide analogs 1 and 2 demonstrated more potent activity to suppress expression levels of IL-6, IL-8, TNF-α, VEGF165, and MMP-2 than thalidomide. Analog 1 consistently, showed the highest potency and efficacy in all the assays. Taken together, our results support further development and evaluation of novel thalidomide analogs as anti-tumor and anti-angiogenic agents. Copyright © 2014. Published by Elsevier B.V. JF - International immunopharmacology AU - El-Aarag, Bishoy Y A AU - Kasai, Tomonari AU - Zahran, Magdy A H AU - Zakhary, Nadia I AU - Shigehiro, Tsukasa AU - Sekhar, Sreeja C AU - Agwa, Hussein S AU - Mizutani, Akifumi AU - Murakami, Hiroshi AU - Kakuta, Hiroki AU - Seno, Masaharu AD - Chemistry Department, Faculty of Science, Menofia University, Egypt; Division of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University, Okayama 7008530, Japan. ; Division of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University, Okayama 7008530, Japan. Electronic address: t-kasai@cc.okayama-u.ac.jp. ; Chemistry Department, Faculty of Science, Menofia University, Egypt. ; Cancer Biology Department, National Cancer Institute, Cairo University, Egypt. ; Division of Chemistry and Biotechnology, Graduate School of Natural Science and Technology, Okayama University, Okayama 7008530, Japan. ; Division of Pharmaceutical Sciences, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 7008530, Japan. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 283 EP - 292 VL - 21 IS - 2 KW - Angiogenesis Inhibitors KW - 0 KW - Interleukin-6 KW - Interleukin-8 KW - Thiocarbamates KW - Tumor Necrosis Factor-alpha KW - VEGFA protein, human KW - Vascular Endothelial Growth Factor A KW - Nitric Oxide KW - 31C4KY9ESH KW - Thalidomide KW - 4Z8R6ORS6L KW - Matrix Metalloproteinase 2 KW - EC 3.4.24.24 KW - Index Medicus KW - VEGF KW - Angiogenesis KW - Thalidomide dithiocarbamate analogs KW - Migration KW - NO KW - Breast Neoplasms -- drug therapy KW - Humans KW - Interleukin-6 -- metabolism KW - Breast Neoplasms -- metabolism KW - Nitric Oxide -- metabolism KW - Cell Line, Tumor KW - Human Umbilical Vein Endothelial Cells KW - Matrix Metalloproteinase 2 -- metabolism KW - Interleukin-8 -- metabolism KW - Tumor Necrosis Factor-alpha -- metabolism KW - Cell Line KW - Female KW - Vascular Endothelial Growth Factor A -- metabolism KW - Cell Proliferation -- drug effects KW - Angiogenesis Inhibitors -- pharmacology KW - Neovascularization, Pathologic -- drug therapy KW - Neovascularization, Pathologic -- metabolism KW - Thiocarbamates -- pharmacology KW - Thalidomide -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547832584?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+immunopharmacology&rft.atitle=In+vitro+anti-proliferative+and+anti-angiogenic+activities+of+thalidomide+dithiocarbamate+analogs.&rft.au=El-Aarag%2C+Bishoy+Y+A%3BKasai%2C+Tomonari%3BZahran%2C+Magdy+A+H%3BZakhary%2C+Nadia+I%3BShigehiro%2C+Tsukasa%3BSekhar%2C+Sreeja+C%3BAgwa%2C+Hussein+S%3BMizutani%2C+Akifumi%3BMurakami%2C+Hiroshi%3BKakuta%2C+Hiroki%3BSeno%2C+Masaharu&rft.aulast=El-Aarag&rft.aufirst=Bishoy+Y&rft.date=2014-08-01&rft.volume=21&rft.issue=2&rft.spage=283&rft.isbn=&rft.btitle=&rft.title=International+immunopharmacology&rft.issn=1878-1705&rft_id=info:doi/10.1016%2Fj.intimp.2014.05.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-09 N1 - Date created - 2014-07-22 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.intimp.2014.05.007 ER - TY - JOUR T1 - Morphine and codeine concentrations in human urine following controlled poppy seeds administration of known opiate content. AN - 1547543220; 24887324 AB - Opiates are an important component for drug testing due to their high abuse potential. Proper urine opiate interpretation includes ruling out poppy seed ingestion; however, detailed elimination studies after controlled poppy seed administration with known morphine and codeine doses are not available. Therefore, we investigated urine opiate pharmacokinetics after controlled oral administration of uncooked poppy seeds with known morphine and codeine content. Participants were administered two 45 g oral poppy seed doses 8 h apart, each containing 15.7 mg morphine and 3mg codeine. Urine was collected ad libitum up to 32 h after the first dose. Specimens were analyzed with the Roche Opiates II immunoassay at 2000 and 300 μg/L cutoffs, and the ThermoFisher CEDIA(®) heroin metabolite (6-acetylmorphine, 6-AM) and Lin-Zhi 6-AM immunoassays with 10 μg/L cutoffs to determine if poppy seed ingestion could produce positive results in these heroin marker assays. In addition, all specimens were quantified for morphine and codeine by GC/MS. Participants (N=22) provided 391 urine specimens over 32 h following dosing; 26.6% and 83.4% were positive for morphine at 2000 and 300 μg/L GC/MS cutoffs, respectively. For the 19 subjects who completed the study, morphine concentrations ranged from <300 to 7522 μg/L with a median peak concentration of 5239 μg/L. The median first morphine-positive urine sample at 2000 μg/L cutoff concentration occurred at 6.6 h (1.2-12.1), with the last positive from 2.6 to 18 h after the second dose. No specimens were positive for codeine at a cutoff concentration of 2000 μg/L, but 20.2% exceeded 300 μg/L, with peak concentrations of 658 μg/L (284-1540). The Roche Opiates II immunoassay had efficiencies greater than 96% for the 2000 and 300 μg/L cutoffs. The CEDIA 6-AM immunoassay had a specificity of 91%, while the Lin-Zhi assay had no false positive results. These data provide valuable information for interpreting urine opiate results. Copyright © 2014. Published by Elsevier Ireland Ltd. JF - Forensic science international AU - Smith, Michael L AU - Nichols, Daniel C AU - Underwood, Paula AU - Fuller, Zachary AU - Moser, Matthew A AU - LoDico, Charles AU - Gorelick, David A AU - Newmeyer, Matthew N AU - Concheiro, Marta AU - Huestis, Marilyn A AD - U.S. Army Forensic Toxicology Drug Testing Laboratory, Fort Meade, MD, USA. ; Division of Workplace Programs, Substance Abuse Mental Health Services Administration, Department of Health and Human Services, Rockville, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Currently at Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. Electronic address: mhuestis@intra.nida.nih.gov. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 87 EP - 90 VL - 241 KW - Analgesics, Opioid KW - 0 KW - Morphine KW - 76I7G6D29C KW - Codeine KW - Q830PW7520 KW - Index Medicus KW - Poppy seeds KW - Urine KW - Controlled dose KW - Humans KW - Gas Chromatography-Mass Spectrometry KW - Male KW - Female KW - Immunoassay KW - Seeds KW - Morphine -- urine KW - Papaver KW - Codeine -- urine KW - Analgesics, Opioid -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547543220?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Forensic+science+international&rft.atitle=Morphine+and+codeine+concentrations+in+human+urine+following+controlled+poppy+seeds+administration+of+known+opiate+content.&rft.au=Smith%2C+Michael+L%3BNichols%2C+Daniel+C%3BUnderwood%2C+Paula%3BFuller%2C+Zachary%3BMoser%2C+Matthew+A%3BLoDico%2C+Charles%3BGorelick%2C+David+A%3BNewmeyer%2C+Matthew+N%3BConcheiro%2C+Marta%3BHuestis%2C+Marilyn+A&rft.aulast=Smith&rft.aufirst=Michael&rft.date=2014-08-01&rft.volume=241&rft.issue=&rft.spage=87&rft.isbn=&rft.btitle=&rft.title=Forensic+science+international&rft.issn=1872-6283&rft_id=info:doi/10.1016%2Fj.forsciint.2014.04.042 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-21 N1 - Date created - 2014-07-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Drug Test Anal. 2014 Mar;6(3):194-201 [24339374] Ther Drug Monit. 2010 Feb;32(1):11-8 [19901868] J Anal Toxicol. 2001 Oct;25(7):504-14 [11599592] Forensic Sci Int. 1985 Feb;27(2):111-7 [3979930] Ther Drug Monit. 2006 Aug;28(4):552-8 [16885724] Anesthesiology. 1999 Apr;90(4):1026-38 [10201674] Clin Chem. 1999 Apr;45(4):510-9 [10102911] Forensic Sci Int. 1998 Jul 6;95(1):1-10 [9718666] Clin Chem. 1997 Jun;43(6 Pt 1):1029-32 [9191557] Planta Med. 1996 Dec;62(6):544-7 [9000887] J Anal Toxicol. 1991 Jul-Aug;15(4):161-6 [1943064] J Anal Toxicol. 1991 Mar-Apr;15(2):49-53 [2051744] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.forsciint.2014.04.042 ER - TY - JOUR T1 - Impact of neoadjuvant single or dual HER2 inhibition and chemotherapy backbone upon pathological complete response in operable and locally advanced breast cancer: Sensitivity analysis of randomized trials. AN - 1546219126; 24877987 AB - The role of the dual HER2 inhibition, and the best chemotherapy backbone for neoadjuvant chemotherapy still represent an issue for clinical practice. A literature-based meta-analysis exploring single versus dual HER2 inhibition in terms of pathological complete response (pCR, breast plus axilla) rate and testing the interaction according to the chemotherapy (anthracyclines-taxanes or taxanes) was conducted. In addition, an event-based pooled analysis by extracting activity and safety events and deriving 95% confidence intervals (CI) was accomplished. Fourteen trials (4149 patients) were identified, with 6 trials (1820 patients) included in the meta-analysis and 31 arms (14 trials, 3580 patients) in the event-based pooled analysis. The dual HER2 inhibition significantly improves pCR rate, in the range of 16-19%, regardless of the chemotherapy backbone (relative risk 1.37, 95% CI 1.23-1.53, p<0.0001); pCR was significantly higher in the hormonal receptor negative population, regardless of the HER2 inhibition and type of chemotherapy. pCR and the rate of breast conserving surgery was higher when anthracyclines were added to taxanes, regardless of the HER2 inhibition. Severe neutropenia was higher with the addition of anthracyclines to taxanes, with an absolute difference of 19.7%, despite no differences in febrile neutropenia. While no significant differences according to the HER2 inhibition were found in terms of cardiotoxicity, a slightly difference for grade 3-4 (1.2%) against the addition of anthracyclines was calculated. The dual HER2 inhibition for the neoadjuvant treatment of HER2-positive breast cancer significantly increases pCR; the combination of anthracyclines, taxanes and anti-Her2 agents should be currently considered the standard of care. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - Cancer treatment reviews AU - Bria, Emilio AU - Carbognin, Luisa AU - Furlanetto, Jenny AU - Pilotto, Sara AU - Bonomi, Maria AU - Guarneri, Valentina AU - Vicentini, Cecilia AU - Brunelli, Matteo AU - Nortilli, Rolando AU - Pellini, Francesca AU - Sperduti, Isabella AU - Giannarelli, Diana AU - Pollini, Giovanni Paolo AU - Conte, Pierfranco AU - Tortora, Giampaolo AD - Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: emiliobria@yahoo.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: luisa.carbognin@gmail.com. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: jenny.furlanetto@hotmail.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: sara.pilotto.85@alice.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: mari.bonomi0429@gmail.com. ; Medical Oncology, Istituto Oncologico Veneto IRCCS, University of Padova, Padova, Italy. Electronic address: valentina.guarneri@unipd.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: cecivice@gmail.com. ; Department of Pathology and Diagnostic, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: matteo.brunelli@univr.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: rolando.nortilli@ospedaleuniverona.it. ; Chirurgia 'A', Department of Surgery and Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: francesca.pellini@ospedaleuniverona.it. ; Biostatistics, Regina Elena National Cancer Institute, Roma, Italy. Electronic address: isperduti@yahoo.it. ; Biostatistics, Regina Elena National Cancer Institute, Roma, Italy. Electronic address: giannarelli@ifo.it. ; Chirurgia 'A', Department of Surgery and Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: giovanni.pollini@ospedaleuniverona.it. ; Medical Oncology, Istituto Oncologico Veneto IRCCS, University of Padova, Padova, Italy. Electronic address: pierfranco.conte@unipd.it. ; Medical Oncology, Azienda Ospedaliera Universitaria Integrata, University of Verona, Verona, Italy. Electronic address: giampaolo.tortora@univr.it. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 847 EP - 856 VL - 40 IS - 7 KW - Anthracyclines KW - 0 KW - Protein Kinase Inhibitors KW - Taxoids KW - ERBB2 protein, human KW - EC 2.7.10.1 KW - Receptor, ErbB-2 KW - Index Medicus KW - Neoadjuvant KW - Meta-analysis KW - Trastuzumab KW - Breast cancer KW - HER2-positive KW - Randomized Controlled Trials as Topic KW - Protein Kinase Inhibitors -- therapeutic use KW - Humans KW - Protein Kinase Inhibitors -- administration & dosage KW - Neoadjuvant Therapy KW - Anthracyclines -- administration & dosage KW - Female KW - Taxoids -- administration & dosage KW - Breast Neoplasms -- pathology KW - Receptor, ErbB-2 -- antagonists & inhibitors KW - Breast Neoplasms -- therapy KW - Breast Neoplasms -- enzymology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1546219126?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+treatment+reviews&rft.atitle=Impact+of+neoadjuvant+single+or+dual+HER2+inhibition+and+chemotherapy+backbone+upon+pathological+complete+response+in+operable+and+locally+advanced+breast+cancer%3A+Sensitivity+analysis+of+randomized+trials.&rft.au=Bria%2C+Emilio%3BCarbognin%2C+Luisa%3BFurlanetto%2C+Jenny%3BPilotto%2C+Sara%3BBonomi%2C+Maria%3BGuarneri%2C+Valentina%3BVicentini%2C+Cecilia%3BBrunelli%2C+Matteo%3BNortilli%2C+Rolando%3BPellini%2C+Francesca%3BSperduti%2C+Isabella%3BGiannarelli%2C+Diana%3BPollini%2C+Giovanni+Paolo%3BConte%2C+Pierfranco%3BTortora%2C+Giampaolo&rft.aulast=Bria&rft.aufirst=Emilio&rft.date=2014-08-01&rft.volume=40&rft.issue=7&rft.spage=847&rft.isbn=&rft.btitle=&rft.title=Cancer+treatment+reviews&rft.issn=1532-1967&rft_id=info:doi/10.1016%2Fj.ctrv.2014.05.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-05 N1 - Date created - 2014-06-10 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ctrv.2014.05.001 ER - TY - JOUR T1 - Analytic and clinical performance of cobas HPV testing in anal specimens from HIV-positive men who have sex with men. AN - 1546214580; 24899025 AB - Anal human papillomavirus (HPV) infections are common, and the incidence of anal cancer is high in HIV-infected men who have sex with men (MSM). To evaluate the performance of HPV assays in anal samples, we compared the cobas HPV test (cobas) to the Roche Linear Array HPV genotyping assay (LA) and cytology in HIV-infected MSM. Cytology and cobas and LA HPV testing were conducted for 342 subjects. We calculated agreement between the HPV assays and the clinical performance of HPV testing and HPV genotyping alone and in combination with anal cytology. We observed high agreement between cobas and LA, with cobas more likely than LA to show positive results for HPV16, HPV18, and other carcinogenic types. Specimens testing positive in cobas but not in LA were more likely to be positive for other markers of HPV-related disease compared to those testing negative in both assays, suggesting that at least some of these were true positives for HPV. cobas and LA showed high sensitivities but low specificities for the detection of anal intraepithelial neoplasia grade 2/3 (AIN2/3) in this population (100% sensitivity and 26% specificity for cobas versus 98.4% sensitivity and 28.9% specificity for LA). A combination of anal cytology and HPV genotyping provided the highest accuracy for detecting anal precancer. A higher HPV load was associated with a higher risk of AIN2/3 with HPV16 (P(trend) < 0.001), HPV18 (P(trend) = 0.07), and other carcinogenic types (P(trend) < 0.001). We demonstrate that cobas can be used for HPV detection in anal cytology specimens. Additional tests are necessary to identify men at the highest risk of anal cancer among those infected with high-risk HPV. Copyright © 2014, American Society for Microbiology. All Rights Reserved. JF - Journal of clinical microbiology AU - Wentzensen, Nicolas AU - Follansbee, Stephen AU - Borgonovo, Sylvia AU - Tokugawa, Diane AU - Sahasrabuddhe, Vikrant V AU - Chen, Jie AU - Lorey, Thomas S AU - Gage, Julia C AU - Fetterman, Barbara AU - Boyle, Sean AU - Sadorra, Mark AU - Tang, Scott Dahai AU - Darragh, Teresa M AU - Castle, Philip E AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA wentzenn@mail.nih.gov. ; Kaiser Permanente Medical Center, San Francisco, California, USA. ; Kaiser Permanente TPMG Regional Laboratory, Berkeley, California, USA. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Roche Molecular Systems, Pleasanton, California, USA. ; University of California, San Francisco, California, USA. ; Global Cancer Initiative, Chestertown, Maryland, USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 2892 EP - 2897 VL - 52 IS - 8 KW - Index Medicus KW - Sensitivity and Specificity KW - Young Adult KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - Cytological Techniques -- methods KW - Male KW - Homosexuality, Male KW - Papillomavirus Infections -- diagnosis KW - Papillomaviridae -- classification KW - Anus Diseases -- diagnosis KW - Papillomaviridae -- isolation & purification KW - Papillomavirus Infections -- virology KW - Papillomaviridae -- genetics KW - Anus Diseases -- virology KW - Genotyping Techniques -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1546214580?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Analytic+and+clinical+performance+of+cobas+HPV+testing+in+anal+specimens+from+HIV-positive+men+who+have+sex+with+men.&rft.au=Wentzensen%2C+Nicolas%3BFollansbee%2C+Stephen%3BBorgonovo%2C+Sylvia%3BTokugawa%2C+Diane%3BSahasrabuddhe%2C+Vikrant+V%3BChen%2C+Jie%3BLorey%2C+Thomas+S%3BGage%2C+Julia+C%3BFetterman%2C+Barbara%3BBoyle%2C+Sean%3BSadorra%2C+Mark%3BTang%2C+Scott+Dahai%3BDarragh%2C+Teresa+M%3BCastle%2C+Philip+E&rft.aulast=Wentzensen&rft.aufirst=Nicolas&rft.date=2014-08-01&rft.volume=52&rft.issue=8&rft.spage=2892&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+microbiology&rft.issn=1098-660X&rft_id=info:doi/10.1128%2FJCM.03517-13 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-20 N1 - Date created - 2014-07-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Discov. 2013 Feb;3(2):148-57 [23299199] J Infect Dis. 2013 Feb 1;207(3):392-401 [23162133] J Infect Dis. 2013 Dec 1;208(11):1768-75 [23908478] Int J Cancer. 2015 Jan 1;136(1):98-107 [24817381] JAMA. 2002 Apr 24;287(16):2114-9 [11966386] Int J Cancer. 2007 Dec 15;121(12):2787-93 [17722112] Int J Cancer. 2009 Feb 1;124(3):516-20 [18973271] Int J Cancer. 2009 Apr 1;124(7):1626-36 [19115209] BMJ. 2009;339:b2569 [19638649] J Natl Cancer Inst. 2009 Aug 19;101(16):1120-30 [19648510] Am J Clin Pathol. 2011 Mar;135(3):468-75 [21350104] Lancet Oncol. 2011 Sep;12(9):880-90 [21865084] Am J Clin Pathol. 2011 Oct;136(4):578-86 [21917680] J Clin Microbiol. 2012 Jan;50(1):61-5 [22075592] Clin Infect Dis. 2012 Apr;54(7):1026-34 [22291097] Lancet Oncol. 2012 May;13(5):487-500 [22445259] CA Cancer J Clin. 2012 May-Jun;62(3):147-72 [22422631] AIDS. 2012 Nov 13;26(17):2185-92 [23018436] Cancer Epidemiol Biomarkers Prev. 2013 Jan;22(1):42-9 [23155136] Cancer Cytopathol. 2013 Feb;121(2):72-8 [22811048] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/JCM.03517-13 ER - TY - JOUR T1 - Risk of neurobehavioral disinhibition in prenatal methamphetamine-exposed young children with positive hair toxicology results. AN - 1545420583; 24518561 AB - The objective was to evaluate the effects of prenatal methamphetamine exposure (PME) and postnatal drug exposures identified by child hair analysis on neurobehavioral disinhibition at 6.5 years of age. Mother-infant pairs were enrolled in the Infant Development, Environment, and Lifestyle (IDEAL) Study in Los Angeles, Honolulu, Tulsa, and Des Moines. PME was determined by maternal self-report and/or positive meconium results. At the 6.5-year follow-up visit, hair was collected and analyzed for methamphetamine, tobacco, cocaine, and cannabinoid markers. Child behavioral and executive function test scores were aggregated to evaluate child neurobehavioral disinhibition. Hierarchical linear regression models assessed the impact of PME, postnatal substances, and combined PME with postnatal drug exposures on the child's neurobehavioral disinhibition aggregate score. Past year caregiver substance use was compared with child hair results. A total of 264 children were evaluated. Significantly more PME children (n = 133) had hair positive for methamphetamine/amphetamine (27.1% versus 8.4%) and nicotine/cotinine (38.3% versus 25.2%) than children without PME (n = 131). Overall, no significant differences in analyte hair concentrations were noted between groups. Significant differences in behavioral and executive function were observed between children with and without PME. No independent effects of postnatal methamphetamine or tobacco exposure, identified by positive hair test, were noted and no additional neurobehavioral disinhibition was observed in PME children with postnatal drug exposures, as compared with PME children without postnatal exposure. Child hair testing offered a noninvasive means to evaluate postnatal environmental drug exposure, although no effects from postnatal drug exposure alone were seen. PME, alone and in combination with postnatal drug exposures, was associated with behavioral and executive function deficits at 6.5 years. JF - Therapeutic drug monitoring AU - Himes, Sarah K AU - LaGasse, Linda L AU - Derauf, Chris AU - Newman, Elana AU - Smith, Lynne M AU - Arria, Amelia M AU - Della Grotta, Sheri A AU - Dansereau, Lynne M AU - Abar, Beau AU - Neal, Charles R AU - Lester, Barry M AU - Huestis, Marilyn A AD - *Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland; †Department of Pediatrics, Brown Center for the Study of Children at Risk, Warren Alpert Medical School of Brown University, Women and Infants Hospital of Rhode Island, Providence, RI; ‡Division of Community Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota; §Department of Psychology, The University of Tulsa, Tulsa, Oklahoma; ¶Department of Pediatrics, LABioMed Institute at Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA, Torrance, California; ‖Department of Family Science, Center on Young Adult Health and Development, University of Maryland School of Public Health, College Park, Maryland; **Department of Emergency Medicine and Psychiatry, University of Rochester Medical Center, Rochester, New York; and ††Department of Pediatrics, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 535 EP - 543 VL - 36 IS - 4 KW - Methamphetamine KW - 44RAL3456C KW - Nicotine KW - 6M3C89ZY6R KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Risk KW - Tobacco -- chemistry KW - Mothers KW - Humans KW - Case-Control Studies KW - Cocaine -- chemistry KW - Child Development -- drug effects KW - Child KW - Female KW - Pregnancy KW - Nicotine -- chemistry KW - Hair -- chemistry KW - Methamphetamine -- chemistry KW - Prenatal Exposure Delayed Effects -- diagnosis KW - Amphetamine-Related Disorders -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1545420583?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Risk+of+neurobehavioral+disinhibition+in+prenatal+methamphetamine-exposed+young+children+with+positive+hair+toxicology+results.&rft.au=Himes%2C+Sarah+K%3BLaGasse%2C+Linda+L%3BDerauf%2C+Chris%3BNewman%2C+Elana%3BSmith%2C+Lynne+M%3BArria%2C+Amelia+M%3BDella+Grotta%2C+Sheri+A%3BDansereau%2C+Lynne+M%3BAbar%2C+Beau%3BNeal%2C+Charles+R%3BLester%2C+Barry+M%3BHuestis%2C+Marilyn+A&rft.aulast=Himes&rft.aufirst=Sarah&rft.date=2014-08-01&rft.volume=36&rft.issue=4&rft.spage=535&rft.isbn=&rft.btitle=&rft.title=Therapeutic+drug+monitoring&rft.issn=1536-3694&rft_id=info:doi/10.1097%2FFTD.0000000000000049 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-02 N1 - Date created - 2014-07-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pediatrics. 2002 May;109(5):815-25 [11986441] Psychol Addict Behav. 2013 Sep;27(3):662-73 [23067308] Am J Psychiatry. 2003 Jun;160(6):1078-85 [12777265] Anal Chem. 2004 Aug 1;76(15):4358-63 [15283573] Forensic Sci Int. 1997 Jan 17;84(1-3):123-8 [9042716] J Abnorm Child Psychol. 1998 Aug;26(4):257-68 [9700518] Drug Metab Dispos. 2005 Feb;33(2):258-61 [15528319] Matern Child Health J. 2006 May;10(3):293-302 [16395620] Ther Drug Monit. 2006 Jun;28(3):442-6 [16778731] Am J Drug Alcohol Abuse. 2007;33(2):281-9 [17497551] Forensic Sci Int. 2007 Jul 4;169(2-3):129-36 [16963215] J Dev Behav Pediatr. 2007 Jun;28(3):219-24 [17565289] Arch Dis Child Fetal Neonatal Ed. 2007 Sep;92(5):F351-5 [17077112] Obstet Gynecol. 2008 Feb;111(2 Pt 1):341-7 [18238971] Obstet Gynecol. 2009 Jun;113(6):1285-91 [19461424] J Dev Behav Pediatr. 2009 Jun;30(3):185-92 [19525715] J Burn Care Res. 2009 Jul-Aug;30(4):587-92 [19506505] J Chromatogr B Analyt Technol Biomed Life Sci. 2009 Nov 1;877(29):3701-6 [19783234] Ther Drug Monit. 2009 Dec;31(6):769-75 [19935364] Forensic Sci Int. 2010 Mar 20;196(1-3):38-42 [20056364] Annu Rev Public Health. 2010;31:385-98 [20070191] J Addict Dis. 2010 Apr;29(2):259-76 [20407981] Clin Chem. 2010 May;56(5):856-60 [20185623] Neurotoxicol Teratol. 2011 Jan-Feb;33(1):166-75 [20615464] Neurotoxicol Teratol. 2011 Jan-Feb;33(1):176-84 [21256431] J Forensic Leg Med. 2011 Apr;18(3):110-4 [21420647] Dev Psychopathol. 2011 Aug;23(3):777-88 [21756431] Pediatrics. 2012 Apr;129(4):681-8 [22430455] Anal Chim Acta. 2012 May 13;726:35-43 [22541011] Ther Drug Monit. 2012 Jun;34(3):337-44 [22495425] Forensic Sci Int. 2012 Jun 10;219(1-3):179-82 [22300795] J Pediatr. 2012 Sep;161(3):452-9 [22424953] Child Psychiatry Hum Dev. 2012 Dec;43(6):943-57 [22552952] Drug Alcohol Depend. 2012 Nov 1;126(1-2):80-6 [22608010] J Dev Behav Pediatr. 2013 Jan;34(1):31-7 [23275056] J Subst Abuse Treat. 2013 May-Jun;44(5):548-56 [23313146] Pediatr Emerg Care. 2002 Aug;18(4):327-32 [12187145] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/FTD.0000000000000049 ER - TY - JOUR T1 - MicroRNA expression profiling of thymic epithelial tumors. AN - 1545416547; 24863004 AB - Thymic epithelial tumors (TET) are the most frequent human primary mediastinal tumors in adults. A deep biological characterization of the processes at the basis of the transformed phenotype could strongly improve our understanding of the morphological and clinical heterogeneity of these diseases. MicroRNAs (miRNAs) are non-coding RNAs involved in post-transcriptional regulation and their altered expression accounts for the pathogenesis of several tumors. The aim of this study was to identify the miRNAs that are differentially expressed in tumor vs normal thymic tissues or among the different tumor histotypes and that could impact on the biology of TET. microRNAs expression profiling was performed by microarray analysis of formalin-fixed paraffin embedded (FFPE) tissue from 54 thymic tumor samples and 12 normal counterparts, derived from two patient cohorts. We identified groups of miRNAs differentially expressed between: (i) TET and normal thymic tissues, (ii) thymomas and thymic carcinomas, (iii) histotype groups. Moreover, we identified putative molecular pathways targeted by these differentially expressed miRNAs that could be involved in thymic carcinogenesis and in the maintenance and spreading of this tumor. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Lung cancer (Amsterdam, Netherlands) AU - Ganci, Federica AU - Vico, Carmen AU - Korita, Etleva AU - Sacconi, Andrea AU - Gallo, Enzo AU - Mori, Federica AU - Cambria, Annamaria AU - Russo, Emanuele AU - Anile, Marco AU - Vitolo, Domenico AU - Pescarmona, Edoardo AU - Blandino, Rosario AU - Facciolo, Francesco AU - Venuta, Federico AU - Blandino, Giovanni AU - Marino, Mirella AU - Fazi, Francesco AD - Translational Oncogenomics Unit, "Regina Elena" National Cancer Institute, Rome, Italy. ; Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Section of Histology & Medical Embryology, Sapienza University of Rome, Rome, Italy. ; Department of Pathology, "Regina Elena" National Cancer Institute, Rome, Italy. ; Molecular Chemoprevention Unit, "Regina Elena" National Cancer Institute, Rome, Italy. ; Department of Oncology, Division of Pathology, S. Vincenzo Hospital, Taormina, Italy. ; Department of Thoracic Surgery, Azienda Policlinico Umberto I, Sapienza University of Rome, Rome, Italy; Fondazione Eleonora Lorillard Spencer Cenci, Italy. ; Department of Pathology, Azienda Policlinico Umberto I, "Sapienza" University of Rome, Rome, Italy. ; Department of Oncology, Division of Oncological Surgery S. Vincenzo Hospital, Taormina, Italy. ; Thoracic Surgery, "Regina Elena" National Cancer Institute, Rome, Italy. ; Department of Pathology, "Regina Elena" National Cancer Institute, Rome, Italy. Electronic address: marino@ifo.it. ; Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Section of Histology & Medical Embryology, Sapienza University of Rome, Rome, Italy. Electronic address: francesco.fazi@uniroma1.it. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 197 EP - 204 VL - 85 IS - 2 KW - MicroRNAs KW - 0 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - EGFR KW - microRNAs KW - miR-145 KW - Thymic epithelial tumors KW - Receptor, Epidermal Growth Factor -- genetics KW - Humans KW - Thymus Gland -- metabolism KW - Cluster Analysis KW - Gene Expression Regulation, Neoplastic KW - Gene Expression Profiling KW - Neoplasms, Glandular and Epithelial -- genetics KW - MicroRNAs -- genetics KW - Thymus Neoplasms -- genetics KW - Thymus Neoplasms -- pathology KW - Neoplasms, Glandular and Epithelial -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1545416547?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.atitle=MicroRNA+expression+profiling+of+thymic+epithelial+tumors.&rft.au=Ganci%2C+Federica%3BVico%2C+Carmen%3BKorita%2C+Etleva%3BSacconi%2C+Andrea%3BGallo%2C+Enzo%3BMori%2C+Federica%3BCambria%2C+Annamaria%3BRusso%2C+Emanuele%3BAnile%2C+Marco%3BVitolo%2C+Domenico%3BPescarmona%2C+Edoardo%3BBlandino%2C+Rosario%3BFacciolo%2C+Francesco%3BVenuta%2C+Federico%3BBlandino%2C+Giovanni%3BMarino%2C+Mirella%3BFazi%2C+Francesco&rft.aulast=Ganci&rft.aufirst=Federica&rft.date=2014-08-01&rft.volume=85&rft.issue=2&rft.spage=197&rft.isbn=&rft.btitle=&rft.title=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.issn=1872-8332&rft_id=info:doi/10.1016%2Fj.lungcan.2014.04.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-09 N1 - Date created - 2014-07-15 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.lungcan.2014.04.008 ER - TY - JOUR T1 - Reversible cerebellar ataxia due to ovarian teratoma. AN - 1545414798; 24726236 AB - Cerebellar dysfunction is a classic paraneoplastic syndrome associated with various types of cancer, including gynecological and breast tumors, small-cell lung cancer, thymoma, and Hodgkin's lymphoma. We present a 22-year-old woman with acute cerebellar ataxia that subsided upon removal of an ovarian teratoma. This patient may represent a new category of immune-mediated cerebellar ataxia that is reversible with removal of an underlying tumor. Published by Elsevier Ltd. JF - Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia AU - Park, Jung E AU - Liang, Tsao-Wei AD - Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive Room 7D42, Bethesda, MD 20892, USA. Electronic address: junge.park@nih.gov. ; The Parkinson's Disease and Movement Disorders Program, Department of Neurology, Thomas Jefferson University, Philadelphia, PA, USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1467 EP - 1469 VL - 21 IS - 8 KW - Index Medicus KW - Ovarian teratoma KW - Paraneoplastic KW - Ataxia KW - Oscillopsia KW - Nystagmus KW - Young Adult KW - Humans KW - Treatment Outcome KW - Recovery of Function KW - Follow-Up Studies KW - Paraneoplastic Syndromes, Nervous System KW - Female KW - Teratoma -- complications KW - Cerebellar Ataxia -- etiology KW - Teratoma -- pathology KW - Ovarian Neoplasms -- pathology KW - Ovarian Neoplasms -- complications KW - Ovarian Neoplasms -- surgery KW - Teratoma -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1545414798?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuroscience+%3A+official+journal+of+the+Neurosurgical+Society+of+Australasia&rft.atitle=Reversible+cerebellar+ataxia+due+to+ovarian+teratoma.&rft.au=Park%2C+Jung+E%3BLiang%2C+Tsao-Wei&rft.aulast=Park&rft.aufirst=Jung&rft.date=2014-08-01&rft.volume=21&rft.issue=8&rft.spage=1467&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+neuroscience+%3A+official+journal+of+the+Neurosurgical+Society+of+Australasia&rft.issn=1532-2653&rft_id=info:doi/10.1016%2Fj.jocn.2013.12.019 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-04 N1 - Date created - 2014-07-15 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jocn.2013.12.019 ER - TY - JOUR T1 - A phase II trial of the Src-kinase inhibitor saracatinib after four cycles of chemotherapy for patients with extensive stage small cell lung cancer: NCCTG trial N-0621. AN - 1545414555; 24957683 AB - To assess the efficacy and the Src-kinase inhibitor saracatinib (AZD-0530) after four cycles of platinum-based chemotherapy for extensive stage small cell lung cancer (SCLC). Patients with at least stable disease received saracatinib at a dose of 175 mg/day by mouth until disease progression, unacceptable toxicity, or patient refusal. The primary endpoint was the 12-week progression-free survival (PFS) rate from initiation of saracatinib treatment. Planned interim analysis in first 20 patients, where 13 or more patients alive and progression-free at 12-weeks would allow continued enrollment to 40 total patients. All 23 evaluable patients received platinum based standard chemotherapy. Median age was 58 years (range: 48-82). 96% of patients had a performance status of 0/1. Median of two cycles given (range: 1-34). All 23 (100%) patients have ended treatment, most for disease progression (19/23). The 12-week PFS rate was 26% (6/23; 95% CI: 10-48%). From start of standard chemotherapy, median PFS was 4.7 months (95% CI: 4.5-5.1) and median OS was 11.2 months (95% CI: 9.9-13.8). Eight (35%) and three (13%) patients experienced at least one grade 3/4 or grade 4 AE, respectively. Commonly occurring grade 3/4 adverse events were thrombocytopenia (13%), fatigue (9%), nausea (9%), and vomiting (9%). Saracatinib at a dose of 175 mg/day by mouth is well tolerated. However, the PFS rate observed at the pre-planned interim analysis did not meet the criteria for additional enrollment. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Lung cancer (Amsterdam, Netherlands) AU - Molina, Julian R AU - Foster, Nathan R AU - Reungwetwattana, Thanyanan AU - Nelson, Garth D AU - Grainger, Andrew V AU - Steen, Preston D AU - Stella, Philip J AU - Marks, Randolph AU - Wright, John AU - Adjei, Alex A AD - Division of Medical Oncology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, United States. Electronic address: molina.julian@mayo.edu. ; Division of Biomedical Statistics and Informatics, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, United States. ; Division of Medical Oncology, Department of Internal Medicine, Ramathibodi Hospital, Bangkok, Thailand. ; Columbus Oncology & Hematology, Inc., 810 Jasonway Avenue, Suite A, Columbus, OH 43214l, United States. ; MeritCare Hospital CCOP, 820 4(th) Street North, Fargo, ND 58102, United States. ; St. Joseph Mercy Cancer Center, 5301 McAuley Drive, Suite C-139, Ypsilanti, MI 48197, United States. ; Division of Medical Oncology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, United States. ; CTEP Program, National Cancer Institute, Executive Plaza North, Suite 7115A, Rockville, MD 20852-7426, United States. ; Roswell Park Cancer Institute, Elm and Carlton Street, Buffalo, NY 14263, United States. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 245 EP - 250 VL - 85 IS - 2 KW - Antineoplastic Agents KW - 0 KW - Benzodioxoles KW - Protein Kinase Inhibitors KW - Quinazolines KW - saracatinib KW - 9KD24QGH76 KW - src-Family Kinases KW - EC 2.7.10.2 KW - Index Medicus KW - Small cell lung cancer KW - Extensive stage KW - C-Src KW - Maintenance KW - Saracatinib KW - Neoplasm Staging KW - Humans KW - Disease Progression KW - Aged KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - src-Family Kinases -- antagonists & inhibitors KW - Aged, 80 and over KW - Treatment Outcome KW - Follow-Up Studies KW - Middle Aged KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Retreatment KW - Female KW - Male KW - Benzodioxoles -- therapeutic use KW - Antineoplastic Agents -- administration & dosage KW - Small Cell Lung Carcinoma -- mortality KW - Small Cell Lung Carcinoma -- drug therapy KW - Lung Neoplasms -- drug therapy KW - Protein Kinase Inhibitors -- administration & dosage KW - Antineoplastic Agents -- adverse effects KW - Quinazolines -- administration & dosage KW - Protein Kinase Inhibitors -- therapeutic use KW - Small Cell Lung Carcinoma -- pathology KW - Benzodioxoles -- administration & dosage KW - Protein Kinase Inhibitors -- adverse effects KW - Quinazolines -- therapeutic use KW - Benzodioxoles -- adverse effects KW - Lung Neoplasms -- mortality KW - Quinazolines -- adverse effects KW - Antineoplastic Agents -- therapeutic use KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1545414555?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.atitle=A+phase+II+trial+of+the+Src-kinase+inhibitor+saracatinib+after+four+cycles+of+chemotherapy+for+patients+with+extensive+stage+small+cell+lung+cancer%3A+NCCTG+trial+N-0621.&rft.au=Molina%2C+Julian+R%3BFoster%2C+Nathan+R%3BReungwetwattana%2C+Thanyanan%3BNelson%2C+Garth+D%3BGrainger%2C+Andrew+V%3BSteen%2C+Preston+D%3BStella%2C+Philip+J%3BMarks%2C+Randolph%3BWright%2C+John%3BAdjei%2C+Alex+A&rft.aulast=Molina&rft.aufirst=Julian&rft.date=2014-08-01&rft.volume=85&rft.issue=2&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.issn=1872-8332&rft_id=info:doi/10.1016%2Fj.lungcan.2014.03.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-09 N1 - Date created - 2014-07-15 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.lungcan.2014.03.004 ER - TY - JOUR T1 - Seroprevalence of 8 oncogenic human papillomavirus genotypes and acquired immunity against reinfection. AN - 1544739307; 24569064 AB - Natural human papillomavirus (HPV) antibody titers have shown protection against subsequent HPV infection, but previous studies were restricted to few HPV genotypes. We examined the association of naturally occurring antibodies against 8 carcinogenic HPV types with subsequent infections. A total of 2302 women enrolled in the Atypical Squamous Cells of Undetermined Significance/Low-Grade Squamous Intraepithelial Lesion Triage Study provided blood samples at baseline. Serum samples were tested for antibodies against 8 carcinogenic HPV genotypes (16, 18, 31, 33, 35, 45, 52, and 58) using a multiplex serology assay. We analyzed the relationship between HPV antibodies and HPV infection during 2 years of follow-up among women negative for the specific HPV type at baseline. Baseline seroprevalence for HPV16 L1 was associated with decreased risk of DNA positivity for HPV16 (odds ratio, 0.39 [95% confidence interval, .18-.86]) at ≥2 follow-up visits. We observed similar but nonsignificant decreased risks for HPV18 and 31. These findings were restricted to women reporting a new sex partner during follow-up. There was no association between baseline seroprevalence and detection of precancer during follow-up. Seroprevalence conferred protection against subsequent HPV infection for HPV16 and indicated possible protection for 2 other genotypes, suggesting that this effect is common to several HPV genotypes. Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - The Journal of infectious diseases AU - Wilson, Lauren AU - Pawlita, Michael AU - Castle, Phillip E AU - Waterboer, Tim AU - Sahasrabuddhe, Vikrant AU - Gravitt, Patti E AU - Schiffman, Mark AU - Wentzensen, Nicolas AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health (NIH), Bethesda Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina. ; German Cancer Research Center, Heidelberg, Germany. ; Global Cancer Initiative, Chestertown. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health (NIH), Bethesda. ; Department of Epidemiology Department of Molecular Microbiology and Immunology, Johns Hopkins University, Baltimore, Maryland. Y1 - 2014/08/01/ PY - 2014 DA - 2014 Aug 01 SP - 448 EP - 455 VL - 210 IS - 3 KW - Abridged Index Medicus KW - Index Medicus KW - serology KW - natural immunity KW - Human papillomavirus KW - Genotype KW - Odds Ratio KW - Adaptive Immunity KW - Humans KW - Seroepidemiologic Studies KW - Cervical Intraepithelial Neoplasia -- virology KW - Female KW - Papillomavirus Infections -- epidemiology KW - Papillomaviridae -- classification KW - Papillomavirus Infections -- blood KW - Papillomaviridae -- genetics KW - Oncogenic Viruses KW - Papillomaviridae -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544739307?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Seroprevalence+of+8+oncogenic+human+papillomavirus+genotypes+and+acquired+immunity+against+reinfection.&rft.au=Wilson%2C+Lauren%3BPawlita%2C+Michael%3BCastle%2C+Phillip+E%3BWaterboer%2C+Tim%3BSahasrabuddhe%2C+Vikrant%3BGravitt%2C+Patti+E%3BSchiffman%2C+Mark%3BWentzensen%2C+Nicolas&rft.aulast=Wilson&rft.aufirst=Lauren&rft.date=2014-08-01&rft.volume=210&rft.issue=3&rft.spage=448&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjiu104 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-25 N1 - Date created - 2014-07-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Microbiol. 2000 Jan;38(1):357-61 [10618116] Int J Cancer. 2013 Nov;133(9):2172-81 [23588935] Lancet. 2001 Jun 9;357(9271):1831-6 [11410191] J Infect Dis. 2002 Sep 15;186(6):737-42 [12198606] J Med Virol. 2002 Nov;68(3):417-23 [12226831] J Virol Methods. 2002 Oct;106(1):61-70 [12367730] Cancer Epidemiol Biomarkers Prev. 2004 Feb;13(2):324-7 [14973086] Am J Obstet Gynecol. 2004 Aug;191(2):430-4 [15343217] Br J Cancer. 2004 Oct 4;91(7):1269-74 [15292929] J Natl Cancer Inst. 1995 Jun 7;87(11):796-802 [7791229] J Clin Microbiol. 1998 Oct;36(10):3020-7 [9738060] J Infect Dis. 2004 Dec 15;190(12):2077-87 [15551205] Lancet Oncol. 2005 May;6(5):271-8 [15863374] Clin Chem. 2005 Oct;51(10):1845-53 [16099939] Am J Clin Pathol. 2005 Nov;124(5):722-32 [16203281] Obstet Gynecol. 2006 Aug;108(2):264-72 [16880294] J Infect Dis. 2007 Jun 1;195(11):1582-9 [17471427] N Engl J Med. 2007 May 10;356(19):1915-27 [17494925] N Engl J Med. 2007 May 10;356(19):1928-43 [17494926] Cancer Epidemiol Biomarkers Prev. 2007 Sep;16(9):1874-9 [17855708] J Gen Virol. 2008 Jan;89(Pt 1):117-29 [18089735] J Clin Microbiol. 2008 Jan;46(1):109-17 [17989194] Lancet Oncol. 2008 May;9(5):425-34 [18407790] PLoS Pathog. 2008 Jun;4(6):e1000091 [18566657] Vaccine. 2008 Jul 4;26(29-30):3608-16 [18541349] Cancer Epidemiol Biomarkers Prev. 2009 May;18(5):1341-9 [19423515] Sex Transm Dis. 2009 Nov;36(11):696-703 [19652630] Viral Immunol. 2009 Dec;22(6):445-9 [19951181] Clin Vaccine Immunol. 2010 May;17(5):818-27 [20237197] Cancer Epidemiol Biomarkers Prev. 2010 Jun;19(6):1585-94 [20530494] Cancer Res. 2010 Nov 1;70(21):8569-77 [20978200] J Natl Cancer Inst. 2010 Nov 3;102(21):1653-62 [20944077] Cancer Epidemiol Biomarkers Prev. 2011 Feb;20(2):287-96 [21300618] J Infect Dis. 2011 Jul 1;204(1):94-102 [21628663] J Clin Invest. 2011 Dec;121(12):4593-9 [22133884] BJOG. 2012 Jan;119(1):20-5 [21624034] Am J Clin Pathol. 2012 Aug;138(2):241-6 [22904136] Cancer Res. 2012 Dec 1;72(23):6183-90 [23019223] J Infect Dis. 2013 Jan 15;207(2):272-80 [23242540] Acta Cytol. 2000 Sep-Oct;44(5):726-42 [11015972] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/infdis/jiu104 ER - TY - JOUR T1 - Mechanism and synergism in epithelial fluid and electrolyte secretion. AN - 1544737734; 24240699 AB - A central function of epithelia is the control of the volume and electrolyte composition of bodily fluids through vectorial transport of electrolytes and the obligatory H2O. In exocrine glands, fluid and electrolyte secretion is carried out by both acinar and duct cells, with the portion of fluid secreted by each cell type varying among glands. All acinar cells secrete isotonic, plasma-like fluid, while the duct determines the final electrolyte composition of the fluid by absorbing most of the Cl(-) and secreting HCO3 (-). The key transporters mediating acinar fluid and electrolyte secretion are the basolateral Na(+)/K(+) /2Cl(-) cotransporter, the luminal Ca(2+)-activated Cl(-) channel ANO1 and basolateral and luminal Ca(2+)-activated K(+) channels. Ductal fluid and HCO3 (-) secretion are mediated by the basolateral membrane Na(+)-HCO3 (-) cotransporter NBCe1-B and the luminal membrane Cl(-)/HCO3 (-) exchanger slc26a6 and the Cl(-) channel CFTR. The function of the transporters is regulated by multiple inputs, which in the duct include major regulation by the WNK/SPAK pathway that inhibit secretion and the IRBIT/PP1 pathway that antagonize the effects of the WNK/SPAK pathway to both stimulate and coordinate the secretion. The function of these regulatory pathways in secretory glands acinar cells is yet to be examined. An important concept in biology is synergism among signaling pathways to generate the final physiological response that ensures regulation with high fidelity and guards against cell toxicity. While synergism is observed in all epithelial functions, the molecular mechanism mediating the synergism is not known. Recent work reveals a central role for IRBIT as a third messenger that integrates and synergizes the function of the Ca(2+) and cAMP signaling pathways in activation of epithelial fluid and electrolyte secretion. These concepts are discussed in this review using secretion by the pancreatic and salivary gland ducts as model systems. JF - Pflugers Archiv : European journal of physiology AU - Hong, Jeong Hee AU - Park, Seonghee AU - Shcheynikov, Nikolay AU - Muallem, Shmuel AD - Epithelial Signaling and Transport Section, Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institute of Health, Bethesda, MD, 20892, USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1487 EP - 1499 VL - 466 IS - 8 KW - Electrolytes KW - 0 KW - Index Medicus KW - Animals KW - Pancreatic Ducts -- secretion KW - Humans KW - Salivary Ducts -- secretion KW - Water-Electrolyte Balance -- physiology KW - Signal Transduction -- physiology KW - Epithelium -- secretion KW - Body Fluids -- metabolism KW - Electrolytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544737734?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pflugers+Archiv+%3A+European+journal+of+physiology&rft.atitle=Mechanism+and+synergism+in+epithelial+fluid+and+electrolyte+secretion.&rft.au=Hong%2C+Jeong+Hee%3BPark%2C+Seonghee%3BShcheynikov%2C+Nikolay%3BMuallem%2C+Shmuel&rft.aulast=Hong&rft.aufirst=Jeong&rft.date=2014-08-01&rft.volume=466&rft.issue=8&rft.spage=1487&rft.isbn=&rft.btitle=&rft.title=Pflugers+Archiv+%3A+European+journal+of+physiology&rft.issn=1432-2013&rft_id=info:doi/10.1007%2Fs00424-013-1390-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-23 N1 - Date created - 2014-07-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Acta Physiol (Oxf). 2006 May-Jun;187(1-2):159-67 [16734752] Kidney Int. 2006 Jun;69(12):2162-70 [16688122] Proc Natl Acad Sci U S A. 2006 Jun 20;103(25):9542-7 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- TY - JOUR T1 - A mutation in the extracellular domain of the α7 nAChR reduces calcium permeability. AN - 1544736798; 24177919 AB - The α7 neuronal nicotinic acetylcholine receptor (nAChR) displays the highest calcium permeability among the different subtypes of nAChRs expressed in the mammalian brain and can impact cellular events including neurotransmitter release, second messenger cascades, cell survival, and apoptosis. The selectivity for cations in nAChRs is thought to be achieved in part by anionic residues which are located on either side of the channel mouth and increase relative cationic concentration. Mutagenesis studies have improved our understanding of the role of the second transmembrane domain and the intracellular loop of the channel in ion selectivity. However, little is known about the influence that the extracellular domain (ECD) plays in ion permeation. In the α7 nAChR, it has been found that the ECD contains a ring of ten aspartates (two per subunit) that is believed to face the lumen of the pore and could attract cations for permeation. Using mutagenesis and a combination of electrophysiology and imaging techniques, we tested the possible involvement of these aspartate residues in the calcium permeability of the rat α7 nAChR. We found that one of these residues (the aspartate at position 44) appears to be essential since mutating it to alanine resulted in a decrease in amplitude for both whole cell and single-channel responses and in the complete disappearance of detectable calcium changes in most cells, which indicates that the ECD of the α7 nAChR plays a key role in calcium permeation. JF - Pflugers Archiv : European journal of physiology AU - Colón-Sáez, José O AU - Yakel, Jerrel L AD - Laboratory of Neurobiology, National Institute of Environmental Health Science, National Institutes of Health, Department of Health and Human Services, PO Box 12233, Research Triangle Park, NC, 27709, USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1571 EP - 1579 VL - 466 IS - 8 KW - Protein Subunits KW - 0 KW - alpha7 Nicotinic Acetylcholine Receptor KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Animals KW - Protein Structure, Tertiary -- genetics KW - Patch-Clamp Techniques KW - Extracellular Space -- metabolism KW - Cells, Cultured KW - Calcium -- metabolism KW - Protein Subunits -- genetics KW - Neurons -- metabolism KW - alpha7 Nicotinic Acetylcholine Receptor -- metabolism KW - alpha7 Nicotinic Acetylcholine Receptor -- genetics KW - Protein Subunits -- metabolism KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544736798?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pflugers+Archiv+%3A+European+journal+of+physiology&rft.atitle=A+mutation+in+the+extracellular+domain+of+the+%CE%B17+nAChR+reduces+calcium+permeability.&rft.au=Col%C3%B3n-S%C3%A1ez%2C+Jos%C3%A9+O%3BYakel%2C+Jerrel+L&rft.aulast=Col%C3%B3n-S%C3%A1ez&rft.aufirst=Jos%C3%A9&rft.date=2014-08-01&rft.volume=466&rft.issue=8&rft.spage=1571&rft.isbn=&rft.btitle=&rft.title=Pflugers+Archiv+%3A+European+journal+of+physiology&rft.issn=1432-2013&rft_id=info:doi/10.1007%2Fs00424-013-1385-y LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-23 N1 - Date created - 2014-07-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3643-8 [10716716] J Biol Chem. 2011 May 6;286(18):16008-17 [21454663] Neuropharmacology. 2000 Oct;39(13):2799-807 [11044750] Biol Psychiatry. 2001 Feb 1;49(3):233-9 [11230874] Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):4148-53 [11259680] Eur J Neurosci. 2001 May;13(10):1849-60 [11403678] J Physiol. 2002 Apr 15;540(Pt 2):425-34 [11956333] Mol Cell Neurosci. 2002 Dec;21(4):616-25 [12504594] Nature. 2003 Jan 23;421(6921):384-8 [12508119] Neuron. 2003 Jun 19;38(6):929-39 [12818178] J Neurosci. 2003 Nov 5;23(31):10093-9 [14602824] Cell Calcium. 2004 Jan;35(1):1-8 [14670366] Trends Pharmacol Sci. 2004 Jun;25(6):317-24 [15165747] J Physiol. 2011 Jul 1;589(Pt 13):3163-74 [21540349] J Clin Pharm Ther. 2011 Aug;36(4):437-45 [21729110] Neuron. 2011 Jul 14;71(1):155-65 [21745645] Biochem Pharmacol. 2011 Oct 15;82(8):931-42 [21763291] Nat Neurosci. 2011 Oct;14(10):1253-9 [21909087] Neuroscience. 2011 Nov 10;195:21-36 [21884762] Int J Mol Sci. 2012;13(2):2219-38 [22408449] Curr Drug Targets. 2012 May;13(5):623-30 [22300030] J Mol Neurosci. 2012 Sep;48(1):14-21 [22351110] J Neurosci. 2012 Sep 5;32(36):12337-48 [22956824] Mol Pharmacol. 2013 Sep;84(3):459-75 [23839567] J Neurosci. 1990 Oct;10(10):3413-20 [2170596] Nature. 1992 Oct 8;359(6395):500-5 [1383829] Proc Natl Acad Sci U S A. 1993 Aug 1;90(15):6971-5 [7688468] Biophys J. 1995 Feb;68(2):516-24 [7696505] J Pharmacol Exp Ther. 1997 Jan;280(1):428-38 [8996225] J Physiol. 1998 Mar 15;507 ( Pt 3):749-57 [9508836] J Neurosci. 1998 Sep 1;18(17):6871-81 [9712657] J Physiol. 2005 Aug 1;566(Pt 3):759-68 [15932886] Mol Pharmacol. 2005 Nov;68(5):1431-8 [16120769] J Physiol. 2006 May 15;573(Pt 1):35-43 [16527851] J Physiol. 2007 Mar 15;579(Pt 3):753-63 [17204496] Proc Natl Acad Sci U S A. 2007 May 8;104(19):8059-64 [17470817] J Neurosci. 2007 May 23;27(21):5683-93 [17522313] Front Biosci. 2007;12:5030-8 [17569627] Eur J Neurosci. 2008 Mar;27(5):1097-110 [18312591] PLoS Comput Biol. 2008 Feb;4(2):e41 [18282090] J Physiol. 2009 Mar 1;587(Pt 5):1033-42 [19124535] Glia. 2009 Aug 1;57(10):1104-14 [19170184] Neurochem Res. 2009 Oct;34(10):1805-15 [19381804] Nat Methods. 2009 Dec;6(12):875-81 [19898485] Annu Rev Pharmacol Toxicol. 2000;40:431-58 [10836143] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00424-013-1385-y ER - TY - JOUR T1 - Disposition of fragrance ingredient [14C]1-(1,2,3,4,5,6,7,8-octahydro-2,3,8,8-tetramethyl-2-naphthalenyl)ethanone in male Fisher rats following oral administration and dermal application. AN - 1544322611; 24533629 AB - 1. Disposition of 1-(1,2,3,4,5,6,7,8-octahydro-2,3,8,8-tetramethyl-2-naphthalenyl)ethanone (β-OTNE), a fragrance ingredient in variety of consumer products, was investigated following a single oral (20 mg/kg) or a dermal (55 or 550 mg/kg) dose of [(14)C]β-OTNE to male Fisher rats. 2. Following oral administration, 28% and 39% of the dose was recovered in urine and feces, respectively, 48 h following administration. About 73% of a 20 mg/kg dose was excreted in bile within 48 h post-administration supporting significant oral absorption of [(14)C]β-OTNE. 3. Following dermal application to a covered site, absorption of [(14)C]β-OTNE 96 h following application was low (ca. 14%) and dose-independent. When the dose site was uncovered, the absorption increased to ca. 33% (55 mg/kg) and ca. 72% (550 mg/kg). 4. [(14)C]β-OTNE was distributed to tissues following both routes of exposure with the highest radioactive equivalents found in bladder, liver, kidney, adipose and pancreas. 5. Elimination of [(14)C]β-OTNE equivalents in blood and tissues was slow following both oral and dermal application suggesting potential for accumulation following multiple exposure. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Waidyanatha, Suramya AU - Ryan, Kristen AD - Division of National Toxicology Program, National Institute of Environmental Health Sciences , Research Triangle Park, NC , USA. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 749 EP - 756 VL - 44 IS - 8 KW - Carbon Radioisotopes KW - 0 KW - Naphthalenes KW - Perfume KW - 1-(1,2,3,4,5,6,7,8-octahydro-2,3,8,8-tetramethyl-2-naphthalenyl)ethanone KW - 1GD7ODM28Y KW - Index Medicus KW - oral absorption KW - dermal absorption KW - enterohepatic recirculation KW - biliary excretion KW - 1-(1,2,3,4,5,6,7,8-Octahydro-2,3,8,8-tetramethyl-2-naphthalenyl)ethanone KW - fragrance ingredient KW - Administration, Oral KW - Animals KW - Rats, Inbred F344 KW - Administration, Cutaneous KW - Isomerism KW - Tissue Distribution -- drug effects KW - Radioactivity KW - Time Factors KW - Male KW - Naphthalenes -- blood KW - Perfume -- analysis KW - Naphthalenes -- administration & dosage KW - Naphthalenes -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544322611?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.atitle=Disposition+of+fragrance+ingredient+%5B14C%5D1-%281%2C2%2C3%2C4%2C5%2C6%2C7%2C8-octahydro-2%2C3%2C8%2C8-tetramethyl-2-naphthalenyl%29ethanone+in+male+Fisher+rats+following+oral+administration+and+dermal+application.&rft.au=Waidyanatha%2C+Suramya%3BRyan%2C+Kristen&rft.aulast=Waidyanatha&rft.aufirst=Suramya&rft.date=2014-08-01&rft.volume=44&rft.issue=8&rft.spage=749&rft.isbn=&rft.btitle=&rft.title=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.issn=1366-5928&rft_id=info:doi/10.3109%2F00498254.2014.888489 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-02 N1 - Date created - 2014-07-09 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/00498254.2014.888489 ER - TY - JOUR T1 - Poisoning of mitochondrial topoisomerase I by lamellarin D. AN - 1542650962; 24890608 AB - Lamellarin D (Lam-D) is a hexacyclic pyrole alkaloid isolated from marine invertebrates, whose biologic properties have been attributed to mitochondrial targeting. Mitochondria contain their own DNA (mtDNA), and the only specific mitochondrial topoisomerase in vertebrates is mitochondrial topoisomerase I (Top1mt). Here, we show that Top1mt is a direct mitochondrial target of Lam-D. In vitro Lam-D traps Top1mt and induces Top1mt cleavage complexes (Top1mtcc). Using single-molecule analyses, we also show that Lam-D slows down supercoil relaxation of Top1mt and strongly inhibits Top1mt religation in contrast to the inefficacy of camptothecin on Top1mt. In living cells, we show that Lam-D accumulates rapidly inside mitochondria, induces cellular Top1mtcc, and leads to mtDNA damage. This study provides evidence that Top1mt is a direct mitochondrial target of Lam-D and suggests that developing Top1mt inhibitors represents a novel strategy for targeting mitochondrial DNA. U.S. Government work not protected by U.S. copyright. JF - Molecular pharmacology AU - Khiati, Salim AU - Seol, Yeonee AU - Agama, Keli AU - Dalla Rosa, Ilaria AU - Agrawal, Surbhi AU - Fesen, Katherine AU - Zhang, Hongliang AU - Neuman, Keir C AU - Pommier, Yves AD - Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute (S.K., K.A., I.D.R., S.A., K.F., H.Z., Y.P.) and Laboratory of Molecular Biophysics, National Heart, Lung, and Blood Institute (Y.S., K.C.N.), National Institutes of Health, Bethesda, Maryland. ; Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute (S.K., K.A., I.D.R., S.A., K.F., H.Z., Y.P.) and Laboratory of Molecular Biophysics, National Heart, Lung, and Blood Institute (Y.S., K.C.N.), National Institutes of Health, Bethesda, Maryland pommier@nih.gov. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 193 EP - 199 VL - 86 IS - 2 KW - Coumarins KW - 0 KW - DNA, Mitochondrial KW - Heterocyclic Compounds, 4 or More Rings KW - Isoquinolines KW - lamellarin D KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - Index Medicus KW - Humans KW - DNA, Mitochondrial -- metabolism KW - Cell Line, Tumor KW - DNA, Mitochondrial -- genetics KW - Isoquinolines -- pharmacology KW - Coumarins -- pharmacology KW - Mitochondria -- drug effects KW - Heterocyclic Compounds, 4 or More Rings -- pharmacology KW - Mitochondria -- metabolism KW - DNA Topoisomerases, Type I -- genetics KW - Mitochondria -- genetics KW - DNA Topoisomerases, Type I -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542650962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Poisoning+of+mitochondrial+topoisomerase+I+by+lamellarin+D.&rft.au=Khiati%2C+Salim%3BSeol%2C+Yeonee%3BAgama%2C+Keli%3BDalla+Rosa%2C+Ilaria%3BAgrawal%2C+Surbhi%3BFesen%2C+Katherine%3BZhang%2C+Hongliang%3BNeuman%2C+Keir+C%3BPommier%2C+Yves&rft.aulast=Khiati&rft.aufirst=Salim&rft.date=2014-08-01&rft.volume=86&rft.issue=2&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.114.092833 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-15 N1 - Date created - 2014-07-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncogene. 1999 Nov 18;18(48):6641-6 [10597269] ACS Chem Biol. 2013 Jan 18;8(1):82-95 [23259582] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10608-13 [11526219] Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12114-9 [12209014] Eur J Biochem. 2003 Oct;270(20):4173-86 [14519130] Cancer Res. 2003 Nov 1;63(21):7392-9 [14612538] Curr Med Chem Anticancer Agents. 2004 Jul;4(4):363-78 [15281908] J Biol Chem. 1985 Nov 25;260(27):14873-8 [2997227] Proc Natl Acad Sci U S A. 1988 Oct;85(20):7501-5 [2845409] Cancer Res. 1989 Sep 15;49(18):5016-22 [2548707] Annu Rev Cell Biol. 1991;7:453-78 [1809353] J Med Chem. 1994 Jan 7;37(1):40-6 [8289200] IUBMB Life. 2013 Mar;65(3):273-81 [23441041] Mitochondrion. 2013 May;13(3):199-208 [22846431] Br Med Bull. 2013;106:135-59 [23704099] Nucleic Acids Res. 2013 Nov;41(21):9848-57 [23982517] Chem Biol. 2013 Nov 21;20(11):1323-8 [24183971] ACS Chem Biol. 2013 Jul 19;8(7):1389-95 [23590228] J Natl Cancer Inst. 1994 Jun 1;86(11):836-42 [8182764] Cancer Res. 1995 May 15;55(10):2097-103 [7743509] Science. 1998 Mar 6;279(5356):1534-41 [9488652] J Biol Chem. 1999 Mar 26;274(13):8516-23 [10085084] Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7196-201 [10377391] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):719-24 [15647368] J Med Chem. 2005 Jul 28;48(15):4803-14 [16033260] Cancer Res. 2005 Sep 1;65(17):8028-33 [16140977] Cancer Res. 2006 Mar 15;66(6):3177-87 [16540669] Nature. 2007 Jul 12;448(7150):213-7 [17589503] Cancer Res. 2007 Nov 1;67(21):10397-405 [17974983] Int J Cancer. 2008 Apr 1;122(7):1506-11 [17990320] Anticancer Agents Med Chem. 2008 Oct;8(7):746-60 [18855577] Nat Protoc. 2008;3(11):1736-50 [18927559] Biochemistry. 2008 Oct 28;47(43):11196-203 [18826252] Cell Res. 2009 Jul;19(7):802-15 [19532122] Chembiochem. 2009 Aug 17;10(12):1939-50 [19637148] Mol Cancer Ther. 2009 Dec;8(12):3307-17 [19952118] Chem Biol. 2010 May 28;17(5):421-33 [20534341] Breast J. 2010 May-Jun;16(3):264-70 [20408822] Apoptosis. 2010 Jul;15(7):769-81 [20151196] Methods. 2010 Aug;51(4):444-51 [20123023] Proc Natl Acad Sci U S A. 2010 Nov 16;107(46):19790-5 [21041670] Org Lett. 2011 Jan 21;13(2):312-5 [21175172] Am J Physiol Cell Physiol. 2011 Feb;300(2):C338-48 [21123731] Nucleic Acids Res. 2011 Feb;39(3):1014-22 [20855291] J Pathol. 2012 Jan;226(2):274-86 [21989606] Nat Rev Drug Discov. 2012 Jan;11(1):25-36 [22173432] Nat Struct Mol Biol. 2012 Apr;19(4):417-23 [22388737] PLoS One. 2012;7(7):e41094 [22911747] Eur J Pharm Biopharm. 2012 Sep;82(1):1-18 [22687572] Proc Natl Acad Sci U S A. 2012 Oct 2;109(40):16125-30 [22991469] Proc Natl Acad Sci U S A. 2012 Oct 2;109(40):16288-93 [22991470] Adv Drug Deliv Rev. 2001 Jul 2;49(1-2):175-87 [11377810] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/mol.114.092833 ER - TY - JOUR T1 - Regulation of human CYP2C9 expression by electrophilic stress involves activator protein 1 activation and DNA looping. AN - 1541378763; 24830941 AB - Cytochrome P450 (CYP)2C9 and CYP2C19 are important human enzymes that metabolize therapeutic drugs, environmental chemicals, and physiologically important endogenous compounds. Initial studies using primary human hepatocytes showed induction of both the CYP2C9 and CYP2C19 genes by tert-butylhydroquinone (tBHQ). As a pro-oxidant, tBHQ regulates the expression of cytoprotective genes by activation of redox-sensing transcription factors, such as the nuclear factor E2-related factor 2 (Nrf2) and members of the activator protein 1 (AP-1) family of proteins. The promoter region of CYP2C9 contains two putative AP-1 sites (TGAGTCA) at positions -2201 and -1930, which are also highly conserved in CYP2C19. The CYP2C9 promoter is activated by ectopic expression of cFos and JunD, whereas Nrf2 had no effect. Using specific kinase inhibitors for mitogen-activated protein kinase, we showed that extracellular signal-regulated kinase and Jun N-terminal kinase are essential for tBHQ-induced expression of CYP2C9. Electrophoretic mobility shift assays demonstrate that cFos distinctly interacts with the distal AP-1 site and JunD with the proximal site. Because cFos regulates target genes as heterodimers with Jun proteins, we hypothesized that DNA looping might be required to bring the distal and proximal AP-1 sites together to activate the CYP2C9 promoter. Chromosome conformation capture analyses confirmed the formation of a DNA loop in the CYP2C9 promoter, possibly allowing interaction between cFos at the distal site and JunD at the proximal site to activate CYP2C9 transcription in response to electrophiles. These results indicate that oxidative stress generated by exposure to electrophilic xenobiotics and metabolites induces the expression of CYP2C9 and CYP2C19 in human hepatocytes. U.S. Government work not protected by U.S. copyright. JF - Molecular pharmacology AU - Makia, Ngome L AU - Surapureddi, Sailesh AU - Monostory, Katalin AU - Prough, Russell A AU - Goldstein, Joyce A AD - Human Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina (N.L.M., S.S., J.A.G.); Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, Kentucky (R.A.P.); and Research Centre for Natural Sciences, Hungarian Academy of Science, Budapest, Hungary (K.M.). ; Human Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina (N.L.M., S.S., J.A.G.); Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, Kentucky (R.A.P.); and Research Centre for Natural Sciences, Hungarian Academy of Science, Budapest, Hungary (K.M.) goldste1@niehs.nih.gov. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 125 EP - 137 VL - 86 IS - 2 KW - Proto-Oncogene Proteins c-fos KW - 0 KW - Proto-Oncogene Proteins c-jun KW - Transcription Factor AP-1 KW - Xenobiotics KW - DNA KW - 9007-49-2 KW - CYP2C9 protein, human KW - EC 1.14.13.- KW - Cytochrome P-450 CYP2C9 KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - CYP2C19 protein, human KW - Cytochrome P-450 CYP2C19 KW - Extracellular Signal-Regulated MAP Kinases KW - EC 2.7.11.24 KW - Index Medicus KW - Hep G2 Cells KW - Xenobiotics -- metabolism KW - Humans KW - Transcription, Genetic -- genetics KW - Liver -- metabolism KW - Promoter Regions, Genetic -- genetics KW - Oxidative Stress -- genetics KW - Cell Line, Tumor KW - Binding Sites -- genetics KW - Hepatocytes -- metabolism KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - Proto-Oncogene Proteins c-fos -- metabolism KW - Transcription Factor AP-1 -- metabolism KW - Proto-Oncogene Proteins c-fos -- genetics KW - DNA -- genetics KW - Proto-Oncogene Proteins c-jun -- genetics KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Extracellular Signal-Regulated MAP Kinases -- metabolism KW - Aryl Hydrocarbon Hydroxylases -- genetics KW - Transcription Factor AP-1 -- genetics KW - Extracellular Signal-Regulated MAP Kinases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541378763?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Regulation+of+human+CYP2C9+expression+by+electrophilic+stress+involves+activator+protein+1+activation+and+DNA+looping.&rft.au=Makia%2C+Ngome+L%3BSurapureddi%2C+Sailesh%3BMonostory%2C+Katalin%3BPrough%2C+Russell+A%3BGoldstein%2C+Joyce+A&rft.aulast=Makia&rft.aufirst=Ngome&rft.date=2014-08-01&rft.volume=86&rft.issue=2&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.114.092585 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-15 N1 - Date created - 2014-06-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2008 Sep 12;283(37):25209-17 [18596035] FEBS Lett. 2009 Jun 18;583(12):2126-30 [19467232] Curr Drug Metab. 2009 Dec;10(10):1066-74 [20167002] Br J Pharmacol. 2010 Apr;159(7):1440-9 [20180943] Mol Pharmacol. 2010 Oct;78(4):704-13 [20624854] Antioxid Redox Signal. 2010 Dec 1;13(11):1713-48 [20446772] J Immunol. 2011 Mar 1;186(5):3173-9 [21257959] Mol Pharmacol. 2012 Sep;82(3):529-40 [22723340] J Biol Chem. 2012 Sep 7;287(37):31342-8 [22822070] Mol Pharmacol. 2012 Oct;82(4):601-13 [22740640] Curr Drug Metab. 2013 Jan;14(1):137-50 [22497566] Pharmacol Ther. 2013 Apr;138(1):103-41 [23333322] Mol Carcinog. 2014 Apr;53(4):300-13 [23138933] Drug Metab Dispos. 2001 Mar;29(3):242-51 [11181490] Clin Pharmacol Ther. 2001 Jun;69(6):400-6 [11406737] Br J Clin Pharmacol. 2001 Oct;52(4):349-55 [11678778] J Biol Chem. 2002 Jan 4;277(1):209-17 [11679585] Pharmacogenetics. 2002 Apr;12(3):251-63 [11927841] J Biol Chem. 2002 Aug 16;277(33):29710-8 [12052834] Mol Pharmacol. 2002 Sep;62(3):737-46 [12181452] Oncogene. 2002 Sep 19;21(42):6434-45 [12226747] Mol Cell Biol. 2003 Apr;23(8):2871-82 [12665585] Methods Mol Biol. 1998;107:341-52 [14577243] Nat Rev Cancer. 2003 Nov;3(11):859-68 [14668816] J Pharmacol Exp Ther. 2004 Feb;308(2):495-501 [14600250] Methods Enzymol. 2004;378:286-301 [15038976] Eur J Clin Pharmacol. 1975 Dec 19;9(2-3):219-27 [1233266] Br J Clin Pharmacol. 1985 Oct;20(4):323-6 [4074601] Microbiol Rev. 1992 Mar;56(1):123-36 [1579106] Mol Cell Biol. 1993 Sep;13(9):5479-89 [8355695] Genes Dev. 1993 Dec;7(12B):2497-509 [8276234] J Biol Chem. 1994 Dec 16;269(50):31756-62 [7527395] Pharmacogenetics. 1994 Dec;4(6):285-99 [7704034] Biochemistry. 1995 Jun 27;34(25):8028-36 [7794915] J Biol Chem. 1996 Jun 7;271(23):13422-9 [8662787] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):12908-13 [8917518] Cancer Res. 1997 May 15;57(10):1946-54 [9157990] J Biol Chem. 1997 Nov 14;272(46):28962-70 [9360968] Nature. 1999 Sep 30;401(6752):493-7 [10519554] Annu Rev Pharmacol Toxicol. 2005;45:477-94 [15822186] J Pharmacol Exp Ther. 2005 Sep;314(3):1125-33 [15919766] Oncogene. 2005 Nov 17;24(51):7567-78 [16007120] Nat Methods. 2006 Jan;3(1):17-21 [16369547] AAPS J. 2006;8(1):E101-11 [16584116] J Biol Chem. 2006 Nov 17;281(46):34833-47 [16984917] Expert Opin Drug Metab Toxicol. 2006 Dec;2(6):923-46 [17125409] Nat Protoc. 2007;2(7):1722-33 [17641637] J Biol Chem. 2008 Mar 28;283(13):8164-72 [18252719] Drug Metab Dispos. 2008 May;36(5):816-23 [18227147] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/mol.114.092585 ER - TY - JOUR T1 - CMT-associated mutations in glycyl- and tyrosyl-tRNA synthetases exhibit similar pattern of toxicity and share common genetic modifiers in Drosophila. AN - 1539472304; 24807208 AB - Aminoacyl-tRNA synthetases are ubiquitously expressed proteins that charge tRNAs with their cognate amino acids. By ensuring the fidelity of protein synthesis, these enzymes are essential for the viability of every cell. Yet, mutations in six tRNA synthetases specifically affect the peripheral nerves and cause Charcot-Marie-Tooth (CMT) disease. The CMT-causing mutations in tyrosyl- and glycyl-tRNA synthetases (YARS and GARS, respectively) alter the activity of the proteins in a range of ways (some mutations do not impact charging function, while others abrogate it), making a loss of function in tRNA charging unlikely to be the cause of disease pathology. It is currently unknown which cellular mechanisms are triggered by the mutant enzymes and how this leads to neurodegeneration. Here, by expressing two pathogenic mutations (G240R, P234KY) in Drosophila, we generated a model for GARS-associated neuropathy. We observed compromised viability, and behavioral, electrophysiological and morphological impairment in flies expressing the cytoplasmic isoform of mutant GARS. Their features recapitulated several hallmarks of CMT pathophysiology and were similar to the phenotypes identified in our previously described Drosophila model of YARS-associated neuropathy. Furthermore, CG8316 and CG15599 - genes identified in a retinal degeneration screen to modify mutant YARS, also modified the mutant GARS phenotypes. Our study presents genetic evidence for common mutant-specific interactions between two CMT-associated aminoacyl-tRNA synthetases, lending support for a shared mechanism responsible for the synthetase-induced peripheral neuropathies. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Neurobiology of disease AU - Ermanoska, Biljana AU - Motley, William W AU - Leitão-Gonçalves, Ricardo AU - Asselbergh, Bob AU - Lee, LaTasha H AU - De Rijk, Peter AU - Sleegers, Kristel AU - Ooms, Tinne AU - Godenschwege, Tanja A AU - Timmerman, Vincent AU - Fischbeck, Kenneth H AU - Jordanova, Albena AD - Molecular Neurogenomics Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA; Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Molecular Neurogenomics Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium; Peripheral Neuropathy Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium; Centralized Service Facility, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Department of Biological Sciences, Florida Atlantic University, Jupiter, FL 33458, USA. ; Applied Molecular Genomics Unit, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium; Neurodegenerative Brain Diseases Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium; Peripheral Neuropathy Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium. ; Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA. ; Molecular Neurogenomics Group, Department of Molecular Genetics, VIB, University of Antwerp, Antwerp 2610, Belgium; Neurogenetics Laboratory, Institute Born-Bunge, University of Antwerp, Antwerp 2610, Belgium. Electronic address: albena.jordanova@molgen.vib-ua.be. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 180 EP - 189 VL - 68 KW - Dextrans KW - 0 KW - Drosophila Proteins KW - Fluoro-Ruby KW - Rhodamines KW - Tyrosine-tRNA Ligase KW - EC 6.1.1.1 KW - Glycine-tRNA Ligase KW - EC 6.1.1.14 KW - Index Medicus KW - Aminoacyl-tRNA synthetase KW - Charcot–Marie–Tooth disease KW - Drosophila KW - Animals KW - Retina -- ultrastructure KW - Retinal Degeneration -- diagnosis KW - Humans KW - Membrane Potentials -- physiology KW - Disease Models, Animal KW - Animals, Genetically Modified KW - Neurons -- pathology KW - Nerve Fibers -- physiology KW - Membrane Potentials -- genetics KW - Wings, Animal -- pathology KW - Wings, Animal -- ultrastructure KW - Neurons -- physiology KW - Drosophila Proteins -- genetics KW - Retina -- pathology KW - Retinal Degeneration -- etiology KW - Drosophila Proteins -- metabolism KW - Female KW - Male KW - Retinal Degeneration -- genetics KW - Charcot-Marie-Tooth Disease -- pathology KW - Tyrosine-tRNA Ligase -- genetics KW - Peripheral Nervous System Diseases -- etiology KW - Peripheral Nervous System Diseases -- genetics KW - Charcot-Marie-Tooth Disease -- complications KW - Mutation -- genetics KW - Glycine-tRNA Ligase -- genetics KW - Charcot-Marie-Tooth Disease -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1539472304?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+disease&rft.atitle=CMT-associated+mutations+in+glycyl-+and+tyrosyl-tRNA+synthetases+exhibit+similar+pattern+of+toxicity+and+share+common+genetic+modifiers+in+Drosophila.&rft.au=Ermanoska%2C+Biljana%3BMotley%2C+William+W%3BLeit%C3%A3o-Gon%C3%A7alves%2C+Ricardo%3BAsselbergh%2C+Bob%3BLee%2C+LaTasha+H%3BDe+Rijk%2C+Peter%3BSleegers%2C+Kristel%3BOoms%2C+Tinne%3BGodenschwege%2C+Tanja+A%3BTimmerman%2C+Vincent%3BFischbeck%2C+Kenneth+H%3BJordanova%2C+Albena&rft.aulast=Ermanoska&rft.aufirst=Biljana&rft.date=2014-08-01&rft.volume=68&rft.issue=&rft.spage=180&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+disease&rft.issn=1095-953X&rft_id=info:doi/10.1016%2Fj.nbd.2014.04.020 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2014-06-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lancet Neurol. 2009 Jul;8(7):654-67 [19539237] Mol Cell. 2009 Jun 12;34(5):603-11 [19524539] Proc Natl Acad Sci U S A. 2009 Jul 14;106(28):11782-7 [19561293] Nucleic Acids Res. 2010 Jan;38(Database issue):D196-203 [19892828] Am J Hum Genet. 2010 Jan;86(1):77-82 [20045102] Trends Neurosci. 2010 Feb;33(2):59-66 [20152552] PLoS One. 2010;5(4):e9931 [20368981] Cold Spring Harb Protoc. 2010 Jul;2010(7):pdb.prot5453 [20647357] J Neurogenet. 2010 Sep;24(3):158-67 [20615087] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14366-71 [10588711] Genes Dev. 2000 Apr 1;14(7):830-40 [10766739] J Cell Biol. 2000 May 1;149(3):567-74 [10791971] Annu Rev Biochem. 2000;69:617-50 [10966471] J Biol Chem. 2000 Oct 13;275(41):31559-62 [10930398] Development. 2000 Dec;127(23):5203-12 [11060245] J Mol Biol. 2001 Jun 29;310(1):243-57 [11419950] Neuron. 2002 May 16;34(4):509-19 [12062036] Nat Neurosci. 2002 Dec;5(12):1294-301 [12436113] Nat Genet. 2003 Apr;33(4):455-6 [12627231] Am J Hum Genet. 2003 May;72(5):1293-9 [12690580] Nucleic Acids Res. 2003 Jul 1;31(13):3625-30 [12824381] Nat Genet. 2004 Mar;36(3):283-7 [14981521] Protein Sci. 2004 May;13(5):1402-6 [15096640] Genetics. 2004 Jun;167(2):761-81 [15238527] Neurology. 2004 Aug 24;63(4):724-6 [15326253] J Embryol Exp Morphol. 1981 Dec;66:57-80 [6802923] J Mol Biol. 1990 Oct 5;215(3):403-10 [2231712] Development. 1993 Jun;118(2):401-15 [8223268] Eur J Cell Biol. 1994 Oct;65(1):60-9 [7889996] Proc Natl Acad Sci U S A. 1996 Oct 29;93(22):12418-22 [8901596] Development. 1997 Apr;124(8):1497-507 [9108366] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694] J Comp Neurol. 1998 Aug 10;397(4):519-31 [9699913] Science. 1998 Dec 11;282(5396):2082-5 [9851929] Ann Neurol. 2005 Nov;58(5):777-80 [16240349] Nat Genet. 2006 Feb;38(2):197-202 [16429158] Nucleic Acids Res. 2006 Jul 1;34(Web Server issue):W335-9 [16845021] Neuron. 2006 Sep 21;51(6):715-26 [16982418] J Neurosci. 2006 Oct 11;26(41):10397-406 [17035524] Am J Hum Genet. 2010 Oct 8;87(4):560-6 [20920668] Nucleic Acids Res. 2011 Jan;39(Database issue):D225-9 [21109532] Science. 2010 Dec 24;330(6012):1787-97 [21177974] Mol Cell Neurosci. 2011 Feb;46(2):432-43 [21115117] J Vis Exp. 2011;(52). pii: 3080. doi: 10.3791/3080 [21673644] Mol Syst Biol. 2011;7:539 [21988835] PLoS Genet. 2011 Dec;7(12):e1002399 [22144914] J Biol Chem. 2012 Mar 16;287(12):9330-4 [22291016] Nat Methods. 2012 Jul;9(7):671-5 [22930834] Nucleic Acids Res. 2013 Jan;41(Database issue):D358-65 [23180791] Hum Mutat. 2013 Jan;34(1):191-9 [22930593] J Peripher Nerv Syst. 2012 Dec;17(4):418-21 [23279345] Lancet Neurol. 2013 Jun;12(6):609-22 [23684085] J Neurol Neurosurg Psychiatry. 2013 Nov;84(11):1247-9 [23729695] Clin Genet. 2014 Dec;86(6):592-4 [24354524] Nat Neurosci. 2007 Jul;10(7):828-37 [17529987] Proc Natl Acad Sci U S A. 2007 Jul 3;104(27):11239-44 [17595294] Genome Biol. 2007;8(5):R68 [17472741] Dev Cell. 2008 Feb;14(2):239-51 [18267092] Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W197-201 [18463136] Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W297-302 [18463141] Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):13901-5 [18779587] Dis Model Mech. 2009 Jul-Aug;2(7-8):359-73 [19470612] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.nbd.2014.04.020 ER - TY - JOUR T1 - Correlation of plasma viral loads and presence of Chikungunya IgM antibodies with cytokine/chemokine levels during acute Chikungunya virus infection AN - 1534838879; 20079634 AB - Chikungunya (CHIKV) is an emerging arboviral infection of public health concern in India contributing to widespread morbidity. The precise molecular events occurring early in the infection have not been well understood. Cytokines/chemokines are suspected to play a key role in its pathogenesis. Very few studies have correlated the plasma levels of cytokines/chemokines with diagnostic markers such as viral loads and presence of CHIKV IgM antibodies. Understanding these dynamics in the early phase of CHIKV infection is likely to provide an insight into the evolution of the immune response, identify biomarkers for assessing severity, and for development of newer therapeutic strategies. This study was therefore undertaken to estimate the levels of various cytokines/chemokines in plasma samples of patients infected with CHIKV and correlate to viral load and CHIKV IgM antibodies. Cytokine/chemokine levels and viral loads in plasma were measured using cytometric bead array and TaqMan real time PCR assay, respectively. The findings revealed that acute phase of CHIKV infection is characterized by predominant inflammatory responses mediated by IL-6, IL-8, IP-10, MCP-1, and MIG (P<0.003). Plasma levels of IL-6 (r=0.53, P<0.05) and MCP-1 (r=0.83, P<0.05) emerged as reliable biomarkers of high viral loads in Chikungunya patients. Further, presence of elevated levels of MCP-1 and MIG during the chronic phase of the disease suggests that these chemokines may contribute to perpetuation of symptoms. Hence, these chemokines might serve as targets for the development of treatment to ameliorate the symptoms during the acute phase and prevent the development of chronic manifestations. JF - Journal of Medical Virology AU - Reddy, Vijayalakshmi AU - Mani, Reeta Subramaniam AU - Desai, Anita AU - Ravi, Vasanthapuram AD - Department of Neurovirology, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1393 EP - 1401 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 86 IS - 8 SN - 0146-6615, 0146-6615 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts; Virology & AIDS Abstracts KW - Interleukin 6 KW - Virology KW - Symptoms KW - Chemokines KW - Nucleotide sequence KW - Disease control KW - Biomarkers KW - Defence mechanisms KW - Morbidity KW - Interleukin 8 KW - India KW - Public health KW - IP-10 protein KW - Cytokines KW - Polymerase chain reaction KW - Chikungunya virus KW - Monocyte chemoattractant protein 1 KW - biomarkers KW - Inflammation KW - Plasma levels KW - Antibodies KW - Viral diseases KW - Immune response KW - Evolution KW - Immunoglobulin M KW - V 22350:Immunology 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/1534838879?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medical+Virology&rft.atitle=Correlation+of+plasma+viral+loads+and+presence+of+Chikungunya+IgM+antibodies+with+cytokine%2Fchemokine+levels+during+acute+Chikungunya+virus+infection&rft.au=Reddy%2C+Vijayalakshmi%3BMani%2C+Reeta+Subramaniam%3BDesai%2C+Anita%3BRavi%2C+Vasanthapuram&rft.aulast=Reddy&rft.aufirst=Vijayalakshmi&rft.date=2014-08-01&rft.volume=86&rft.issue=8&rft.spage=1393&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Virology&rft.issn=01466615&rft_id=info:doi/10.1002%2Fjmv.23875 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Virology; Symptoms; Antibodies; Viral diseases; Nucleotide sequence; Disease control; Biomarkers; Defence mechanisms; Public health; Interleukin 6; Chemokines; Monocyte chemoattractant protein 1; biomarkers; Interleukin 8; Morbidity; Inflammation; Plasma levels; IP-10 protein; Polymerase chain reaction; Cytokines; Immune response; Immunoglobulin M; Evolution; Chikungunya virus; India DO - http://dx.doi.org/10.1002/jmv.23875 ER - TY - JOUR T1 - PCR-based assay to detect sheeppox virus in ocular, nasal, and rectal swabs from infected Moroccan sheep. AN - 1529846215; 24698762 AB - Sheeppox is now enzootic in Morocco. The development of a reliable method for rapid diagnosis of the disease is a central part of any control strategy. The aim of this study is to determine the diagnostic value of a variety of clinical samples such as ovine nasal, ocular or rectal swabs for the detection of sheeppox virus (SPPV) by qualitative conventional polymerase chain reaction (PCR), using a single pair of primers targeting the inverted terminal repeats of the SPPV InS-1 strain, a virulent field isolate. Swab and blood samples were collected from forty animals naturally infected with SPPV who had clinical signs of sheeppox. All animals tested PCR-positive for SPPV. Positive results were obtained infrequently with blood samples, whereas swab samples from at least two sites (nasal, ocular, rectal) were positive per evaluated animal. These results indicate that swab samples are suitable for quantitative molecular SPPV diagnosis. PCR product sequences obtained from all types of sheep samples proved to be identical to the corresponding regions of sheeppox virus strain Romania 65. Copyright © 2014. Published by Elsevier B.V. JF - Journal of virological methods AU - Zro, K AU - Azelmat, S AU - Bendouro, Y AU - Kuhn, J H AU - El Fahime, E AU - Ennaji, M M AD - Laboratory of Virology, Microbiology and Quality/Ecotoxicology and Biodiversity, Hassan II University Mohammedia-Casablanca, Faculty of Science and Technology Mohammedia, BP 146 Mohammedia 20650, Morocco; Regional Laboratory of Analysis and Research of Oujda, National Office for the Safety of Food Products, 60 000 Oujda, Morocco. ; Military Hospital of Instruction Mohammed V, Rabat 14 000, Morocco. ; Regional Laboratory of Analysis and Research of Oujda, National Office for the Safety of Food Products, 60 000 Oujda, Morocco. ; Integrated Research Facility at Fort Detrick, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 8200 Research Plaza, Fort Detrick, Frederick, MD, United States. ; Functional Genomics Platform Scientific Research Technical Support Unit - Biology - National Center of Scientific and Technical Research, Rabat 14 000, Morocco. ; Laboratory of Virology, Microbiology and Quality/Ecotoxicology and Biodiversity, Hassan II University Mohammedia-Casablanca, Faculty of Science and Technology Mohammedia, BP 146 Mohammedia 20650, Morocco. Electronic address: m.ennaji@yahoo.fr. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 38 EP - 43 VL - 204 KW - DNA Primers KW - 0 KW - DNA, Viral KW - Index Medicus KW - Capripoxvirus KW - Sheeppox virus KW - Poxvirus KW - Poxviridae KW - PCR KW - Genotype KW - Rectum -- virology KW - Eye -- virology KW - Animals KW - Morocco KW - DNA Primers -- genetics KW - Sheep KW - Nasal Mucosa -- virology KW - DNA, Viral -- genetics KW - Blood -- virology KW - Capripoxvirus -- isolation & purification KW - Capripoxvirus -- genetics KW - Veterinary Medicine -- methods KW - Polymerase Chain Reaction -- methods KW - Sheep Diseases -- diagnosis KW - Capripoxvirus -- classification KW - Poxviridae Infections -- diagnosis KW - Poxviridae Infections -- virology KW - Molecular Diagnostic Techniques -- methods KW - Sheep Diseases -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1529846215?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+virological+methods&rft.atitle=PCR-based+assay+to+detect+sheeppox+virus+in+ocular%2C+nasal%2C+and+rectal+swabs+from+infected+Moroccan+sheep.&rft.au=Zro%2C+K%3BAzelmat%2C+S%3BBendouro%2C+Y%3BKuhn%2C+J+H%3BEl+Fahime%2C+E%3BEnnaji%2C+M+M&rft.aulast=Zro&rft.aufirst=K&rft.date=2014-08-01&rft.volume=204&rft.issue=&rft.spage=38&rft.isbn=&rft.btitle=&rft.title=Journal+of+virological+methods&rft.issn=1879-0984&rft_id=info:doi/10.1016%2Fj.jviromet.2014.03.019 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-05 N1 - Date created - 2014-05-26 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jviromet.2014.03.019 ER - TY - JOUR T1 - Fenretinide induces ubiquitin-dependent proteasomal degradation of stearoyl-CoA desaturase in human retinal pigment epithelial cells. AN - 1518817344; 24357007 AB - Stearoyl-CoA desaturase (SCD, SCD1), an endoplasmic reticulum (ER) resident protein and a rate-limiting enzyme in monounsaturated fatty acid biosynthesis, regulates cellular functions by controlling the ratio of saturated to monounsaturated fatty acids. Increase in SCD expression is strongly implicated in the proliferation and survival of cancer cells, whereas its decrease is known to impair proliferation, induce apoptosis, and restore insulin sensitivity. We examined whether fenretinide, (N-(4-hydroxyphenyl)retinamide, 4HPR), which induces apoptosis in cancer cells and recently shown to improve insulin sensitivity, can modulate the expression of SCD. We observed that fenretinide decreased SCD protein and enzymatic activity in the ARPE-19 human retinal pigment epithelial cell line. Increased expression of BiP/GRP78, ATF4, and GADD153 implicated ER stress. Tunicamycin and thapsigargin, compounds known to induce ER stress, also decreased the SCD protein. This decrease was completely blocked by the proteasome inhibitor MG132. In addition, PYR41, an inhibitor of ubiquitin activating enzyme E1, blocked the fenretinide-mediated decrease in SCD. Immunoprecipitation analysis using anti-ubiquitin and anti-SCD antibodies and the blocking of SCD loss by PYR41 inhibition of ubiquitination further corroborate that fenretinide mediates the degradation of SCD in human RPE cells via the ubiquitin-proteasome dependent pathway. Therefore, the effect of fenretinide on SCD should be considered in its potential therapeutic role against cancer, type-2 diabetes, and retinal diseases. © 2013 Wiley Periodicals, Inc. JF - Journal of cellular physiology AU - Samuel, William AU - Kutty, R Krishnan AU - Duncan, Todd AU - Vijayasarathy, Camasamudram AU - Kuo, Bryan C AU - Chapa, Krysten M AU - Redmond, T Michael AD - Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/08// PY - 2014 DA - August 2014 SP - 1028 EP - 1038 VL - 229 IS - 8 KW - Antineoplastic Agents KW - 0 KW - Ubiquitin KW - Fenretinide KW - 187EJ7QEXL KW - Stearoyl-CoA Desaturase KW - EC 1.14.19.1 KW - Index Medicus KW - Gene Expression Regulation, Enzymologic -- drug effects KW - Humans KW - Apoptosis -- physiology KW - Apoptosis -- drug effects KW - Stress, Physiological -- drug effects KW - Antineoplastic Agents -- pharmacology KW - Cell Line KW - Endoplasmic Reticulum -- drug effects KW - Stearoyl-CoA Desaturase -- metabolism KW - Ubiquitin -- metabolism KW - Epithelial Cells -- enzymology KW - Epithelial Cells -- drug effects KW - Retinal Pigment Epithelium -- cytology KW - Fenretinide -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518817344?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fenretinide+induces+ubiquitin-dependent+proteasomal+degradation+of+stearoyl-CoA+desaturase+in+human+retinal+pigment+epithelial+cells.&rft.au=Samuel%2C+William%3BKutty%2C+R+Krishnan%3BDuncan%2C+Todd%3BVijayasarathy%2C+Camasamudram%3BKuo%2C+Bryan+C%3BChapa%2C+Krysten+M%3BRedmond%2C+T+Michael&rft.aulast=Samuel&rft.aufirst=William&rft.date=2014-08-01&rft.volume=229&rft.issue=8&rft.spage=1028&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24527 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-21 N1 - Date created - 2014-04-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Carcinogenesis. 2010 Sep;31(9):1509-15 [20595235] J Biol Chem. 2010 Sep 17;285(38):29078-90 [20628055] Mol Med. 2010 Nov-Dec;16(11-12):535-42 [20683548] Curr Mol Med. 2010 Dec;10(9):802-23 [21091424] Mol Med. 2011 Mar-Apr;17(3-4):273-80 [21060977] J Clin Invest. 2011 May;121(5):1858-70 [21490391] J Biol Chem. 2011 May 13;286(19):16596-605 [21454530] PLoS One. 2011;6(5):e19734 [21573029] Exp Biol Med (Maywood). 2011 Jun 1;236(6):707-13 [21565896] J Biol Chem. 2011 Jul 15;286(28):24754-64 [21543327] Biochem Pharmacol. 2011 Nov 1;82(9):1110-25 [21819973] Adv Exp Med Biol. 2012;723:167-74 [22183330] Biol Pharm Bull. 2012;35(3):369-75 [22382323] J Biol Chem. 2012 May 18;287(21):17426-37 [22474281] Biochem Pharmacol. 2013 Mar 1;85(5):653-66 [23000916] Retina. 2013 Mar;33(3):498-507 [23023528] Diabetes. 2006 Nov;55(11):3121-6 [17065351] Cell Metab. 2007 Mar;5(3):167-79 [17339025] J Biol Chem. 2007 Jun 8;282(23):16718-28 [17283068] Endocrinology. 2007 Jul;148(7):3258-70 [17431003] Am J Pathol. 2007 Aug;171(2):513-24 [17620365] Cancer Res. 2007 Oct 1;67(19):9472-81 [17909057] Invest Ophthalmol Vis Sci. 2008 Mar;49(3):1210-20 [18326751] Biophys J. 2008 Apr 1;94(7):2869-83 [18096630] Am J Physiol Endocrinol Metab. 2008 Aug;295(2):E339-49 [18523127] Anal Chim Acta. 2008 Oct 3;627(1):99-104 [18790132] Mol Cancer Ther. 2008 Sep;7(9):2967-76 [18790777] J Clin Oncol. 2001 Mar 15;19(6):1664-70 [11250995] Cancer Res. 2001 Jul 1;61(13):5102-5 [11431347] J Biol Chem. 2001 Aug 3;276(31):28744-50 [11397803] J Biol Chem. 2002 Jan 4;277(1):59-66 [11677241] Physiol Rev. 2002 Apr;82(2):373-428 [11917093] Carcinogenesis. 2002 Nov;23(11):1933-6 [12419843] J Neurochem. 2003 Feb;84(4):655-68 [12562510] Mol Cell Biol. 2003 Aug;23(16):5790-802 [12897149] Proc Natl Acad Sci U S A. 2003 Sep 16;100(19):11110-5 [12960377] J Biol Chem. 1976 Aug 25;251(16):5095-103 [8453] Int J Cancer. 1994 May 1;57(3):348-52 [7909540] Int J Cancer. 1994 Nov 1;59(3):422-6 [7927952] Prog Lipid Res. 1995;34(2):139-50 [7480063] Int J Cancer. 1996 Feb 8;65(4):491-7 [8621233] J Natl Cancer Inst. 1997 Aug 20;89(16):1191-8 [9274913] Mol Biol Cell. 1997 Nov;8(11):2281-90 [9362069] Annu Rev Biochem. 1998;67:425-79 [9759494] Trends Cell Biol. 1998 Oct;8(10):397-403 [9789328] Clin Cancer Res. 1996 May;2(5):855-63 [9816241] Mol Biol Cell. 1998 Dec;9(12):3445-53 [9843580] J Lipid Res. 1999 Sep;40(9):1549-58 [10484602] Am J Physiol Endocrinol Metab. 2005 Mar;288(3):E599-607 [15562249] Methods. 2005 Apr;35(4):373-81 [15804610] J Clin Invest. 2005 Apr;115(4):1030-8 [15761499] Oncogene. 2005 May 5;24(20):3319-27 [15735697] J Biol Chem. 2005 Jul 8;280(27):25339-49 [15851470] Nature. 2005 Jul 21;436(7049):356-62 [16034410] Invest Ophthalmol Vis Sci. 2005 Dec;46(12):4393-401 [16303925] Cell Biol Int. 2006 Jan;30(1):31-43 [16275144] J Cell Sci. 2006 Jun 1;119(Pt 11):2342-53 [16723740] J Clin Invest. 2006 Jun;116(6):1686-95 [16741579] EMBO Rep. 2006 Sep;7(9):880-5 [16953201] J Cell Physiol. 2006 Dec;209(3):854-65 [16972258] Biochem J. 2009 Feb 1;417(3):791-801 [18922131] Biochem Biophys Res Commun. 2009 Mar 20;380(4):818-22 [19338759] Am J Physiol Endocrinol Metab. 2009 Jul;297(1):E28-37 [19066317] Diabetes. 2009 Aug;58(8):1757-65 [19478146] Expert Opin Ther Pat. 2009 Sep;19(9):1169-91 [19691439] Mol Pharmacol. 2009 Sep;76(3):503-15 [19520899] Blood. 2010 Mar 18;115(11):2251-9 [20075161] Age (Dordr). 2010 Jun;32(2):231-7 [20431990] Curr Opin Lipidol. 2010 Jun;21(3):192-7 [20216310] Mol Cancer Ther. 2010 Jun;9(6):1740-54 [20530718] Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):1189-94 [20153289] PLoS One. 2010;5(6):e11394 [20613975] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/jcp.24527 ER - TY - CPAPER T1 - Diversity of Anti-Cancer Activity among a Subset of the USDA Apple Germplasm Core Collection T2 - 2014 Annual Conference of the American Society for Horticultural Science (ASHS 2014) AN - 1541353518; 6288750 JF - 2014 Annual Conference of the American Society for Horticultural Science (ASHS 2014) AU - Thompson, Matthew AU - Stushnoff, Cecil Y1 - 2014/07/28/ PY - 2014 DA - 2014 Jul 28 KW - Germplasm KW - Species diversity KW - Malus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Conference+of+the+American+Society+for+Horticultural+Science+%28ASHS+2014%29&rft.atitle=Diversity+of+Anti-Cancer+Activity+among+a+Subset+of+the+USDA+Apple+Germplasm+Core+Collection&rft.au=Thompson%2C+Matthew%3BStushnoff%2C+Cecil&rft.aulast=Thompson&rft.aufirst=Matthew&rft.date=2014-07-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Conference+of+the+American+Society+for+Horticultural+Science+%28ASHS+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://ashs.confex.com/ashs/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Selecting pharmacological interventions through rapid screening motifs and proper cell models T2 - 2014 American Dairy Science Association- American Society of Animal Science and and the Canadian Society of Animal Science Annual Meeting (JAM 2014) AN - 1548625018; 6289697 JF - 2014 American Dairy Science Association- American Society of Animal Science and and the Canadian Society of Animal Science Annual Meeting (JAM 2014) AU - Zudaire, E Y1 - 2014/07/20/ PY - 2014 DA - 2014 Jul 20 KW - Screening KW - Intervention KW - Cell culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548625018?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Dairy+Science+Association-+American+Society+of+Animal+Science+and+and+the+Canadian+Society+of+Animal+Science+Annual+Meeting+%28JAM+2014%29&rft.atitle=Selecting+pharmacological+interventions+through+rapid+screening+motifs+and+proper+cell+models&rft.au=Zudaire%2C+E&rft.aulast=Zudaire&rft.aufirst=E&rft.date=2014-07-20&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Dairy+Science+Association-+American+Society+of+Animal+Science+and+and+the+Canadian+Society+of+Animal+Science+Annual+Meeting+%28JAM+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://www.asas.org/docs/default-source/jam2014/jam_program_june4.pdf?sfvrsn=0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-30 N1 - Last updated - 2014-07-28 ER - TY - JOUR T1 - A cell-penetrating antibody fragment against HIV-1 Rev has high antiviral activity: characterization of the paratope. AN - 1549630918; 24878961 AB - The HIV-1 protein Rev oligomerizes on viral transcripts and directs their nuclear export. Previously, a Fab against Rev generated by phage display was used to crystallize and solve the structure of the Rev oligomerization domain. Here we have investigated the capability of this Fab to block Rev oligomerization and inhibit HIV-1 replication. The Fab itself did not have antiviral activity, but when a Tat-derived cell-penetrating peptide was appended, the resulting molecule (FabRev1-Tat) was strongly inhibitory of three different CCR5-tropic HIV-1 isolates (IC50 = 0.09-0.44 μg/ml), as assessed by suppression of reverse transcriptase activity in infected peripheral blood mononuclear cells, and had low cell toxicity (TC50 > 100 μg/ml). FabRev1-Tat was taken up by both peripheral blood mononuclear and HEK293T cells, appearing in both the cytoplasm and nucleus, as shown by immunofluorescence confocal laser scanning microscopy. Computational alanine scanning was used to identify key residues in the complementarity-determining regions to guide mutagenesis experiments. Residues in the light chain CDR3 (LCDR3) were assessed to be important. Residues in LCDR3 were mutated, and LCDR3-Tyr(92) was found to be critical for binding to Rev, as judged by surface plasmon resonance and electron microscopy. Peptides corresponding to all six CDR regions were synthesized and tested for Rev binding. None of the linear peptides had significant affinity for Rev, but four of the amide-cyclic forms did. Especially cyclic-LCDR3 (LGGYPAASYRTA) had high affinity for Rev and was able to effectively depolymerize Rev filaments, as shown by both surface plasmon resonance and electron microscopy. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Zhuang, Xiaolei AU - Stahl, Stephen J AU - Watts, Norman R AU - DiMattia, Michael A AU - Steven, Alasdair C AU - Wingfield, Paul T AD - From the Protein Expression Laboratory and. ; the Laboratory of Structural Biology Research, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892. ; From the Protein Expression Laboratory and pelpw@helix.nih.gov. Y1 - 2014/07/18/ PY - 2014 DA - 2014 Jul 18 SP - 20222 EP - 20233 VL - 289 IS - 29 KW - Anti-HIV Agents KW - 0 KW - Cell-Penetrating Peptides KW - Complementarity Determining Regions KW - Immunoglobulin Fab Fragments KW - rev Gene Products, Human Immunodeficiency Virus KW - rev protein, Human Immunodeficiency Virus-1 KW - Index Medicus KW - Monoclonal Antibody KW - AIDS KW - Phage Display KW - Cyclic Peptide KW - Cell-penetrating peptide (CPP) KW - Models, Molecular KW - HEK293 Cells KW - Humans KW - Protein Multimerization -- drug effects KW - Amino Acid Sequence KW - Protein Binding KW - Mutagenesis, Site-Directed KW - Microscopy, Electron, Transmission KW - Protein Engineering KW - Virus Replication -- drug effects KW - Binding Sites, Antibody -- genetics KW - Kinetics KW - Molecular Sequence Data KW - Binding Sites, Antibody -- immunology KW - Virus Replication -- immunology KW - Anti-HIV Agents -- chemistry KW - Cell-Penetrating Peptides -- immunology KW - HIV-1 -- immunology KW - Cell-Penetrating Peptides -- genetics KW - Anti-HIV Agents -- immunology KW - rev Gene Products, Human Immunodeficiency Virus -- metabolism KW - rev Gene Products, Human Immunodeficiency Virus -- genetics KW - Immunoglobulin Fab Fragments -- genetics KW - Anti-HIV Agents -- pharmacology KW - rev Gene Products, Human Immunodeficiency Virus -- antagonists & inhibitors KW - Immunoglobulin Fab Fragments -- immunology KW - HIV-1 -- physiology KW - Cell-Penetrating Peptides -- pharmacology KW - HIV-1 -- drug effects KW - Immunoglobulin Fab Fragments -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549630918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=A+cell-penetrating+antibody+fragment+against+HIV-1+Rev+has+high+antiviral+activity%3A+characterization+of+the+paratope.&rft.au=Zhuang%2C+Xiaolei%3BStahl%2C+Stephen+J%3BWatts%2C+Norman+R%3BDiMattia%2C+Michael+A%3BSteven%2C+Alasdair+C%3BWingfield%2C+Paul+T&rft.aulast=Zhuang&rft.aufirst=Xiaolei&rft.date=2014-07-18&rft.volume=289&rft.issue=29&rft.spage=20222&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.581090 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-06 N1 - Date created - 2014-07-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11466-71 [11027346] AIDS Res Hum Retroviruses. 2000 Jan 1;16(1):59-65 [10628817] FEBS Lett. 2001 Nov 9;508(1):67-74 [11707270] J Immunol Methods. 2002 Sep 1;267(1):53-70 [12135800] Biochem Biophys Res Commun. 2003 Jul 18;307(1):198-205 [12850000] Trends Biochem Sci. 2003 Aug;28(8):419-24 [12932730] Sci STKE. 2004 Feb 10;2004(219):pl2 [14872095] Cell. 1989 Jul 14;58(1):205-14 [2752419] Biochemistry. 1991 Jul 30;30(30):7527-34 [1854752] Proc Natl Acad Sci U S A. 1993 May 15;90(10):4374-8 [7685100] Science. 1996 Sep 13;273(5281):1547-51 [8703216] J Struct Biol. 1998 Jan;121(1):41-52 [9573619] Annu Rev Biochem. 1998;67:1-25 [9759480] Mol Cell Biol. 1999 Feb;19(2):1210-7 [9891055] Annu Rev Microbiol. 1998;52:491-532 [9891806] J Biol Chem. 1999 Feb 5;274(6):3789-96 [9920932] J Gen Virol. 2005 Jun;86(Pt 6):1791-800 [15914858] Biomaterials. 2008 May;29(15):2408-14 [18295328] Proc Natl Acad Sci U S A. 2009 Feb 3;106(5):1404-8 [19164515] Mol Pharm. 2009 Mar-Apr;6(2):337-44 [19718791] J Mol Biol. 2010 Apr 2;397(3):697-708 [20138059] Proc Natl Acad Sci U S A. 2010 Mar 30;107(13):5810-4 [20231488] Nucleic Acids Res. 2010 Jul;38(Web Server issue):W402-6 [20444871] Nucleic Acids Res. 2010 Jul;38(Web Server issue):W480-6 [20511591] Nucleic Acids Res. 2010 Jul;38(Web Server issue):W407-11 [20525787] Int J Biochem Cell Biol. 2010 Sep;42(9):1482-8 [20580677] PLoS One. 2010;5(8):e12352 [20808810] Methods Mol Biol. 2011;683:21-9 [21053119] BMC Biotechnol. 2010;10:79 [21029412] Nat Struct Mol Biol. 2010 Nov;17(11):1337-42 [20953181] J Control Release. 2011 May 10;151(3):220-8 [21078351] Proteins. 2011 Sep;79(9):2671-83 [21735484] Nature. 2012 Jan 19;481(7381):365-70 [22190034] Chem Biol Drug Des. 2012 May;79(5):683-90 [22188730] PLoS One. 2012;7(11):e48839 [23144991] PLoS One. 2013;8(4):e60259 [23565213] J Virol. 2013 Oct;87(20):11173-86 [23926352] Nucleic Acids Res. 2013 Nov;41(20):9471-83 [23945945] Cell. 2013 Oct 24;155(3):594-605 [24243017] Microb Cell Fact. 2014;13:17 [24475978] Mol Cell. 2001 Mar;7(3):603-14 [11463385] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.581090 ER - TY - JOUR T1 - The nuclear receptor peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) promotes oncogene-induced cellular senescence through repression of endoplasmic reticulum stress. AN - 1549630858; 24898257 AB - Endoplasmic reticulum (ER) stress and ER stress-associated unfolded protein response (UPR) can promote cancer cell survival, but it remains unclear whether they can influence oncogene-induced senescence. The present study examined the role of ER stress in senescence using oncogene-dependent models. Increased ER stress attenuated senescence in part by up-regulating phosphorylated protein kinase B (p-AKT) and decreasing phosphorylated extracellular signal-regulated kinase (p-ERK). A positive feed forward loop between p-AKT, ER stress, and UPR was discovered whereby a transient increase of ER stress caused reduced senescence and promotion of tumorigenesis. Decreased ER stress was further correlated with increased senescence in both mouse and human tumors. Interestingly, H-RAS-expressing Pparβ/δ null cells and tumors having increased cell proliferation exhibited enhanced ER stress, decreased cellular senescence, and/or enhanced tumorigenicity. Collectively, these results demonstrate a new role for ER stress and UPR that attenuates H-RAS-induced senescence and suggest that PPARβ/δ can repress this oncogene-induced ER stress to promote senescence in accordance with its role as a tumor modifier that suppresses carcinogenesis. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Zhu, Bokai AU - Ferry, Christina H AU - Markell, Lauren K AU - Blazanin, Nicholas AU - Glick, Adam B AU - Gonzalez, Frank J AU - Peters, Jeffrey M AD - From the Department of Veterinary and Biomedical Sciences and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802 and. ; the Laboratory of Metabolism, NCI, National Institutes of Health, Bethesda, Maryland 20892. ; From the Department of Veterinary and Biomedical Sciences and The Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802 and jmp21@psu.edu. Y1 - 2014/07/18/ PY - 2014 DA - 2014 Jul 18 SP - 20102 EP - 20119 VL - 289 IS - 29 KW - ATF4 protein, human KW - 0 KW - Atf4 protein, mouse KW - DNA-Binding Proteins KW - Heat-Shock Proteins KW - PPAR delta KW - PPAR-beta KW - RNA, Small Interfering KW - Regulatory Factor X Transcription Factors KW - Transcription Factors KW - molecular chaperone GRP78 KW - Activating Transcription Factor 4 KW - 145891-90-3 KW - TOR Serine-Threonine Kinases KW - EC 2.7.1.1 KW - mTOR protein, mouse KW - Proto-Oncogene Proteins c-akt KW - EC 2.7.11.1 KW - Index Medicus KW - Cancer Therapy KW - Keratinocyte KW - Oncogene-induced Endoplasmic Reticulum Stress KW - H-RAS-induced Senescence KW - Tumor Suppressor Gene KW - Peroxisome Proliferator-activated Receptor β/δ KW - Cancer Biology KW - Cancer KW - Animals KW - TOR Serine-Threonine Kinases -- metabolism KW - Humans KW - DNA-Binding Proteins -- genetics KW - Gene Expression KW - Models, Biological KW - Skin Neoplasms -- genetics KW - Genes, p53 KW - Keratinocytes -- cytology KW - Keratinocytes -- metabolism KW - Colonic Neoplasms -- pathology KW - Adenoma -- pathology KW - Signal Transduction KW - Cell Transformation, Neoplastic -- genetics KW - Proto-Oncogene Proteins c-akt -- metabolism KW - Colonic Neoplasms -- genetics KW - Activating Transcription Factor 4 -- genetics KW - Cell Transformation, Neoplastic -- metabolism KW - Skin Neoplasms -- pathology KW - Mice KW - RNA, Small Interfering -- genetics KW - Transcription Factors -- genetics KW - Skin Neoplasms -- metabolism KW - Adenoma -- metabolism KW - Gene Knockdown Techniques KW - Cells, Cultured KW - Unfolded Protein Response KW - Colonic Neoplasms -- metabolism KW - Adenoma -- genetics KW - Heat-Shock Proteins -- genetics KW - Genes, ras KW - PPAR-beta -- metabolism KW - PPAR delta -- deficiency KW - PPAR delta -- genetics KW - PPAR-beta -- genetics KW - Endoplasmic Reticulum Stress KW - Cell Aging -- physiology KW - PPAR-beta -- deficiency KW - PPAR delta -- metabolism KW - Cell Aging -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549630858?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+nuclear+receptor+peroxisome+proliferator-activated+receptor-%CE%B2%2F%CE%B4+%28PPAR%CE%B2%2F%CE%B4%29+promotes+oncogene-induced+cellular+senescence+through+repression+of+endoplasmic+reticulum+stress.&rft.au=Zhu%2C+Bokai%3BFerry%2C+Christina+H%3BMarkell%2C+Lauren+K%3BBlazanin%2C+Nicholas%3BGlick%2C+Adam+B%3BGonzalez%2C+Frank+J%3BPeters%2C+Jeffrey+M&rft.aulast=Zhu&rft.aufirst=Bokai&rft.date=2014-07-18&rft.volume=289&rft.issue=29&rft.spage=20102&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.551069 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-06 N1 - Date created - 2014-07-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cancer Res. 2007 Dec;5(12):1263-75 [18171984] Trends Mol Med. 2007 Oct;13(10):433-42 [17905659] Oncogene. 2008 May 1;27(20):2801-9 [18193093] Cell. 2008 Jun 13;133(6):1019-31 [18555778] Toxicology. 2008 Dec 5;254(1-2):112-7 [18950674] Carcinogenesis. 2008 Dec;29(12):2406-14 [18799709] Oncogene. 2009 Jun 18;28(24):2324-36 [19421146] Nat Protoc. 2009;4(12):1798-806 [20010931] Toxicol Sci. 2010 Jan;113(1):27-36 [19748995] Mol Pharmacol. 2010 Sep;78(3):419-30 [20516370] Cancer Res. 2010 Nov 1;70(21):8526-36 [20959475] Mol Cancer Ther. 2010 Dec;9(12):3267-77 [21159610] Biochem J. 2011 Mar 1;434(2):181-8 [21309747] Mol Cell. 2011 Apr 8;42(1):36-49 [21474066] Cell Signal. 2011 Dec;23(12):2039-50 [21843636] Cancer Res. 2012 Jan 15;72(2):395-401 [22102693] Mol Cell Biol. 2012 Jun;32(11):2065-82 [22473992] Mol Cell Biol. 2012 Jun;32(12):2268-78 [22493067] Oncogene. 2014 Nov 13;33(46):5348-59 [24213576] Gastroenterology. 2000 Oct;119(4):929-42 [11040180] Cancer Res. 2003 Jul 1;63(13):3447-52 [12839923] J Biol Chem. 2004 May 28;279(22):23719-27 [15033975] Mol Cell Biol. 2004 Jun;24(12):5459-74 [15169907] Nature. 1981 Sep 3;293(5827):72-4 [6791032] Cancer Res. 1988 Jan 1;48(1):165-9 [3121168] Cancer Res. 1992 Jun 1;52(11):3145-56 [1375535] Methods Enzymol. 1995;254:3-20 [8531694] Cancer Res. 1996 Sep 1;56(17):3895-7 [8752154] Nature. 2005 Aug 4;436(7051):642 [16079833] Carcinogenesis. 2006 May;27(5):1105-12 [16418176] Nat Cell Biol. 2006 Oct;8(10):1053-63 [16964246] Cancer Cell. 2006 Dec;10(6):459-72 [17157787] Cancer Cell. 2007 Apr;11(4):349-60 [17418411] Cancer Res. 2007 Apr 15;67(8):3496-9 [17440054] Biochem Biophys Res Commun. 2007 Aug 3;359(3):778-83 [17560942] Biochem Biophys Res Commun. 2007 Aug 3;359(3):643-8 [17560946] Cell. 2007 Jun 29;129(7):1261-74 [17604717] Annu Rev Pathol. 2008;3:399-425 [18039139] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.551069 ER - TY - JOUR T1 - Super-suppression of mitochondrial reactive oxygen species signaling impairs compensatory autophagy in primary mitophagic cardiomyopathy. AN - 1546213634; 24874428 AB - Mitochondrial reactive oxygen species (ROS) are implicated in aging, chronic degenerative neurological syndromes, and myopathies. On the basis of free radical hypothesis, dietary, pharmacological, and genetic ROS suppression has been tested to minimize tissue damage, with remarkable therapeutic efficacy. The effects of mitochondrial-specific ROS suppression in primary mitophagic dysfunction are unknown. An in vivo dose-ranging analysis of ROS suppression in an experimental cardiomyopathy provoked by defective mitochondrial clearance. Mice lacking mitofusin 2 (Mfn2) in hearts have impaired parkin-mediated mitophagy leading to accumulation of damaged ROS-producing organelles and progressive heart failure. As expected, cardiomyocyte-directed expression of mitochondrial-targeted catalase at modest levels normalized mitochondrial ROS production and prevented mitochondrial depolarization, respiratory impairment, and structural degeneration in Mfn2 null hearts. In contrast, catalase expression at higher levels that supersuppressed mitochondrial ROS failed to improve either mitochondrial fitness or cardiomyopathy, revealing that ROS toxicity is not the primary mechanism for cardiac degeneration. Lack of benefit from supersuppressing ROS was associated with failure to invoke secondary autophagic pathways of mitochondrial quality control, revealing a role for ROS signaling in mitochondrial clearance. Mitochondrial permeability transition pore function was normal, and genetic inhibition of mitochondrial permeability transition pore function did not alter mitochondrial or cardiac degeneration, in Mfn2 null hearts. Local mitochondrial ROS (1) contribute to mitochondrial degeneration and (2) activate mitochondrial quality control mechanisms. A therapeutic window for mitochondrial ROS suppression should minimize the former while retaining the latter, which we achieved by expressing lower levels of catalase. © 2014 American Heart Association, Inc. JF - Circulation research AU - Song, Moshi AU - Chen, Yun AU - Gong, Guohua AU - Murphy, Elizabeth AU - Rabinovitch, Peter S AU - Dorn, Gerald W AD - From the Department of Internal Medicine, Center for Pharmacogenomics, Washington University School of Medicine, St. Louis, MO (M.S., G.G., G.W.D.); National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD (E.M.); and Department of Pathology, University of Washington, Seattle (P.S.R.). ; From the Department of Internal Medicine, Center for Pharmacogenomics, Washington University School of Medicine, St. Louis, MO (M.S., G.G., G.W.D.); National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD (E.M.); and Department of Pathology, University of Washington, Seattle (P.S.R.). gdorn@dom.wustl.edu. Y1 - 2014/07/18/ PY - 2014 DA - 2014 Jul 18 SP - 348 EP - 353 VL - 115 IS - 3 KW - Mitochondrial Membrane Transport Proteins KW - 0 KW - Myh6 protein, mouse KW - Oxidants KW - Reactive Oxygen Species KW - mitochondrial permeability transition pore KW - Hydrogen Peroxide KW - BBX060AN9V KW - GTP Phosphohydrolases KW - EC 3.6.1.- KW - Mfn2 protein, mouse KW - Myosin Heavy Chains KW - EC 3.6.4.1 KW - Cyclophilins KW - EC 5.2.1.- KW - cyclophilin D KW - EC 5.2.1.8 KW - Index Medicus KW - mitochondria KW - mitochondrial degradation KW - cardiomyopathies KW - mitofusin 1 KW - catalase KW - Mitochondrial Membrane Transport Proteins -- metabolism KW - Animals KW - Myosin Heavy Chains -- genetics KW - Cyclophilins -- genetics KW - Hydrogen Peroxide -- metabolism KW - Humans KW - Oxidants -- metabolism KW - Myocardium -- metabolism KW - Male KW - Female KW - Mitochondrial Membranes -- metabolism KW - Mice, Knockout KW - Signal Transduction -- physiology KW - Reactive Oxygen Species -- metabolism KW - Cardiomyopathies -- metabolism KW - GTP Phosphohydrolases -- genetics KW - Cardiomyopathies -- pathology KW - Mitochondria, Heart -- metabolism KW - Autophagy -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1546213634?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Circulation+research&rft.atitle=Super-suppression+of+mitochondrial+reactive+oxygen+species+signaling+impairs+compensatory+autophagy+in+primary+mitophagic+cardiomyopathy.&rft.au=Song%2C+Moshi%3BChen%2C+Yun%3BGong%2C+Guohua%3BMurphy%2C+Elizabeth%3BRabinovitch%2C+Peter+S%3BDorn%2C+Gerald+W&rft.aulast=Song&rft.aufirst=Moshi&rft.date=2014-07-18&rft.volume=115&rft.issue=3&rft.spage=348&rft.isbn=&rft.btitle=&rft.title=Circulation+research&rft.issn=1524-4571&rft_id=info:doi/10.1161%2FCIRCRESAHA.115.304384 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-16 N1 - Date created - 2014-07-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Cell Biol. 2010 Apr 19;189(2):211-21 [20404107] Circulation. 2009 Jun 2;119(21):2789-97 [19451351] Proc Natl Acad Sci U S A. 2010 May 18;107(20):9035-42 [20418503] Circ Res. 2010 Jun 11;106(11):1681-91 [20413785] Trends Biochem Sci. 2011 Jan;36(1):30-8 [20728362] Mol Cell Biol. 2011 Mar;31(6):1309-28 [21245373] Circ Res. 2011 Apr 1;108(7):837-46 [21311045] Circ Res. 2012 Sep 14;111(7):863-75 [22777004] J Biol Chem. 2013 Jan 18;288(3):1979-90 [23204527] Science. 2013 Apr 26;340(6131):471-5 [23620051] PLoS Biol. 2010 Jan;8(1):e1000298 [20126261] Nature. 2003 Jun 12;423(6941):769-73 [12802338] Int J Biochem Cell Biol. 2004 Dec;36(12):2463-72 [15325585] Nature. 2005 Mar 31;434(7033):658-62 [15800627] Science. 2005 Jun 24;308(5730):1909-11 [15879174] Circ Res. 2006 Mar 31;98(6):837-45 [16514068] J Clin Invest. 2009 Jan;119(1):203-12 [19065046] Mol Cell. 2009 May 15;34(3):259-69 [19450525] Comment In: Circ Res. 2014 Jul 18;115(3):329-31 [25035131] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1161/CIRCRESAHA.115.304384 ER - TY - JOUR T1 - Genetic instability in lymphoblastoid cell lines expressing biallelic and monoallelic variants in the human MUTYH gene. AN - 1539466318; 24569162 AB - The MUTYH DNA glycosylase counteracts mutagenesis by removing adenine misincorporated opposite DNA 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG). Biallelic germline mutations in MUTYH cause the autosomal recessive MUTYH-associated polyposis (MAP). The impact on genetic instability of the p.Tyr179Cys and p.Arg245His MUTYH variants was evaluated in lymphoblastoid cell lines (LCLs) derived from MAP patients and their relatives in comparison to wild-type LCLs. No difference in MUTYH expression was identified between wild type and LCLs with the p.Tyr179Cys, while the p.Arg245His mutation was associated with an unstable MUTYH protein. LCLs homozygous for the p.Tyr179Cys or the p.Arg245His variant contained increased DNA 8-oxodG levels and exhibited a mutator phenotype at the PIG-A gene. The extent of the increased spontaneous mutation frequency was 3-fold (range 1.6- to 4.6-fold) in four independent LCLs carrying the p.Tyr179Cys variant, while a larger increase (6-fold) was observed in two p.Arg245His LCLs. A similar hypermutability and S-phase delay following treatment with KBrO3 was observed in LCLs homozygous for either variant. When genetic instability was investigated in monoallelic p.Arg245His carriers, mutant frequencies showed an increase which is intermediate between wild-type and homozygous cells, whereas the mutator effect in heterozygous p.Tyr179Cys LCLs was similar to that in homozygotes. These findings indicate that the type of MUTYH mutation can affect the extent of genome instability associated with MUTYH inactivation. In addition, the mild spontaneous mutator phenotype observed in monoallelic carriers highlights the biological importance of this gene in the protection of the genome against endogenous DNA damage. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Human molecular genetics AU - Grasso, Francesca AU - Giacomini, Elisa AU - Sanchez, Massimo AU - Degan, Paolo AU - Gismondi, Viviana AU - Mazzei, Filomena AU - Varesco, Liliana AU - Viel, Alessandra AU - Bignami, Margherita AD - Department of Environment and Primary Prevention and. ; Experimental Oncology 1, CRO Aviano National Cancer Institute, Aviano, Italy. ; Department of Cell Biology and Neuroscience, Istituto Superiore di Sanità, Rome, Italy. ; Department of Translational Oncology and. ; Unit of Hereditary Cancer, IRCCS AOU San Martino-IST, Genoa, Italy. ; Department of Environment and Primary Prevention and margherita.bignami@iss.it. Y1 - 2014/07/15/ PY - 2014 DA - 2014 Jul 15 SP - 3843 EP - 3852 VL - 23 IS - 14 KW - Bromates KW - 0 KW - Membrane Proteins KW - phosphatidylinositol glycan-class A protein KW - potassium bromate KW - 04MB35W6ZA KW - 8-oxo-7-hydrodeoxyguanosine KW - 88847-89-6 KW - DNA Glycosylases KW - EC 3.2.2.- KW - mutY adenine glycosylase KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Young Adult KW - Genetic Variation KW - Polymorphism, Single Nucleotide KW - Protein Stability KW - Humans KW - Membrane Proteins -- metabolism KW - Membrane Proteins -- genetics KW - Adult KW - Bromates -- pharmacology KW - Middle Aged KW - Deoxyguanosine -- analysis KW - Cell Cycle -- drug effects KW - Cell Line KW - Male KW - Deoxyguanosine -- analogs & derivatives KW - Adenomatous Polyposis Coli -- genetics KW - Genomic Instability KW - DNA Glycosylases -- metabolism KW - DNA Glycosylases -- genetics KW - Adenomatous Polyposis Coli -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1539466318?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genetic+instability+in+lymphoblastoid+cell+lines+expressing+biallelic+and+monoallelic+variants+in+the+human+MUTYH+gene.&rft.au=Grasso%2C+Francesca%3BGiacomini%2C+Elisa%3BSanchez%2C+Massimo%3BDegan%2C+Paolo%3BGismondi%2C+Viviana%3BMazzei%2C+Filomena%3BVaresco%2C+Liliana%3BViel%2C+Alessandra%3BBignami%2C+Margherita&rft.aulast=Grasso&rft.aufirst=Francesca&rft.date=2014-07-15&rft.volume=23&rft.issue=14&rft.spage=3843&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=1460-2083&rft_id=info:doi/10.1093%2Fhmg%2Fddu097 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-09 N1 - Date created - 2014-06-21 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/hmg/ddu097 ER - TY - JOUR T1 - The design and discovery of water soluble 4-substituted-2,6-dimethylfuro[2,3-d]pyrimidines as multitargeted receptor tyrosine kinase inhibitors and microtubule targeting antitumor agents. AN - 1536685001; 24890652 AB - The design, synthesis and biological evaluations of fourteen 4-substituted 2,6-dimethylfuro[2,3-d]pyrimidines are reported. Four compounds (11-13, 15) inhibit vascular endothelial growth factor receptor-2 (VEGFR-2), platelet-derived growth factor receptor β (PDGFR-β), and target tubulin leading to cytotoxicity. Compound 11 has nanomolar potency, comparable to sunitinib and semaxinib, against tumor cell lines overexpressing VEGFR-2 and PDGFR-β. Further, 11 binds at the colchicine site on tubulin, depolymerizes cellular microtubules and inhibits purified tubulin assembly and overcomes both βIII-tubulin and P-glycoprotein-mediated drug resistance, and initiates mitotic arrest leading to apoptosis. In vivo, its HCl salt, 21, reduced tumor size and vascularity in xenograft and allograft murine models and was superior to docetaxel and sunitinib, without overt toxicity. Thus 21 affords potential combination chemotherapy in a single agent. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - Bioorganic & medicinal chemistry AU - Zhang, Xin AU - Raghavan, Sudhir AU - Ihnat, Michael AU - Thorpe, Jessica E AU - Disch, Bryan C AU - Bastian, Anja AU - Bailey-Downs, Lora C AU - Dybdal-Hargreaves, Nicholas F AU - Rohena, Cristina C AU - Hamel, Ernest AU - Mooberry, Susan L AU - Gangjee, Aleem AD - Division of Medicinal Chemistry, Graduate School of Pharmaceutical Sciences, Duquesne University, 600 Forbes Avenue, Pittsburgh, PA 15282, United States. ; College of Pharmacy, University of Oklahoma Health Science Center, 1110 North Stonewall, Oklahoma City, OK 73117, United States. ; Department of Pharmacology, Cancer Therapy & Research Center, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, United States. ; Screening Technologies Branch, Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, Frederick National Laboratory for Cancer Research, National Institutes of Health, 1050 Boyles Street, Frederick, MD 21702, United States. ; Division of Medicinal Chemistry, Graduate School of Pharmaceutical Sciences, Duquesne University, 600 Forbes Avenue, Pittsburgh, PA 15282, United States. Electronic address: gangjee@duq.edu. Y1 - 2014/07/15/ PY - 2014 DA - 2014 Jul 15 SP - 3753 EP - 3772 VL - 22 IS - 14 KW - Aniline Compounds KW - 0 KW - Antineoplastic Agents KW - N-(4-methoxyphenyl)-N,2,6-trimethylfuro(2,3-d)pyrimidin-4-amine KW - Protein Kinase Inhibitors KW - Pyrimidines KW - Water KW - 059QF0KO0R KW - Receptor Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Microtubule targeting agents KW - Anticancer agents KW - Single agent combination chemotherapy KW - Tyrosine kinase inhibitors KW - Cell Proliferation -- drug effects KW - Drug Screening Assays, Antitumor KW - Animals KW - Solubility KW - HeLa Cells KW - Dose-Response Relationship, Drug KW - Humans KW - Mice, Nude KW - Mice KW - Cell Line, Tumor KW - Mice, Inbred BALB C KW - Female KW - Structure-Activity Relationship KW - Pyrimidines -- chemistry KW - Drug Discovery KW - Aniline Compounds -- pharmacology KW - Protein Kinase Inhibitors -- pharmacology KW - Water -- chemistry KW - Pyrimidines -- pharmacology KW - Receptor Protein-Tyrosine Kinases -- antagonists & inhibitors KW - Microtubules -- drug effects KW - Receptor Protein-Tyrosine Kinases -- metabolism KW - Neoplasms, Experimental -- pathology KW - Aniline Compounds -- chemistry KW - Pyrimidines -- chemical synthesis KW - Apoptosis -- drug effects KW - Antineoplastic Agents -- chemical synthesis KW - Protein Kinase Inhibitors -- chemistry KW - Protein Kinase Inhibitors -- chemical synthesis KW - Neoplasms, Experimental -- drug therapy KW - Antineoplastic Agents -- chemistry KW - Antineoplastic Agents -- pharmacology KW - Aniline Compounds -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1536685001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioorganic+%26+medicinal+chemistry&rft.atitle=The+design+and+discovery+of+water+soluble+4-substituted-2%2C6-dimethylfuro%5B2%2C3-d%5Dpyrimidines+as+multitargeted+receptor+tyrosine+kinase+inhibitors+and+microtubule+targeting+antitumor+agents.&rft.au=Zhang%2C+Xin%3BRaghavan%2C+Sudhir%3BIhnat%2C+Michael%3BThorpe%2C+Jessica+E%3BDisch%2C+Bryan+C%3BBastian%2C+Anja%3BBailey-Downs%2C+Lora+C%3BDybdal-Hargreaves%2C+Nicholas+F%3BRohena%2C+Cristina+C%3BHamel%2C+Ernest%3BMooberry%2C+Susan+L%3BGangjee%2C+Aleem&rft.aulast=Zhang&rft.aufirst=Xin&rft.date=2014-07-15&rft.volume=22&rft.issue=14&rft.spage=3753&rft.isbn=&rft.btitle=&rft.title=Bioorganic+%26+medicinal+chemistry&rft.issn=1464-3391&rft_id=info:doi/10.1016%2Fj.bmc.2014.04.049 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-28 N1 - Date created - 2014-06-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncologist. 2010;15(12):1253-61 [21147873] Oncology. 2010;79(1-2):129-35 [21088439] Mini Rev Med Chem. 2011 Jan;11(1):18-31 [21034401] Acta Crystallogr D Biol Crystallogr. 2011 Apr;67(Pt 4):386-94 [21460457] Invest New Drugs. 2011 Jun;29(3):499-505 [20094773] Nature. 2011 May 19;473(7347):398-402 [21460836] J Med Chem. 2011 Sep 8;54(17):6151-5 [21786793] Clin Cancer Res. 2005 Aug 1;11(15):5481-6 [16061864] Bioorg Med Chem. 2005 Sep 15;13(18):5475-91 [16039863] Nature. 2005 Dec 15;438(7070):967-74 [16355214] Cancer Treat Rev. 2006 May;32(3):166-79 [16527420] Clin Cancer Res. 2006 May 1;12(9):2774-9 [16675570] Nat Rev Drug Discov. 2007 Apr;6(4):273-86 [17396134] Int J Cancer. 2007 May 15;120(10):2078-85 [17285590] Ann Oncol. 2007 Jul;18 Suppl 5:v3-8 [17656560] Curr Med Chem. 2007;14(23):2495-516 [17979703] Oncogene. 2008 Aug 7;27(34):4702-11 [18408761] Cancer Res. 2008 Nov 1;68(21):8881-8 [18974132] Mol Cancer Ther. 2008 Dec;7(12):3670-84 [19074844] Bioorg Med Chem. 2009 Oct 15;17(20):7324-36 [19748785] J Med Chem. 2010 Jan 14;53(1):325-34 [19894742] Br J Cancer. 2010 Jan 19;102(2):316-24 [20029418] J Med Chem. 2010 Feb 25;53(4):1563-78 [20092323] J Clin Oncol. 2010 Jun 20;28(18):2947-51 [20458043] Lancet Oncol. 2010 Jul;11(7):619-26 [20570559] J Clin Oncol. 2010 Jul 10;28(20):3248-55 [20530274] J Biol Chem. 1999 Dec 31;274(53):37990-4 [10608867] J Med Chem. 2000 Jun 15;43(12):2310-23 [10882357] J Clin Oncol. 2001 Jul 1;19(13):3267-79 [11432895] Curr Opin Chem Biol. 2001 Aug;5(4):424-31 [11470606] J Mol Biol. 2001 Nov 9;313(5):1045-57 [11700061] Biol Pharm Bull. 2002 May;25(5):597-604 [12033499] Pharmacol Ther. 2002 Feb-Mar;93(2-3):79-98 [12191602] Oncogene. 2002 Sep 12;21(41):6255-63 [12214266] Cancer Res. 2002 Oct 15;62(20):5749-54 [12384534] Expert Opin Ther Targets. 2003 Apr;7(2):215-34 [12667099] Oncogene. 2003 Jun 5;22(23):3548-53 [12789263] Oncologist. 2003;8(5):411-24 [14530494] Semin Oncol. 2003 Oct;30(5 Suppl 16):65-78 [14613028] Lung. 2003;181(5):267-73 [14705770] J Med Chem. 2004 Feb 12;47(4):871-87 [14761189] Nature. 2004 Mar 11;428(6979):198-202 [15014504] Cancer Res. 1992 Jul 15;52(14):3892-900 [1617665] Breast Cancer Res Treat. 1995;36(2):109-18 [8534860] Cell. 1996 Aug 9;86(3):353-64 [8756718] J Med Chem. 1997 May 9;40(10):1519-29 [9154973] Anticancer Res. 1998 Nov-Dec;18(6A):4435-41 [9891506] Pharmacol Ther. 1999 May-Jun;82(2-3):195-206 [10454197] Methods Mol Biol. 1999;129:257-69 [10494570] Clin Cancer Res. 2005 Jan 1;11(1):298-305 [15671559] J Med Chem. 2005 Feb 10;48(3):710-22 [15689155] Bioorg Med Chem Lett. 2005 May 2;15(9):2203-7 [15837294] Br J Cancer. 2005 Jun;92 Suppl 1:S6-13 [15928657] Cancer Chemother Pharmacol. 2010 Sep;66(4):669-80 [20043166] Nat Rev Drug Discov. 2010 Oct;9(10):790-803 [20885410] Invest New Drugs. 2010 Dec;28(6):844-53 [19760364] Nat Rev Cancer. 2010 Nov;10(11):760-74 [20966921] Nat Rev Clin Oncol. 2010 Nov;7(11):618-9 [20981125] Br J Cancer. 2010 Nov 9;103(10):1554-61 [20959830] J Med Chem. 2010 Nov 25;53(22):8116-28 [20973488] Clin Cancer Res. 2010 Dec 1;16(23):5892-9 [21138873] Cancer J. 2011 Sep-Oct;17(5):267-72 [21952273] Clin Exp Rheumatol. 2011 Jul-Aug;29(4 Suppl 67):S77-86 [21968242] Biol Pharm Bull. 2011;34(12):1774-80 [22130229] ChemMedChem. 2012 Jan 2;7(1):33-42 [21990124] Breast Cancer Res Treat. 2012 Feb;131(3):899-906 [22042372] Ann Oncol. 2012 Mar;23(3):688-94 [21821830] Ann Oncol. 2012 Apr;23(4):1023-9 [21778300] Breast. 2012 Aug;21(4):507-13 [22336056] Invest New Drugs. 2012 Oct;30(5):1972-7 [22006161] Br J Cancer. 2012 Oct 9;107(8):1277-85 [22990652] Br J Cancer. 2012 Oct 9;107(8):1268-76 [22996612] Pharm Res. 2012 Nov;29(11):2943-71 [22814904] Breast. 2012 Dec;21(6):716-23 [23022045] Cancer Chemother Pharmacol. 2012 Dec;70(6):843-53 [23014737] Chemotherapy. 2012;58(4):321-9 [23147218] J Med Chem. 2012 Dec 27;55(24):10797-822 [23098265] Breast Cancer Res Treat. 2013 Jan;137(2):457-64 [23224144] J Med Chem. 2013 Jan 10;56(1):241-53 [23270382] Breast Cancer Res Treat. 2013 Apr;138(2):427-35 [23479422] Ann Oncol. 2013 May;24(5):1392-400 [23293114] Curr Cancer Drug Targets. 2013 Mar;13(3):326-46 [23369096] Invest New Drugs. 2013 Jun;31(3):734-41 [23161334] J Med Chem. 2013 May 23;56(10):3889-903 [23611691] J Clin Oncol. 2013 Jun 1;31(16):1947-53 [23509322] J Med Chem. 2013 Sep 12;56(17):6829-44 [23895532] J Med Chem. 2013 Sep 26;56(18):7382-95 [23961916] Eur J Pharmacol. 2013 Oct 5;717(1-3):40-6 [23660368] Nat Rev Clin Oncol. 2009 Jul;6(7):395-404 [19424102] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bmc.2014.04.049 ER - TY - JOUR T1 - The chemical uncoupler 2,4-dinitrophenol (DNP) protects against diet-induced obesity and improves energy homeostasis in mice at thermoneutrality. AN - 1549631531; 24872412 AB - The chemical uncoupler 2,4-dinitrophenol (DNP) was an effective and widely used weight loss drug in the early 1930s. However, the physiology of DNP has not been studied in detail because toxicity, including hyperthermia and death, reduced interest in the clinical use of chemical uncouplers. To investigate DNP action, mice fed a high fat diet and housed at 30 °C (to minimize facultative thermogenesis) were treated with 800 mg/liter DNP in drinking water. DNP treatment increased energy expenditure by ∼ 17%, but did not change food intake. DNP-treated mice weighed 26% less than controls after 2 months of treatment due to decreased fat mass, without a change in lean mass. DNP improved glucose tolerance and reduced hepatic steatosis without observed toxicity. DNP treatment also reduced circulating T3 and T4 levels, Ucp1 expression, and brown adipose tissue activity, demonstrating that DNP-mediated heat generation substituted for brown adipose tissue thermogenesis. At 22 °C, a typical vivarium temperature that is below thermoneutrality, DNP treatment had no effect on body weight, adiposity, or glucose homeostasis. Thus, environmental temperature should be considered when assessing an anti-obesity drug in mice, particularly agents acting on energy expenditure. Furthermore, the beneficial effects of DNP suggest that chemical uncouplers deserve further investigation for the treatment of obesity and its comorbidities. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Goldgof, Margalit AU - Xiao, Cuiying AU - Chanturiya, Tatyana AU - Jou, William AU - Gavrilova, Oksana AU - Reitman, Marc L AD - From the Diabetes, Endocrinology, and Obesity Branch and. ; the Mouse Metabolism Core, NIDDK, National Institutes of Health, Bethesda, Maryland 20892. ; From the Diabetes, Endocrinology, and Obesity Branch and marc.reitman@nih.gov. Y1 - 2014/07/11/ PY - 2014 DA - 2014 Jul 11 SP - 19341 EP - 19350 VL - 289 IS - 28 KW - Ion Channels KW - 0 KW - Mitochondrial Proteins KW - Ucp1 protein, mouse KW - Uncoupling Agents KW - Uncoupling Protein 1 KW - 2,4-Dinitrophenol KW - Q13SKS21MN KW - Index Medicus KW - Obesity KW - Drug Development KW - CL316243 KW - Thermoregulation KW - Uncoupling Protein KW - Thermoneutrality KW - Brown Adipose Tissue KW - Energy Metabolism KW - Adipocyte KW - Eating -- drug effects KW - Mitochondrial Proteins -- biosynthesis KW - Animals KW - Adipose Tissue, Brown -- metabolism KW - Ion Channels -- biosynthesis KW - Mice KW - Gene Expression Regulation -- drug effects KW - Adipose Tissue, Brown -- pathology KW - Obesity -- drug therapy KW - Body Temperature Regulation -- drug effects KW - Obesity -- pathology KW - Obesity -- metabolism KW - Adiposity -- drug effects KW - Energy Metabolism -- drug effects KW - 2,4-Dinitrophenol -- pharmacology KW - Uncoupling Agents -- pharmacology KW - Obesity -- chemically induced KW - Diet -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549631531?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+chemical+uncoupler+2%2C4-dinitrophenol+%28DNP%29+protects+against+diet-induced+obesity+and+improves+energy+homeostasis+in+mice+at+thermoneutrality.&rft.au=Goldgof%2C+Margalit%3BXiao%2C+Cuiying%3BChanturiya%2C+Tatyana%3BJou%2C+William%3BGavrilova%2C+Oksana%3BReitman%2C+Marc+L&rft.aulast=Goldgof&rft.aufirst=Margalit&rft.date=2014-07-11&rft.volume=289&rft.issue=28&rft.spage=19341&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.568204 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-29 N1 - Date created - 2014-07-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Physiol Endocrinol Metab. 2000 Aug;279(2):E293-300 [10913028] Nat Med. 2011 Feb;17(2):200-5 [21258337] J Clin Invest. 2001 Jul;108(1):97-105 [11435461] Physiol Rev. 2004 Jan;84(1):277-359 [14715917] J Physiol. 1971 Sep;217(2):315-26 [5097602] Br J Nutr. 1981 Mar;45(2):257-67 [7213581] J Biol Chem. 1995 Dec 8;270(49):29483-92 [7493988] Nature. 1997 May 1;387(6628):90-4 [9139827] J Biol Chem. 1997 Jul 11;272(28):17686-93 [9211919] Ther Ggw. 1964 Mar;103:232-44 [14129994] Am J Clin Nutr. 1956 Mar-Apr;4(2):169-75 [13302165] J Pharm Pharmacol. 1959 Aug;11:462-74 [14400214] J Biol Chem. 2006 Oct 20;281(42):31894-908 [16914547] Regul Toxicol Pharmacol. 2007 Jul;48(2):115-7 [17475379] Biochem J. 2007 Oct 1;407(1):129-40 [17608618] Aging Cell. 2008 Aug;7(4):552-60 [18505478] FASEB J. 2008 Nov;22(11):3925-37 [18644838] Cell Metab. 2009 Feb;9(2):111-2 [19187768] N Engl J Med. 2009 Apr 9;360(15):1500-8 [19357405] Front Neuroendocrinol. 2010 Apr;31(2):134-56 [20074584] Cell Metab. 2010 Apr 7;11(4):268-72 [20374959] Nat Rev Drug Discov. 2010 Jun;9(6):465-82 [20514071] Nat Med. 2010 Sep;16(9):1001-8 [20802499] Eur J Endocrinol. 2010 Dec;163(6):863-72 [20826525] Int J Obes (Lond). 2010 Nov;34(11):1644-54 [20479763] Int J Obes (Lond). 2010 Dec;34 Suppl 2:S53-8 [21151148] J Exp Biol. 2011 Jan 15;214(Pt 2):242-53 [21177944] Diabetes. 2011 Apr;60(4):1082-9 [21335378] J Clin Endocrinol Metab. 2011 Apr;96(4):E598-605 [21270329] J Med Toxicol. 2011 Sep;7(3):205-12 [21739343] J Exp Med. 2012 Jun 4;209(6):1069-74 [22665703] Nat Med. 2012 Oct;18(10):1575-9 [22961106] Int J Obes (Lond). 2013 Mar;37(3):399-403 [22751256] NCHS Data Brief. 2013 Oct;(131):1-8 [24152742] Cell Metab. 2013 Nov 5;18(5):740-8 [24206666] PLoS One. 2014;9(1):e85876 [24465761] Diabetes. 2000 Nov;49(11):1910-6 [11078459] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.568204 ER - TY - JOUR T1 - Tyrosine 308 is necessary for ligand-directed Gs protein-biased signaling of β2-adrenoceptor. AN - 1549631147; 24831005 AB - Interaction of a given G protein-coupled receptor to multiple different G proteins is a widespread phenomenon. For instance, β2-adrenoceptor (β2-AR) couples dually to Gs and Gi proteins. Previous studies have shown that cAMP-dependent protein kinase (PKA)-mediated phosphorylation of β2-AR causes a switch in receptor coupling from Gs to Gi. More recent studies have demonstrated that phosphorylation of β2-AR by G protein-coupled receptor kinases, particularly GRK2, markedly enhances the Gi coupling. We have previously shown that although most β2-AR agonists cause both Gs and Gi activation, (R,R')-fenoterol preferentially activates β2-AR-Gs signaling. However, the structural basis for this functional selectivity remains elusive. Here, using docking simulation and site-directed mutagenesis, we defined Tyr-308 as the key amino acid residue on β2-AR essential for Gs-biased signaling. Following stimulation with a β2-AR-Gs-biased agonist (R,R')-4'-aminofenoterol, the Gi disruptor pertussis toxin produced no effects on the receptor-mediated ERK phosphorylation in HEK293 cells nor on the contractile response in cardiomyocytes expressing the wild-type β2-AR. Interestingly, Y308F substitution on β2-AR enabled (R,R')-4'-aminofenoterol to activate Gi and to produce these responses in a pertussis toxin-sensitive manner without altering β2-AR phosphorylation by PKA or G protein-coupled receptor kinases. These results indicate that, in addition to the phosphorylation status, the intrinsic structural feature of β2-AR plays a crucial role in the receptor coupling selectivity to G proteins. We conclude that specific interactions between the ligand and the Tyr-308 residue of β2-AR stabilize receptor conformations favoring the receptor-Gs protein coupling and subsequently result in Gs-biased agonism. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Woo, Anthony Yiu-Ho AU - Jozwiak, Krzysztof AU - Toll, Lawrence AU - Tanga, Mary J AU - Kozocas, Joseph A AU - Jimenez, Lucita AU - Huang, Ying AU - Song, Ying AU - Plazinska, Anita AU - Pajak, Karolina AU - Paul, Rajib K AU - Bernier, Michel AU - Wainer, Irving W AU - Xiao, Rui-Ping AD - From the Key Laboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China, the Institute of Molecular Medicine, Centers for Life Sciences, Peking University, Beijing 100871, China, the Laboratory of Cardiovascular Science and yiuhowoo@pkusz.edu.cn. ; the Department of Chemistry, Medical University of Lublin, Lublin, Poland. ; the Torrey Pines Institute for Molecular Studies, Port St. Lucie, Florida 34987, and. ; SRI International, Menlo Park, California 94025. ; From the Key Laboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, China, the Institute of Molecular Medicine, Centers for Life Sciences, Peking University, Beijing 100871, China. ; Laboratory of Clinical Investigation, NIA, National Institutes of Health, Baltimore, Maryland 21224. ; the Institute of Molecular Medicine, Centers for Life Sciences, Peking University, Beijing 100871, China, xiaor@pku.edu.cn. Y1 - 2014/07/11/ PY - 2014 DA - 2014 Jul 11 SP - 19351 EP - 19363 VL - 289 IS - 28 KW - ADRB2 protein, human KW - 0 KW - Adrenergic beta-2 Receptor Agonists KW - Receptors, Adrenergic, beta-2 KW - Tyrosine KW - 42HK56048U KW - Extracellular Signal-Regulated MAP Kinases KW - EC 2.7.11.24 KW - Index Medicus KW - Site-directed Mutagenesis KW - Molecular Pharmacology KW - Cardiomyocyte Contraction KW - Adrenergic Receptor KW - Functional Selectivity KW - Molecular Docking KW - G Protein-coupled Receptor (GPCR) KW - Signal Transduction KW - Cardiovascular KW - Animals KW - HEK293 Cells KW - Humans KW - Mice KW - Extracellular Signal-Regulated MAP Kinases -- metabolism KW - Mutation, Missense KW - Mice, Knockout KW - Phosphorylation -- drug effects KW - Rats KW - Rats, Sprague-Dawley KW - Adrenergic beta-2 Receptor Agonists -- pharmacology KW - Protein Stability -- drug effects KW - Phosphorylation -- physiology KW - Tyrosine -- genetics KW - Tyrosine -- metabolism KW - Amino Acid Substitution KW - Male KW - Extracellular Signal-Regulated MAP Kinases -- genetics KW - Myocytes, Cardiac -- cytology KW - Signal Transduction -- physiology KW - Signal Transduction -- drug effects KW - Receptors, Adrenergic, beta-2 -- genetics KW - Receptors, Adrenergic, beta-2 -- metabolism KW - Myocytes, Cardiac -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549631147?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tyrosine+308+is+necessary+for+ligand-directed+Gs+protein-biased+signaling+of+%CE%B22-adrenoceptor.&rft.au=Woo%2C+Anthony+Yiu-Ho%3BJozwiak%2C+Krzysztof%3BToll%2C+Lawrence%3BTanga%2C+Mary+J%3BKozocas%2C+Joseph+A%3BJimenez%2C+Lucita%3BHuang%2C+Ying%3BSong%2C+Ying%3BPlazinska%2C+Anita%3BPajak%2C+Karolina%3BPaul%2C+Rajib+K%3BBernier%2C+Michel%3BWainer%2C+Irving+W%3BXiao%2C+Rui-Ping&rft.aulast=Woo&rft.aufirst=Anthony&rft.date=2014-07-11&rft.volume=289&rft.issue=28&rft.spage=19351&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.558882 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-29 N1 - Date created - 2014-07-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Circulation. 2003 Sep 30;108(13):1633-9 [12975249] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):940-5 [12552097] J Biol Chem. 1990 Feb 25;265(6):3202-11 [2154473] Symp Soc Exp Biol. 1990;44:225-40 [1983369] Mol Pharmacol. 1995 Feb;47(2):322-9 [7870040] J Biol Chem. 1997 Sep 19;272(38):23871-9 [9295336] Nature. 1997 Nov 6;390(6655):88-91 [9363896] J Biol Chem. 1998 Jul 24;273(30):18677-80 [9668034] Circ Res. 1999 Jan 8-22;84(1):43-52 [9915773] Br J Pharmacol. 2006 Feb;147(3):249-59 [16331289] Chirality. 2006 Nov;18(10):822-7 [16917835] J Pharmacol Exp Ther. 2007 Jan;320(1):1-13 [16803859] Mol Pharmacol. 2007 May;71(5):1200-2 [17293557] J Med Chem. 2007 Jun 14;50(12):2903-15 [17506540] Trends Pharmacol Sci. 2007 Aug;28(8):407-15 [17629960] Trends Pharmacol Sci. 2007 Aug;28(8):390-6 [17629962] Trends Pharmacol Sci. 2007 Aug;28(8):416-22 [17644195] J Biol Chem. 2007 Nov 30;282(48):34968-76 [17890226] J Biol Chem. 2008 Jan 25;283(4):1799-807 [18056263] Mol Pharmacol. 2009 Jan;75(1):158-65 [18838481] Mol Pharmacol. 2009 Jan;75(1):13-8 [19001067] J Biol Chem. 2009 Nov 20;284(47):32279-87 [19706594] Bioorg Med Chem. 2010 Jan 15;18(2):728-36 [20036561] Br J Pharmacol. 2010 Mar;159(5):1022-38 [20132209] Pharmacol Rev. 2010 Jun;62(2):265-304 [20392808] Mol Pharmacol. 2011 Mar;79(3):575-85 [21163968] Trends Pharmacol Sci. 2011 Apr;32(4):213-8 [21414670] J Mol Cell Cardiol. 2011 Jun;50(6):1000-7 [21291891] Proc Natl Acad Sci U S A. 2011 Aug 9;108(32):13118-23 [21778406] Nat Chem Biol. 2011 Oct;7(10):692-700 [21857662] Structure. 2011 Oct 12;19(10):1424-32 [21889352] Circ Res. 2012 Jan 20;110(2):265-74 [22179058] Science. 2012 Mar 2;335(6072):1106-10 [22267580] Mol Pharmacol. 2012 Jun;81(6):820-31 [22416052] Nat Commun. 2012;3:1044 [22948826] Cell. 2013 Jan 31;152(3):532-42 [23374348] J Biol Chem. 2013 Jun 14;288(24):17167-78 [23629648] J Am Chem Soc. 2013 Jun 26;135(25):9465-74 [23721409] Nature. 2013 Oct 24;502(7472):575-9 [24056936] J Mol Model. 2013 Nov;19(11):4919-30 [24043542] Mol Pharmacol. 1999 Nov;56(5):875-85 [10531390] J Biol Chem. 2000 Jul 14;275(28):21773-9 [10787424] Am J Physiol Heart Circ Physiol. 2000 Jul;279(1):H429-36 [10899083] J Biol Chem. 2000 Aug 18;275(33):25342-50 [10840035] J Biol Chem. 2002 Aug 23;277(34):31249-56 [12063255] Mol Pharmacol. 2002 Nov;62(5):971-4 [12391258] Mol Pharmacol. 2002 Nov;62(5):1094-102 [12391272] Mol Pharmacol. 2004 Jan;65(1):196-206 [14722251] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.558882 ER - TY - JOUR T1 - Profiling of the Tox21 10K compound library for agonists and antagonists of the estrogen receptor alpha signaling pathway. AN - 1544736661; 25012808 AB - The U.S. Tox21 program has screened a library of approximately 10,000 (10K) environmental chemicals and drugs in three independent runs for estrogen receptor alpha (ERα) agonist and antagonist activity using two types of ER reporter gene cell lines, one with an endogenous full length ERα (ER-luc; BG1 cell line) and the other with a transfected partial receptor consisting of the ligand binding domain (ER-bla; ERα β-lactamase cell line), in a quantitative high-throughput screening (qHTS) format. The ability of the two assays to correctly identify ERα agonists and antagonists was evaluated using a set of 39 reference compounds with known ERα activity. Although both assays demonstrated adequate (i.e. >80%) predictivity, the ER-luc assay was more sensitive and the ER-bla assay more specific. The qHTS assay results were compared with results from previously published ERα binding assay data and showed >80% consistency. Actives identified from both the ER-bla and ER-luc assays were analyzed for structure-activity relationships (SARs) revealing known and potentially novel ERα active structure classes. The results demonstrate the feasibility of qHTS to identify environmental chemicals with the potential to interact with the ERα signaling pathway and the two different assay formats improve the confidence in correctly identifying these chemicals. JF - Scientific reports AU - Huang, Ruili AU - Sakamuru, Srilatha AU - Martin, Matt T AU - Reif, David M AU - Judson, Richard S AU - Houck, Keith A AU - Casey, Warren AU - Hsieh, Jui-Hua AU - Shockley, Keith R AU - Ceger, Patricia AU - Fostel, Jennifer AU - Witt, Kristine L AU - Tong, Weida AU - Rotroff, Daniel M AU - Zhao, Tongan AU - Shinn, Paul AU - Simeonov, Anton AU - Dix, David J AU - Austin, Christopher P AU - Kavlock, Robert J AU - Tice, Raymond R AU - Xia, Menghang AD - NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, MD 20850, USA. ; National Center for Computational Toxicology, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; ILS Inc., Research Triangle Park, NC 27709, USA. ; Division of Bioinformatics and Biostatistics, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA. Y1 - 2014/07/11/ PY - 2014 DA - 2014 Jul 11 SP - 5664 VL - 4 KW - Estrogen Receptor alpha KW - 0 KW - Ligands KW - Small Molecule Libraries KW - Index Medicus KW - Protein Binding -- drug effects KW - Humans KW - HEK293 Cells KW - High-Throughput Screening Assays -- methods KW - Genes, Reporter -- drug effects KW - Cell Line KW - Structure-Activity Relationship KW - Small Molecule Libraries -- pharmacology KW - Signal Transduction -- drug effects KW - Estrogen Receptor alpha -- antagonists & inhibitors KW - Estrogen Receptor alpha -- agonists UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544736661?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Profiling+of+the+Tox21+10K+compound+library+for+agonists+and+antagonists+of+the+estrogen+receptor+alpha+signaling+pathway.&rft.au=Huang%2C+Ruili%3BSakamuru%2C+Srilatha%3BMartin%2C+Matt+T%3BReif%2C+David+M%3BJudson%2C+Richard+S%3BHouck%2C+Keith+A%3BCasey%2C+Warren%3BHsieh%2C+Jui-Hua%3BShockley%2C+Keith+R%3BCeger%2C+Patricia%3BFostel%2C+Jennifer%3BWitt%2C+Kristine+L%3BTong%2C+Weida%3BRotroff%2C+Daniel+M%3BZhao%2C+Tongan%3BShinn%2C+Paul%3BSimeonov%2C+Anton%3BDix%2C+David+J%3BAustin%2C+Christopher+P%3BKavlock%2C+Robert+J%3BTice%2C+Raymond+R%3BXia%2C+Menghang&rft.aulast=Huang&rft.aufirst=Ruili&rft.date=2014-07-11&rft.volume=4&rft.issue=&rft.spage=5664&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep05664 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-28 N1 - Date created - 2014-07-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Sci. 2000 Mar;54(1):138-53 [10746941] Risk Anal. 2009 Apr;29(4):485-7; discussion 492-7 [19076321] Toxicol Sci. 2000 Sep;57(1):54-60 [10966511] Comb Chem High Throughput Screen. 2000 Oct;3(5):437-44 [11032959] Bioorg Med Chem Lett. 2001 Jul 23;11(14):1839-42 [11459643] Environ Health Perspect. 2002 Aug;110(8):743-8 [12153753] J Appl Toxicol. 2004 Jan-Feb;24(1):1-4 [14745840] J Med Food. 2003 Winter;6(4):387-90 [14977449] Maturitas. 2004 Apr 15;47(4):269-75 [15063479] J Reprod Dev. 2004 Apr;50(2):245-55 [15118252] Arch Environ Contam Toxicol. 2004 May;46(4):445-53 [15253041] Environ Health Perspect. 2004 Aug;112(12):1249-54 [15345371] Environ Health Perspect. 2009 May;117(5):685-95 [19479008] Endocrinology. 2010 Jan;151(1):32-42 [19906814] Annu Rev Physiol. 2010;72:247-72 [20148675] J Steroid Biochem Mol Biol. 2010 Jul;121(1-2):343-8 [20156557] Crit Rev Toxicol. 2010 Nov;40 Suppl 3:1-30 [20932229] Chem Res Toxicol. 2011 Jan 14;24(1):6-19 [21053929] Toxicol Sci. 2011 Mar;120(1):42-58 [21163906] Sci Transl Med. 2011 Apr 27;3(80):80ps16 [21525397] Environ Health Perspect. 2011 Aug;119(8):1142-8 [21543282] Phytochemistry. 2011 Nov;72(16):2062-7 [21802698] J Steroid Biochem Mol Biol. 2012 Oct;132(1-2):186-93 [22634477] Mol Immunol. 2013 Apr;53(4):421-30 [23123408] ALTEX. 2013;30(1):51-6 [23338806] Chem Biol Interact. 2013 May 25;203(3):556-64 [23562765] Environ Health Perspect. 2013 Jul;121(7):756-65 [23603828] Drug Discov Today. 2013 Aug;18(15-16):716-23 [23732176] BMC Struct Biol. 2013;13:27 [24160181] Toxicology. 2004 Dec 1;205(1-2):113-22 [15458796] Science. 1984 Sep 7;225(4666):1032-4 [6474163] Ann N Y Acad Sci. 1995 Jun 12;761:355-60 [7625735] Environ Health Perspect. 1995 Oct;103 Suppl 7:113-22 [8593856] J Steroid Biochem Mol Biol. 1998 Dec;67(5-6):421-9 [10030691] J Mol Endocrinol. 2004 Oct;33(2):387-410 [15525597] Mol Cell. 2005 May 13;18(4):413-24 [15893725] Best Pract Res Clin Endocrinol Metab. 2006 Mar;20(1):15-33 [16522517] Chemosphere. 2006 Jun;64(1):174-7 [16337670] Hum Exp Toxicol. 2004 Nov;23(11):513-7 [15625776] Neural Netw. 2006 Jul-Aug;19(6-7):723-33 [16774731] Mol Aspects Med. 2006 Aug;27(4):299-402 [16914190] Biol Chem. 2006 Sep;387(9):1209-13 [16972788] Environ Toxicol Chem. 2007 Nov;26(11):2440-7 [17941737] Environ Health Perspect. 2007 Nov;115(11):1596-602 [18007991] J Appl Toxicol. 2008 Jan;28(1):78-91 [17992702] Science. 2008 Feb 15;319(5865):906-7 [18276874] Neuroscience. 2009 Jan 23;158(2):811-22 [19027052] In Vitr Mol Toxicol. 2000 Spring;13(1):67-82 [10900408] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep05664 ER - TY - JOUR T1 - Pharmacophore modeling of nilotinib as an inhibitor of ATP-binding cassette drug transporters and BCR-ABL kinase using a three-dimensional quantitative structure-activity relationship approach. AN - 1543682412; 24865254 AB - Nilotinib (Tasigna) is a tyrosine kinase inhibitor approved by the FDA to treat chronic phase chronic myeloid leukemia patients. It is also a transport substrate of the ATP-binding cassette (ABC) drug efflux transporters ABCB1 (P-glycoprotein, P-gp) and ABCG2 (BCRP), which may have an effect on the pharmacokinetics and toxicity of this drug. The goal of this study was to identify pharmacophoric features of nilotinib in order to potentially develop specific inhibitors of BCR-ABL kinase with minimal interactions with ABC drug transporters. Three-dimensional pharmacophore modeling and quantitative structure-activity relationship (QSAR) studies were carried out on a series of nilotinib analogues to identify chemical features that contribute to inhibitory activity of nilotinib against BCR-ABL kinase activity, P-gp, and ABCG2. Twenty-five derivatives of nilotinib were synthesized and were then tested to measure their activity to inhibit BCR-ABL kinase and to inhibit the function of ABC drug transporters. A set of in vitro experiments including kinase activity and cell-based transport assays and photolabeling of P-gp and ABCG2 with a transport substrate, [(125)I]-iodoarylazido-prazosin (IAAP), were carried out in isolated membranes to evaluate the potency of the derivatives to inhibit the function of ABC drug transporters and BCR-ABL kinase. Sixteen, fourteen, and ten compounds were selected as QSAR data sets, respectively, to generate PHASE v3.1 pharmacophore models for BCR-ABL kinase, ABCG2, and P-gp inhibitors. The IC50 values of these derivatives against P-gp, ABCG2, or BCR-ABL kinase were used to generate pharmacophore features required for optimal interactions with these targets. A seven-point pharmacophore (AADDRRR) for BCR-ABL kinase inhibitory activity, a six-point pharmacophore (ADHRRR) for ABCG2 inhibitory activity, and a seven-point pharmacophore (AADDRRR) for P-gp inhibitory activity were generated. The derived models clearly demonstrate high predictive power for test sets of BCR-ABL, ABCG2, and P-gp inhibitors. In aggregate, these results should aid in the development of specific inhibitors of BCR-ABL kinase that exhibit no or minimal interaction with ABC drug transporters. JF - Molecular pharmaceutics AU - Shukla, Suneet AU - Kouanda, Abdul AU - Silverton, Latoya AU - Talele, Tanaji T AU - Ambudkar, Suresh V AD - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH , Bethesda, Maryland 20892, United States. Y1 - 2014/07/07/ PY - 2014 DA - 2014 Jul 07 SP - 2313 EP - 2322 VL - 11 IS - 7 KW - 4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide KW - 0 KW - Antineoplastic Agents KW - P-Glycoproteins KW - Protein Kinase Inhibitors KW - Pyrimidines KW - Fusion Proteins, bcr-abl KW - EC 2.7.10.2 KW - Index Medicus KW - P-Glycoproteins -- chemistry KW - Quantitative Structure-Activity Relationship KW - Humans KW - MCF-7 Cells KW - Cell Line, Tumor KW - Antineoplastic Agents -- chemistry KW - Antineoplastic Agents -- pharmacology KW - Pyrimidines -- chemistry KW - Protein Kinase Inhibitors -- pharmacokinetics KW - Pyrimidines -- pharmacology KW - Protein Kinase Inhibitors -- chemistry KW - Fusion Proteins, bcr-abl -- antagonists & inhibitors KW - ATP-Binding Cassette Transporters -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1543682412?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmaceutics&rft.atitle=Pharmacophore+modeling+of+nilotinib+as+an+inhibitor+of+ATP-binding+cassette+drug+transporters+and+BCR-ABL+kinase+using+a+three-dimensional+quantitative+structure-activity+relationship+approach.&rft.au=Shukla%2C+Suneet%3BKouanda%2C+Abdul%3BSilverton%2C+Latoya%3BTalele%2C+Tanaji+T%3BAmbudkar%2C+Suresh+V&rft.aulast=Shukla&rft.aufirst=Suneet&rft.date=2014-07-07&rft.volume=11&rft.issue=7&rft.spage=2313&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmaceutics&rft.issn=1543-8392&rft_id=info:doi/10.1021%2Fmp400762h LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-04 N1 - Date created - 2014-07-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochem Pharmacol. 2012 Aug 1;84(3):260-7 [22548830] Drug Resist Updat. 2012 Feb-Apr;15(1-2):70-80 [22325423] Bioorg Med Chem Lett. 2013 Feb 1;23(3):682-6 [23273517] N Engl J Med. 2002 Feb 28;346(9):683-93 [11870247] Drug Resist Updat. 2001 Feb;4(1):22-8 [11512149] Leukemia. 2014 Apr;28(4):961-4 [24418991] J Med Chem. 2002 Apr 25;45(9):1737-40 [11960484] J Med Chem. 2002 Dec 19;45(26):5671-86 [12477351] Cancer Res. 2004 Feb 15;64(4):1242-6 [14973080] Mol Pharmacol. 2004 Mar;65(3):675-84 [14978246] Blood. 2004 Nov 1;104(9):2940-2 [15251980] J Biol Chem. 1986 Jun 15;261(17):7762-70 [3711108] Anticancer Drugs. 1996 Jul;7(5):568-78 [8862725] Cancer Cell. 2005 Feb;7(2):117-9 [15710324] Cancer Cell. 2005 Feb;7(2):129-41 [15710326] Cancer Res. 2005 Apr 1;65(7):2577-82 [15805252] Br J Cancer. 2006 Jun 19;94(12):1765-9 [16721371] Biochemistry. 2006 Jul 25;45(29):8940-51 [16846237] Adv Drug Deliv Rev. 2006 Nov 30;58(12-13):1431-50 [17097188] J Comput Aided Mol Des. 2006 Oct-Nov;20(10-11):647-71 [17124629] J Pharmacol Exp Ther. 2007 Oct;323(1):19-30 [17616561] Curr Drug Deliv. 2007 Oct;4(4):324-33 [17979652] J Chem Inf Model. 2007 Nov-Dec;47(6):2429-38 [17956085] ChemMedChem. 2007 Dec;2(12):1783-8 [17994597] Leukemia. 2008 Feb;22(2):445-7 [17690695] Expert Opin Drug Metab Toxicol. 2008 Sep;4(9):1167-80 [18721111] Mol Cancer Ther. 2008 Aug;7(8):2280-7 [18723475] Invest New Drugs. 2009 Feb;27(1):31-40 [18449471] Clin Cancer Res. 2009 Apr 1;15(7):2344-51 [19276246] J Pharmacol Exp Ther. 2009 Sep;330(3):956-63 [19491323] ChemMedChem. 2009 Nov;4(11):1883-96 [19768722] Expert Opin Drug Metab Toxicol. 2011 May;7(5):623-42 [21410427] J Chem Inf Model. 2011 Jun 27;51(6):1315-24 [21604687] Mol Pharm. 2011 Aug 1;8(4):1292-302 [21630681] Nat Biotechnol. 2011 Nov;29(11):1039-45 [22037377] Drug Metab Dispos. 2012 Feb;40(2):304-12 [22041108] Cancer Lett. 2013 Jan 28;328(2):307-17 [23063650] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/mp400762h ER - TY - JOUR T1 - Cu(I)-mediated allosteric switching in a copper-sensing operon repressor (CsoR). AN - 1549631628; 24831014 AB - The copper-sensing operon repressor (CsoR) is representative of a major Cu(I)-sensing family of bacterial metalloregulatory proteins that has evolved to prevent cytoplasmic copper toxicity. It is unknown how Cu(I) binding to tetrameric CsoRs mediates transcriptional derepression of copper resistance genes. A phylogenetic analysis of 227 DUF156 protein members, including biochemically or structurally characterized CsoR/RcnR repressors, reveals that Geobacillus thermodenitrificans (Gt) CsoR characterized here is representative of CsoRs from pathogenic bacilli Listeria monocytogenes and Bacillus anthracis. The 2.56 Å structure of Cu(I)-bound Gt CsoR reveals that Cu(I) binding induces a kink in the α2-helix between two conserved copper-ligating residues and folds an N-terminal tail (residues 12-19) over the Cu(I) binding site. NMR studies of Gt CsoR reveal that this tail is flexible in the apo-state with these dynamics quenched upon Cu(I) binding. Small angle x-ray scattering experiments on an N-terminally truncated Gt CsoR (Δ2-10) reveal that the Cu(I)-bound tetramer is hydrodynamically more compact than is the apo-state. The implications of these findings for the allosteric mechanisms of other CsoR/RcnR repressors are discussed. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Chang, Feng-Ming James AU - Coyne, H Jerome AU - Cubillas, Ciro AU - Vinuesa, Pablo AU - Fang, Xianyang AU - Ma, Zhen AU - Ma, Dejian AU - Helmann, John D AU - García-de los Santos, Alejandro AU - Wang, Yun-Xing AU - Dann, Charles E AU - Giedroc, David P AD - From the Department of Chemistry, Indiana University, Bloomington, Indiana 47405-7102. ; the Programa de Ingeniería Genómica, Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, Apdo. Postal 565-A, Cuernavaca, Morelos, México, 04510. ; the Structural Biophysics Laboratory, Center for Cancer Research, NCI-National Institutes of Health, Frederick, Maryland 21702-1201, and. ; the Department of Microbiology, Cornell University, Ithaca, New York 14853-8101. ; From the Department of Chemistry, Indiana University, Bloomington, Indiana 47405-7102, giedroc@indiana.edu. Y1 - 2014/07/04/ PY - 2014 DA - 2014 Jul 04 SP - 19204 EP - 19217 VL - 289 IS - 27 KW - Bacterial Proteins KW - 0 KW - DNA, Bacterial KW - Repressor Proteins KW - Copper KW - 789U1901C5 KW - Index Medicus KW - X-ray Crystallography KW - Metal Sensor Protein KW - X-ray Scattering KW - Metalloregulation KW - Phylogenetics KW - Transcription Repressor KW - Phylogeny KW - Gene Expression Regulation, Bacterial KW - Bacillus anthracis -- genetics KW - Allosteric Regulation -- drug effects KW - Models, Molecular KW - Transcription, Genetic KW - DNA, Bacterial -- metabolism KW - Geobacillus -- metabolism KW - Protein Multimerization KW - Protein Structure, Quaternary KW - Bacterial Proteins -- genetics KW - Bacterial Proteins -- chemistry KW - Repressor Proteins -- metabolism KW - Copper -- metabolism KW - Bacterial Proteins -- metabolism KW - Operon -- genetics KW - Copper -- pharmacology KW - Repressor Proteins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549631628?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cu%28I%29-mediated+allosteric+switching+in+a+copper-sensing+operon+repressor+%28CsoR%29.&rft.au=Chang%2C+Feng-Ming+James%3BCoyne%2C+H+Jerome%3BCubillas%2C+Ciro%3BVinuesa%2C+Pablo%3BFang%2C+Xianyang%3BMa%2C+Zhen%3BMa%2C+Dejian%3BHelmann%2C+John+D%3BGarc%C3%ADa-de+los+Santos%2C+Alejandro%3BWang%2C+Yun-Xing%3BDann%2C+Charles+E%3BGiedroc%2C+David+P&rft.aulast=Chang&rft.aufirst=Feng-Ming&rft.date=2014-07-04&rft.volume=289&rft.issue=27&rft.spage=19204&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.556704 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-14 N1 - Date created - 2014-07-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Infect Immun. 2001 Feb;69(2):949-58 [11159990] Mol Microbiol. 2014 May;92(4):797-812 [24666373] Syst Biol. 2003 Oct;52(5):696-704 [14530136] Nucleic Acids Res. 2004;32(5):1792-7 [15034147] J Comput Chem. 2004 Oct;25(13):1605-12 [15264254] J Bacteriol. 2004 Oct;186(20):6714-20 [15466022] Anal Biochem. 1996 Jun 1;237(2):260-73 [8660575] Microb Pathog. 1997 Feb;22(2):67-78 [9049996] J Biomol NMR. 1999 Mar;13(3):289-302 [10212987] Science. 1999 Apr 30;284(5415):805-8 [10221913] J Nutr. 1999 Jul;129(7):1251-60 [10395584] J Immunol. 2005 Feb 1;174(3):1491-500 [15661908] Bioinformatics. 2006 Jul 1;22(13):1658-9 [16731699] Mol Microbiol. 2006 Oct;62(1):252-62 [16956381] Nat Chem Biol. 2007 Jan;3(1):60-8 [17143269] J Bacteriol. 2007 Mar;189(5):1616-26 [17189367] Microbiology. 2007 Dec;153(Pt 12):4123-8 [18048925] Nature. 2007 Dec 6;450(7171):913-6 [18026087] J Am Chem Soc. 2008 Jun 18;130(24):7592-606 [18505253] Biochemistry. 2009 Apr 21;48(15):3325-34 [19249860] Proc Natl Acad Sci U S A. 2009 May 19;106(20):8344-9 [19416816] Chem Rev. 2009 Oct;109(10):4644-81 [19788177] J Biol Chem. 2009 Dec 4;284(49):33949-56 [19808669] J Am Chem Soc. 2009 Dec 23;131(50):18044-5 [19928961] J Bacteriol. 2010 May;192(10):2512-24 [20233928] Nucleic Acids Res. 2010 Jul;38(Web Server issue):W540-4 [20507903] Microbiology. 2010 Jul;156(Pt 7):1993-2005 [20395270] Mol Microbiol. 2010 Sep;77(5):1096-110 [20624225] Mol Microbiol. 2011 Jan;79(1):133-48 [21166899] Proc Natl Acad Sci U S A. 2011 Jan 25;108(4):1621-6 [21205886] PLoS One. 2011;6(2):e17367 [21387010] J Biol Chem. 2011 Apr 15;286(15):13522-31 [21339296] Mol Microbiol. 2011 Jul;81(2):457-72 [21564342] Environ Microbiol. 2011 Sep;13(9):2495-507 [21812885] Metallomics. 2011 Nov;3(11):1109-18 [21984219] Anal Chem. 2011 Dec 1;83(23):9092-9 [22007758] J Biol Chem. 2012 Apr 6;287(15):12142-51 [22356910] J Biol Chem. 2012 Apr 20;287(17):13549-55 [22389498] J Biol Chem. 2012 May 18;287(21):17833-47 [22451651] J Am Chem Soc. 2012 Apr 25;134(16):7081-93 [22471551] Nature. 2012 Aug 9;488(7410):236-40 [22801505] Biochemistry. 2013 Jan 8;52(1):84-97 [23215580] Nat Chem Biol. 2013 Mar;9(3):177-83 [23354287] Metallomics. 2013 Apr;5(4):335-42 [23385876] Biophys J. 2013 Aug 20;105(4):962-74 [23972848] Biomol NMR Assign. 2013 Oct;7(2):279-83 [23001947] Metallomics. 2013 Dec;5(12):1634-43 [24077251] Nucleic Acids Res. 2014 Jan;42(2):1326-40 [24121681] Bioinformatics. 2003 Jan;19(1):163-4 [12499312] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.556704 ER - TY - JOUR T1 - Efficacy of ex vivo activated and expanded natural killer cells and T lymphocytes for colorectal cancer patients. AN - 1826605685; 24944796 AB - Immune cell-based therapies using natural killer (NK) cells and cytotoxic T cells are under constant scrutiny, with the aim to design an effective and reduced-toxicity therapy, which will benefit patients via improved quality of life and improved prognosis. Four patients with stage IV colon cancer were administered 1, 3, 5 and 6 effector cell intravenous infusions, respectively. Peripheral blood was collected from the patients and the ex vivo activation and expansion of NK and T cells was performed in Good Manufacturing Practice-certified clean rooms for ~12-15 days. Immunophenotypic analysis of the peripheral blood mononuclear cells (PBMCs) and expanded NK and T cells was conducted using flow cytometry and the patients were followed up. On average, 4.8×107 initial PBMCs and 2.7×109 total expanded cells were obtained. The intravenous infusions of the expanded cells were not accompanied by adverse reactions. Improved prognosis, reflected by a considerable decrease in the cancer markers, accompanied by an improved quality of life in the patients were observed. In conclusion, potential strategies are currently under development for the large-scale production of effectors cells; therefore, autologous immune enhancement therapy (AIET) may be considered as a viable approach to cancer treatment. JF - Biomedical reports AU - Subramani, Baskar AU - Pullai, Chithra Ramanathan AU - Krishnan, Kohila AU - Sugadan, Sheela Devi AU - Deng, Xuewen AU - Hiroshi, Terunuma AU - Ratnavelu, Kananathan AD - Nichi-Asia Life Science, Sdn. Bhd., Petaling Jaya 47810, Malaysia. ; Biotherapy Institute of Japan, Tokyo 135-0051, Japan. ; Nilai Cancer Institute (NCI) Hospital, Nilai 71800, Malaysia. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 505 EP - 508 VL - 2 IS - 4 SN - 2049-9434, 2049-9434 KW - FOLFOX KW - colorectal cancer KW - autologous immune enhancement therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826605685?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomedical+reports&rft.atitle=Efficacy+of+ex+vivo+activated+and+expanded+natural+killer+cells+and+T+lymphocytes+for+colorectal+cancer+patients.&rft.au=Subramani%2C+Baskar%3BPullai%2C+Chithra+Ramanathan%3BKrishnan%2C+Kohila%3BSugadan%2C+Sheela+Devi%3BDeng%2C+Xuewen%3BHiroshi%2C+Terunuma%3BRatnavelu%2C+Kananathan&rft.aulast=Subramani&rft.aufirst=Baskar&rft.date=2014-07-01&rft.volume=2&rft.issue=4&rft.spage=505&rft.isbn=&rft.btitle=&rft.title=Biomedical+reports&rft.issn=20499434&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2014-06-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Oncolytic Viruses Targeting Tumor Stem Cells AN - 1808673543; PQ0003438638 AB - A workshop "Targeting Oncolytic Viruses to Tumor Stem Cells," organized by the Division of Cancer Biology, NCI, NIH, was held on September 6, 2013 in Rockville, MD. Seventeen invited experts presented an overview of their current research in this area and discussed the state of current research on the use of oncolytic viruses targeted to stem cells as a potential cancer therapy. The goal was to evaluate the evidence that this approach might increase the efficacy of oncolytic virus therapy and to identify gaps in knowledge that have retarded progress in this area. Cancer Res; 74(13); 3396-8. copyright 2014 AACR. JF - Cancer Research AU - Chiocca, EAntonio AU - Blair, Donald AU - Mufson, RAllan AD - Department of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA and, mufsonr@mail.nih.gov Y1 - 2014/07/01/ PY - 2014 DA - 2014 Jul 01 SP - 3396 EP - 3398 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 74 IS - 13 SN - 0008-5472, 0008-5472 KW - Biotechnology and Bioengineering Abstracts; Virology & AIDS Abstracts KW - Stem cells KW - Conferences KW - Reviews KW - Oncolysis KW - Tumors KW - Cancer KW - W 30965:Miscellaneous, Reviews KW - V 22370:Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808673543?accountid=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=Oncolytic+Viruses+Targeting+Tumor+Stem+Cells&rft.au=Chiocca%2C+EAntonio%3BBlair%2C+Donald%3BMufson%2C+RAllan&rft.aulast=Chiocca&rft.aufirst=EAntonio&rft.date=2014-07-01&rft.volume=74&rft.issue=13&rft.spage=3396&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-0290 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Stem cells; Conferences; Reviews; Oncolysis; Tumors; Cancer DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0290 ER - TY - JOUR T1 - In Vivo Fluorescence Lifetime Imaging for Monitoring the Efficacy of the Cancer Treatment AN - 1808650030; PQ0003438901 AB - Purpose: Advances in tumor biology created a foundation for targeted therapy aimed at inactivation of specific molecular mechanisms responsible for cell malignancy. In this paper, we used in vivo fluorescence lifetime imaging with HER2-targeted fluorescent probes as an alternative imaging method to investigate the efficacy of targeted therapy with 17-DMAG (an HSP90 inhibitor) on tumors with high expression of HER2 receptors.Experimental Design: HER2-specific Affibody, conjugated to Alexafluor 750, was injected into nude mice bearing HER2-positive tumor xenograft. The fluorescence lifetime was measured before treatment and monitored after the probe injections at 12 hours after the last treatment dose, when the response to the 17-DMAG therapy was the most pronounced as well as a week after the last treatment when the tumors grew back almost to their pretreatment size.Results: Imaging results showed significant difference between the fluorescence lifetimes at the tumor and the contralateral site ( similar to 0.13 ns) in the control group (before treatment) and 7 days after the last treatment when the tumors grew back to their pretreatment dimensions. However, at the time frame that the treatment had its maximum effect (12 hours after the last treatment), the difference between the fluorescence lifetime at the tumor and contralateral site decreased to 0.03 ns.Conclusions: The results showed a good correlation between fluorescence lifetime and the efficacy of the treatment. These findings show that in vivo fluorescence lifetime imaging can be used as a promising molecular imaging tool for monitoring the treatment outcome in preclinical models and potentially in patients. Clin Cancer Res; 20(13); 3531-9. copyright 2014 AACR. JF - Clinical Cancer Research AU - Ardeshirpour, Yasaman AU - Chernomordik, Victor AU - Hassan, Moinuddin AU - Zielinski, Rafal AU - Capala, Jacek AU - Gandjbakhche, Amir AD - NIH/National Institute of Child Health and Human Development, Bethesda; , amir@helix.nih.gov Y1 - 2014/07/01/ PY - 2014 DA - 2014 Jul 01 SP - 3531 EP - 3539 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 20 IS - 13 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Hsp90 protein KW - Molecular modelling KW - Malignancy KW - Fluorescence KW - ErbB-2 protein KW - Animal models KW - Fluorescent indicators KW - Tumors KW - Xenografts KW - imaging KW - Cancer KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808650030?accountid=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=In+Vivo+Fluorescence+Lifetime+Imaging+for+Monitoring+the+Efficacy+of+the+Cancer+Treatment&rft.au=Ardeshirpour%2C+Yasaman%3BChernomordik%2C+Victor%3BHassan%2C+Moinuddin%3BZielinski%2C+Rafal%3BCapala%2C+Jacek%3BGandjbakhche%2C+Amir&rft.aulast=Ardeshirpour&rft.aufirst=Yasaman&rft.date=2014-07-01&rft.volume=20&rft.issue=13&rft.spage=3531&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-13-1826 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Hsp90 protein; Molecular modelling; Malignancy; ErbB-2 protein; Fluorescence; Animal models; Fluorescent indicators; Xenografts; Tumors; imaging; Cancer DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-1826 ER - TY - JOUR T1 - Experimental Effects of Injunctive Norms on Simulated Risky Driving Among Teenage Males AN - 1732820916; PQ0002164767 AB - Objective: Teenage passengers affect teenage driving performance, possibly by social influence. To examine the effect of social norms on driving behavior, male teenagers were randomly assigned to drive in a simulator with a peer-aged confederate to whom participants were primed to attribute either risk-accepting or risk-averse social norms. It was hypothesized that teenage drivers would engage in more risky driving behavior in the presence of peer passengers than no passengers, and with a risk-accepting compared with a risk-averse passenger. Method: 66 male participants aged 16 to 18 years holding a provisional driver license were randomized to drive with a risk-accepting or risk-averse passenger in a simulator. Failure to Stop at a red light and percent Time in Red (light) were measured as primary risk-relevant outcomes of interest at 18 intersections, while driving once alone and once with their assigned passenger. Results: The effect of passenger presence on risky driving was moderated by passenger type for Failed to Stop in a generalized linear mixed model (OR = 1.84, 95% CI [1.19, 2.86], p < .001), and percent Time in Red in a mixed model (B = 7.71, 95% CI [1.54, 13.87], p < .05). Conclusions: Exposure of teenage males to a risk-accepting confederate peer increased teenage males' risky simulated driving behavior compared with exposure to a risk-averse confederate peer. These results indicate that variability in teenage risky driving could be partially explained by social norms. JF - Health Psychology AU - Simons-Morton, Bruce G AU - Bingham, C Raymond AU - Falk, Emily B AU - Li, Kaigang AU - Pradhan, Anuj K AU - Ouimet, Marie Claude AU - Almani, Farideh AU - Shope, Jean T AD - Eunice Kennedy Shriver National Institute of Child Health & Human Development, Bethesda, Maryland, Mortonb@mail.nih.gov PY - 2014 SP - 616 EP - 627 PB - American Psychological Association, 750 First St., N.E. Washington DC 20002-4242 United States VL - 33 IS - 7 SN - 0278-6133, 0278-6133 KW - Risk Abstracts KW - social norms KW - social influence KW - risk behavior KW - adolescents KW - randomized trial KW - Risk aversion KW - Driving ability KW - Behavior KW - Males KW - Risk taking KW - Adolescents KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732820916?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Psychology&rft.atitle=Experimental+Effects+of+Injunctive+Norms+on+Simulated+Risky+Driving+Among+Teenage+Males&rft.au=Simons-Morton%2C+Bruce+G%3BBingham%2C+C+Raymond%3BFalk%2C+Emily+B%3BLi%2C+Kaigang%3BPradhan%2C+Anuj+K%3BOuimet%2C+Marie+Claude%3BAlmani%2C+Farideh%3BShope%2C+Jean+T&rft.aulast=Simons-Morton&rft.aufirst=Bruce&rft.date=2014-07-01&rft.volume=33&rft.issue=7&rft.spage=616&rft.isbn=&rft.btitle=&rft.title=Health+Psychology&rft.issn=02786133&rft_id=info:doi/10.1037%2Fa0034837 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2015-12-09 N1 - SubjectsTermNotLitGenreText - Risk aversion; Driving ability; Behavior; Males; Risk taking; Adolescents DO - http://dx.doi.org/10.1037/a0034837 ER - TY - JOUR T1 - FutureTox II: Contemporary Concepts in Toxicology: "Pathways to Prediction: In Vitro and In Silico Models for Predictive Toxicology" AN - 1683354759; PQ0001555045 AB - The Society of Toxicology (SOT) held a very successful FutureTox II Contemporary Concepts in Toxicology (CCT) Conference in Chapel Hill, North Carolina, on January 16th and 17th, 2014. There were over 291 attendees representing industry, government and academia; the sessions were also telecast to 9 locations, including Health Canada, US FDA/National Center for Toxicologic Research, the US EPA and the California EPA Office of Environmental Health Hazard Assessment. The conference also included more than 50 posters as well as several vendor exhibits. The theme of the meeting was Pathways to Prediction: In Vitro and In Silico Models for Predictive Toxicology. JF - Toxicologic Pathology AU - Elmore, Susan A AU - Ryan, Anne M AU - Wood, Charles E AU - Crabbs, Torrie A AU - Sills, Robert C AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, elmore@niehs.nih.gov Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 940 EP - 942 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 42 IS - 5 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - Conferences KW - Models KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683354759?accountid=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=FutureTox+II%3A+Contemporary+Concepts+in+Toxicology%3A+%22Pathways+to+Prediction%3A+In+Vitro+and+In+Silico+Models+for+Predictive+Toxicology%22&rft.au=Elmore%2C+Susan+A%3BRyan%2C+Anne+M%3BWood%2C+Charles+E%3BCrabbs%2C+Torrie+A%3BSills%2C+Robert+C&rft.aulast=Elmore&rft.aufirst=Susan&rft.date=2014-07-01&rft.volume=42&rft.issue=5&rft.spage=940&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623314537135 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Number of references - 5 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Conferences; Models DO - http://dx.doi.org/10.1177/0192623314537135 ER - TY - JOUR T1 - Spontaneous Mesotheliomas in F344/N Rats Are Characterized by Dysregulation of Cellular Growth and Immune Function Pathways AN - 1683351728; PQ0001555032 AB - Aged male Fischer 344/N rats are prone to developing spontaneous peritoneal mesotheliomas that arise predominantly from the tunica vaginalis of the testes. A definitive cause for the predominance of this neoplasm in F344/N rats is unknown. Investigation of the molecular alterations that occur in spontaneous rat mesotheliomas may provide insight into their pathogenesis as well enable a better understanding regarding the mechanisms underlying chemically induced mesothelioma in rodents. Mesothelial cell function represents a complex interplay of pathways related to host defense mechanisms and maintenance of cellular homeostasis. Global gene expression profiles of spontaneous mesotheliomas from vehicle control male F344/N rats from 2-year National Toxicology Program carcinogenicity bioassays were analyzed to determine the molecular features of these tumors and elucidate tumor-specific gene expression profiles. The resulting gene expression pattern showed that spontaneous mesotheliomas are associated with upregulation of various growth factors, oncogenes, cytokines, pattern recognition response receptors, and pathogen-associated molecular patterns receptors, and the production of reactive oxygen and nitrogen species, as well as downregulation of apoptosis pathways. Alterations in these pathways in turn trigger molecular responses that stimulate cell proliferation and promote tumor survival and progression. JF - Toxicologic Pathology AU - Blackshear, Pamela E AU - Pandiri, Arun R AU - Ton, Thai-Vu T AU - Clayton, Natasha P AU - Shockley, Keith R AU - Peddada, Shyamal D AU - Gerrish, Kevin E AU - Sills, Robert C AU - Hoenerhoff, Mark J AD - Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, USA, hoenerhm@niehs.nih.gov PY - 2014 SP - 863 EP - 876 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 42 IS - 5 SN - 0192-6233, 0192-6233 KW - Immunology Abstracts; Toxicology Abstracts KW - mesothelioma KW - F344/N rat KW - National Toxicology Program KW - microarray KW - gene expression KW - mesothelial cell KW - Fred-PE cells KW - Cell survival KW - Testes KW - Apoptosis KW - Peritoneum KW - Homeostasis KW - Tumors KW - Gene expression KW - Oxygen KW - Pattern recognition KW - Oncogenes KW - Carcinogenicity KW - Cytokines KW - Defense mechanisms KW - Immune response KW - Growth factors KW - Cell proliferation KW - Nitrogen KW - X 24490:Other KW - F 06950:Immunogenetics, MHC, HLA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683351728?accountid=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=Spontaneous+Mesotheliomas+in+F344%2FN+Rats+Are+Characterized+by+Dysregulation+of+Cellular+Growth+and+Immune+Function+Pathways&rft.au=Blackshear%2C+Pamela+E%3BPandiri%2C+Arun+R%3BTon%2C+Thai-Vu+T%3BClayton%2C+Natasha+P%3BShockley%2C+Keith+R%3BPeddada%2C+Shyamal+D%3BGerrish%2C+Kevin+E%3BSills%2C+Robert+C%3BHoenerhoff%2C+Mark+J&rft.aulast=Blackshear&rft.aufirst=Pamela&rft.date=2014-07-01&rft.volume=42&rft.issue=5&rft.spage=863&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313501894 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Number of references - 80 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Testes; Cell survival; Apoptosis; Peritoneum; Tumors; Homeostasis; Gene expression; Pattern recognition; Oxygen; Oncogenes; Carcinogenicity; mesothelioma; Cytokines; Growth factors; Immune response; Defense mechanisms; Cell proliferation; Nitrogen DO - http://dx.doi.org/10.1177/0192623313501894 ER - TY - JOUR T1 - Body size perception and weight control in youth: 9-year international trends from 24 countries AN - 1680441575; 20507744 AB - Objectives: To examine 9-year trends and relationships regarding misperceptions of body size and dieting for weight loss among adolescents from 24 countries, and explore the influence of country-level overweight prevalence. Methods: Sociodemographic characteristics, body size perception and dieting for weight loss were assessed in the Health Behaviour in School-aged Children survey conducted in 24 countries cross-sectionally at three time points (2001/2002, 2005/2006 and 2009/2010). Logistic regression models examined change over time in overestimation of body size in non-overweight adolescents, underestimation of body size in overweight adolescents, dieting for weight loss in non-overweight and overweight adolescents and relationships between body size perception and dieting. Analyses were stratified by weight status and sex. Covariates included country-level overweight prevalence, family affluence and country level of development. Body mass index was only included in models examining dieting for weight loss. Results: Country-level overweight prevalence increased over time (11.6-14.7%). Compared with Time 1, overweight adolescents had greater odds of body size underestimation at Time 3 (odds ratio (OR)=1.68 for girls; OR=1.10 for boys), whereas non-overweight adolescents had lower odds of body size overestimation at Time 3 (OR=0.87 for girls; OR=0.89 for boys). Controlling for country-level overweight prevalence attenuated these relationships. Compared with Time 1, overweight and non-overweight boys were 10% more likely to diet at Time 3, whereas overweight and non-overweight girls were 19% and 16%, respectively, less likely to diet at Time 3. Controlling for country-level overweight prevalence did not impact trends in dieting for weight loss. Additionally, the association of self-perceived overweight with increased odds of dieting diminished over time. Conclusions: Body size perceptions among adolescents may have changed over time concurrent with shifts in country-level body weight. However, controlling for country-level overweight prevalence did not impact trends in dieting for weight loss, suggesting a potentially stronger impact of social comparison on weight-related perceptions than on behavior. JF - International Journal of Obesity AU - Quick, V AU - Nansel, T R AU - Liu, D AU - Lipsky, L M AU - Due, P AU - Iannotti, R J AD - Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development/NIH, Bethesda, MD, USA Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 988 EP - 994 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 38 IS - 7 SN - 0307-0565, 0307-0565 KW - Physical Education Index KW - Anthropometry KW - Obesity KW - Weight control KW - Perception KW - Boys KW - Adolescence KW - Girls KW - Diet (weight control) KW - Trends KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680441575?accountid=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=Body+size+perception+and+weight+control+in+youth%3A+9-year+international+trends+from+24+countries&rft.au=Quick%2C+V%3BNansel%2C+T+R%3BLiu%2C+D%3BLipsky%2C+L+M%3BDue%2C+P%3BIannotti%2C+R+J&rft.aulast=Quick&rft.aufirst=V&rft.date=2014-07-01&rft.volume=38&rft.issue=7&rft.spage=988&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2014.62 LA - English DB - Physical Education Index N1 - Date revised - 2015-05-01 N1 - Last updated - 2015-06-12 N1 - SubjectsTermNotLitGenreText - Anthropometry; Obesity; Weight control; Boys; Perception; Girls; Adolescence; Diet (weight control); Trends DO - http://dx.doi.org/10.1038/ijo.2014.62 ER - TY - JOUR T1 - Ultra-low Dose Interleukin-2 Promotes Immune-modulating Function of Regulatory T Cells and Natural Killer Cells in Healthy Volunteers AN - 1673384558; PQ0001372915 AB - Low-dose interleukin-2 (IL-2) expands regulatory T cells (T sub(regs)) and natural killer (NK) cells after stem cell transplantation (SCT) and may reduce graft-versus-host disease (GVHD). We hypothesized that ultra-low dose (ULD) IL-2 could serve as an immune-modulating agent for stem cell donors to prevent GVHD following SCT. However, the safety, dose level, and immune signatures of ULD IL-2 in immune-competent healthy subjects remain unknown. Here, we have characterized the phenotype and function of T sub(regs) and NK cells as well as the gene expression and cytokine profiles of 21 healthy volunteers receiving 50,000 to 200,000 units/m super(2)/day IL-2 for 5 days. ULD IL-2 was well tolerated and induced a significant increase in the frequency of T sub(regs) with increased suppressive function. There was a marked expansion of CD56 super(bright) NK cells with enhanced interferon- gamma (IFN- gamma ) production. Serum cytokine profiling demonstrated increase of IFN- gamma induced protein 10 (IP-10). Gene expression analysis revealed significant changes in a highly restricted set of genes, including FOXP3, IL-2RA, and CISH. This is the first study to evaluate global immune-modulating function of ULD IL-2 in healthy subjects and to support the future studies administrating ULD IL-2 to stem cell donors. JF - Molecular Therapy AU - Ito, Sawa AU - Bollard, Catherine M AU - Carlsten, Mattias AU - Melenhorst, Jan Joseph AU - Biancotto, Angelique AU - Wang, Ena AU - Chen, Jinguo AU - Kotliarov, Yuri AU - Cheung, Foo AU - Xie, Zhi AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 1388 EP - 1395 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 22 IS - 7 SN - 1525-0016, 1525-0016 KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Gene expression KW - gamma -Interferon KW - Immunoregulation KW - Interleukin 2 KW - IP-10 protein KW - Foxp3 protein KW - Natural killer cells KW - Lymphocytes T KW - Graft-versus-host reaction KW - Immunomodulation KW - Interleukin 2 receptors KW - W 30940:Products KW - F 06960:Molecular Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673384558?accountid=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=Ultra-low+Dose+Interleukin-2+Promotes+Immune-modulating+Function+of+Regulatory+T+Cells+and+Natural+Killer+Cells+in+Healthy+Volunteers&rft.au=Ito%2C+Sawa%3BBollard%2C+Catherine+M%3BCarlsten%2C+Mattias%3BMelenhorst%2C+Jan+Joseph%3BBiancotto%2C+Angelique%3BWang%2C+Ena%3BChen%2C+Jinguo%3BKotliarov%2C+Yuri%3BCheung%2C+Foo%3BXie%2C+Zhi&rft.aulast=Ito&rft.aufirst=Sawa&rft.date=2014-07-01&rft.volume=22&rft.issue=7&rft.spage=1388&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2014.50 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Gene expression; Immunoregulation; gamma -Interferon; IP-10 protein; Interleukin 2; Foxp3 protein; Lymphocytes T; Natural killer cells; Graft-versus-host reaction; Immunomodulation; Interleukin 2 receptors DO - http://dx.doi.org/10.1038/mt.2014.50 ER - TY - JOUR T1 - Toxicity and carcinogenicity studies of Ginkgo biloba extract in rat and mouse: liver, thyroid, and nose are targets. AN - 1672090815; 23960164 AB - Ginkgo biloba extract (GBE) is a popular herbal supplement that is used to improve circulation and brain function. In spite of widespread human exposure to relatively high doses over potentially long periods of time, there is a paucity of data from animal studies regarding the toxicity and carcinogenicity associated with GBE. In order to fill this knowledge gap, 3-month and 2-year toxicity and carcinogenicity studies with GBE administered by oral gavage to B6C3F1/N mice and F344/N rats were performed as part of the National Toxicology Program's Dietary Supplements and Herbal Medicines Initiative. The targets of GBE treatment were the liver, thyroid, and nose. These targets were consistent across exposure period, sex, and species, albeit with varying degrees of effect observed among studies. Key findings included a notably high incidence of hepatoblastomas in male and female mice and evidence of carcinogenic potential in the thyroid gland of both mice and rats. Various nonneoplastic lesions were observed beyond control levels in the liver, thyroid gland, and nose of rats and mice administered GBE. Although these results cannot be directly extrapolated to humans, the findings fill an important data gap in assessing risk associated with GBE use. © 2014 by The Author(s). JF - Toxicologic pathology AU - Rider, Cynthia V AU - Nyska, Abraham AU - Cora, Michelle C AU - Kissling, Grace E AU - Smith, Cynthia AU - Travlos, Gregory S AU - Hejtmancik, Milton R AU - Fomby, Laurene M AU - Colleton, Curtis A AU - Ryan, Michael J AU - Kooistra, Linda AU - Morrison, James P AU - Chan, Po C AD - National Institute of Environmental Health Sciences, Research Triangle Park, Durham, North Carolina, USA ridercv@niehs.nih.gov. ; Integrated Laboratory Systems Incorporated, Research Triangle Park, Durham, North Carolina, USA. ; National Institute of Environmental Health Sciences, Research Triangle Park, Durham, North Carolina, USA. ; Battelle, Columbus, Ohio, USA. ; Charles River Laboratories, Pathology Associates, Durham, North Carolina, USA. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 830 EP - 843 VL - 42 IS - 5 KW - Carcinogens KW - 0 KW - Plant Extracts KW - Index Medicus KW - hepatocarcinogenicity KW - thyroid tumors KW - natural medicine KW - nasal lesions KW - herbal KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Carcinogens -- toxicity KW - Carcinogenicity Tests KW - Mice KW - Drug Evaluation, Preclinical KW - Male KW - Female KW - Organ Size -- drug effects KW - Liver -- pathology KW - Thyroid Gland -- drug effects KW - Ginkgo biloba -- toxicity KW - Thyroid Gland -- pathology KW - Liver -- drug effects KW - Nose -- pathology KW - Plant Extracts -- toxicity KW - Plant Extracts -- chemistry KW - Nose -- drug effects KW - Ginkgo biloba -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1672090815?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Toxicity+and+carcinogenicity+studies+of+Ginkgo+biloba+extract+in+rat+and+mouse%3A+liver%2C+thyroid%2C+and+nose+are+targets.&rft.au=Rider%2C+Cynthia+V%3BNyska%2C+Abraham%3BCora%2C+Michelle+C%3BKissling%2C+Grace+E%3BSmith%2C+Cynthia%3BTravlos%2C+Gregory+S%3BHejtmancik%2C+Milton+R%3BFomby%2C+Laurene+M%3BColleton%2C+Curtis+A%3BRyan%2C+Michael+J%3BKooistra%2C+Linda%3BMorrison%2C+James+P%3BChan%2C+Po+C&rft.aulast=Rider&rft.aufirst=Cynthia&rft.date=2014-07-01&rft.volume=42&rft.issue=5&rft.spage=830&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623313501235 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-20 N1 - Date created - 2015-04-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Int J Immunopharmacol. 2000 Mar;22(3):229-36 [10685005] Toxicol Pathol. 2013 Aug;41(6):826-41 [23262642] Neurochem Int. 2002 Jun;40(7):647-53 [11900860] J Pharm Pharmacol. 2002 May;54(5):661-9 [12005361] Toxicology. 2002 Aug 15;177(2-3):167-77 [12135620] Toxicol Pathol. 2002 Sep-Oct;30(5):580-91 [12371667] Eur J Pharmacol. 2004 Jun 28;494(2-3):131-8 [15212966] Toxicol Pathol. 2004 Jul-Aug;32(4):393-401 [15307212] Biometrics. 1988 Jun;44(2):417-31 [3390507] Fundam Appl Toxicol. 1989 May;12(4):731-7 [2744275] Endocr Rev. 1991 May;12(2):135-50 [2070777] Drug Metab Rev. 1993;25(1-2):173-205 [8449146] Fundam Appl Toxicol. 1994 Aug;23(2):280-97 [7982536] Cancer Lett. 1995 Feb 10;89(1):29-35 [7882299] Toxicol Pathol. 1997 Jan-Feb;25(1):39-48 [9061850] Toxicol Pathol. 1998 Nov-Dec;26(6):717-23 [9864087] J Gen Intern Med. 2005 Jul;20(7):657-61 [16050865] Toxicol Pathol. 2007 Jan;35(1):163-9 [17325985] Toxicol Pathol. 2007 Jan;35(1):170-7 [17325986] J Food Sci. 2008 Jan;73(1):R14-9 [18211362] J Neurochem. 2008 May;105(4):1418-27 [18221374] PLoS One. 2008;3(6):e2493 [18560566] JAMA. 2008 Nov 19;300(19):2253-62 [19017911] J Chromatogr A. 2009 Mar 13;1216(11):2204-10 [18814876] J Chromatogr A. 2009 Mar 13;1216(11):2002-32 [19195661] Pharm Res. 2009 Apr;26(4):872-82 [19034627] JAMA. 2009 Dec 23;302(24):2663-70 [20040554] Circ Cardiovasc Qual Outcomes. 2010 Jan;3(1):41-7 [20123670] OMICS. 2010 Feb;14(1):75-90 [20141330] Am J Hypertens. 2010 May;23(5):528-33 [20168306] Pharmacoepidemiol Drug Saf. 2010 Jul;19(7):694-8 [20582906] Acta Pol Pharm. 2010 Jul-Aug;67(4):335-43 [20635528] Toxicol Pathol. 2010 Aug;38(5):776-95 [20585142] J Pharmacol Exp Ther. 2010 Dec;335(3):771-80 [20739453] Toxicol Pathol. 2011 Feb;39(2):348-60 [21422261] Clin Ther. 2011 Nov;33(11):1749-58 [22030445] Drug Metab Dispos. 2012 Jan;40(1):178-86 [22019630] Drug Metab Dispos. 2012 Jun;40(6):1113-21 [22393123] Natl Toxicol Program Tech Rep Ser. 2013 Mar;(578):1-183 [23652021] Pharmazie. 2000 Nov;55(11):864-5 [11126011] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623313501235 ER - TY - JOUR T1 - The influence of age on serum concentrations of cardiac troponin I: results in rats, monkeys, and commercial sera. AN - 1672090352; 24129761 AB - Cardiac troponins serve as serum biomarkers of myocardial injury. The current study examined the influence of age on serum concentrations of cardiac troponin I (cTnI). An ultrasensitive immunoassay was used to monitor cTnI concentrations in Sprague-Dawley (SD) rats and Erythrocebus patas monkeys of different ages. The mean cTnI concentrations were highest in 10-day-old rats compared to 25-, 40-, and 80-day-old SD rats. Cardiomyocyte remodeling was apparent in hearts from 10-day-old SD rats as evident by hypercellularity, irregularly shaped nuclei, and moderate numbers of myocytes undergoing mitosis and apoptosis. The mean concentration of cTnI in 5 newborn monkeys was considerably higher than that of three 1-year-old monkeys. Evidence of cardiomyocyte remodeling was also observed in these newborn hearts (loss of myofibrils and cytoplasmic vacuolation). Commercial animal serum samples were also analyzed. The concentrations of cTnI detected in fetal equine and porcine serum were considerably higher than that found in adult equine and porcine serum samples Likewise, fetal bovine serum had higher cTnI concentrations (>2,400 pg/ml) than did adult caprine and laprine samples (2.5-2.7 pg/ml). The present study found age-related differences in cTnI concentrations, with higher levels occurring at younger ages. This effect was consistent across several animal species. © 2014 by The Author(s). JF - Toxicologic pathology AU - Herman, Eugene H AU - Knapton, Alan AU - Liu, Yongmin AU - Lipshultz, Steven E AU - Estis, Joel AU - Todd, John AU - Woodward, Ruth A AU - Cochran, Thomas AU - Zhang, Jun AU - Poirier, Miriam C AD - Food and Drug Administration, Division of Drug Safety Research, Silver Spring, Maryland, USA eugene.herman@fda.hhs.gov. ; Food and Drug Administration, Division of Drug Safety Research, Silver Spring, Maryland, USA. ; National Institutes of Health, National Cancer Institute, Carcinogen-DNA Interactions Section, Bethesda, Maryland, USA. ; Department of Pediatrics, Leonard M. Miller School of Medicine, Mailman Center for Child Development, University of Miami, Miami, Florida, USA. ; Singulex, Inc., Alameda, California, USA. ; Shared Animal Facility, NIH Animal Center, Dickerson, Maryland, USA. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 888 EP - 896 VL - 42 IS - 5 KW - Biomarkers KW - 0 KW - Troponin I KW - Index Medicus KW - Sprague-Dawley rats KW - patas monkeys KW - cardiac troponin I KW - young age. KW - Swine KW - Animals KW - Horses KW - Myocardium -- metabolism KW - Rats KW - Myofibrils -- metabolism KW - Cattle KW - Rats, Sprague-Dawley KW - Heart Injuries -- blood KW - Erythrocebus patas KW - Female KW - Male KW - Immunoassay KW - Age Factors KW - Troponin I -- blood KW - Biomarkers -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1672090352?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=The+influence+of+age+on+serum+concentrations+of+cardiac+troponin+I%3A+results+in+rats%2C+monkeys%2C+and+commercial+sera.&rft.au=Herman%2C+Eugene+H%3BKnapton%2C+Alan%3BLiu%2C+Yongmin%3BLipshultz%2C+Steven+E%3BEstis%2C+Joel%3BTodd%2C+John%3BWoodward%2C+Ruth+A%3BCochran%2C+Thomas%3BZhang%2C+Jun%3BPoirier%2C+Miriam+C&rft.aulast=Herman&rft.aufirst=Eugene&rft.date=2014-07-01&rft.volume=42&rft.issue=5&rft.spage=888&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623313505154 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-20 N1 - Date created - 2015-04-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623313505154 ER - TY - JOUR T1 - Social support, self-efficacy for decision-making, and follow-up care use in long-term cancer survivors AN - 1665162096 AB - Objective Cancer survivors play an important role in coordinating their follow-up care and making treatment-related decisions. Little is known about how modifiable factors such as social support are associated with active participation in follow-up care. This study tests associations between social support, cancer-related follow-up care use, and self-efficacy for participation in decision-making related to follow-up care (SEDM). We also identified sociodemographic and clinical factors associated with social support among long-term survivors. Methods The FOllow-up Care Use among Survivors study is a cross-sectional, population-based survey of breast, prostate, colon, and gynecologic cancer survivors ( n=1522) 4–14 years post-diagnosis. Multivariable regression models were used to test associations between perceived social support (tangible and emotional/informational support modeled separately), follow-up care use (past 2 years), and SEDM, as well as to identify factors associated with perceived support. Results Neither support type was associated with follow-up care use (all p>0.05), although marital status was uniquely, positively associated with follow-up care use ( p<0.05). Both tangible support (B for a standard deviation increase (SE)=9.75(3.15), p<0.05) and emotional/informational support (B(SE)=12.61(3.05), p<0.001) were modestly associated with SEDM. Being married, having adequate financial resources, history of recurrence, and better perceived health status were associated with higher perceived tangible and emotional support (all p<0.05). Conclusions While perceived social support may facilitate survivor efficacy for participation in decision-making during cancer follow-up care, other factors, including marital satisfaction, appear to influence follow-up care use. Marital status and social support may be important factors to consider in survivorship care planning. Copyright © 2014 John Wiley & Sons, Ltd. JF - Psycho-Oncology AU - Forsythe, Laura P AU - Alfano, Catherine M AU - Kent, Erin E AU - Weaver, Kathryn E AU - Bellizzi, Keith AU - Arora, Neeraj AU - Aziz, Noreen AU - Keel, Gretchen AU - Rowland, Julia H AD - Patient-Centered Outcomes Research Institute (PCORI), Washington, DC, USA., Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA., Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA. ; Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA. ; Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA., Outcomes Research Branch, Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA. ; Department of Social Sciences & Health Policy, Division of Public Health Sciences, Wake Forest School of Medicine, Winston-Salem, NC, USA. ; Human Development and Family Studies, University of Connecticut, Storrs, CT, USA. ; Outcomes Research Branch, Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA. ; Office of Extramural Programs, National Institute of Nursing Research, NIH/DHHS, Bethesda, MD, USA. ; Information Management Services (IMS), Silver Spring, MD, USA. ; Patient-Centered Outcomes Research Institute (PCORI), Washington, DC, USA.; Office of Cancer Survivorship, Division of Cancer Control and Population Sciences, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA.; Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, NIH/DHHS, Bethesda, MD, USA. Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 788 EP - 796 CY - Chichester PB - Wiley Subscription Services, Inc. VL - 23 IS - 7 SN - 1057-9249 KW - Medical Sciences--Psychiatry And Neurology KW - Breast cancer KW - Care plans KW - Selfefficacy KW - Social support KW - Sociodemographic aspects KW - Survivors KW - Cancer KW - Care management KW - Decision making KW - Deviation KW - Diagnosis KW - Efficacy KW - Emotional support KW - Gynaecological cancer KW - Health status KW - Marital satisfaction KW - Marital status KW - Perceived social support KW - Prostate KW - Recurrence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665162096?accountid=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=Social+support%2C+self-efficacy+for+decision-making%2C+and+follow-up+care+use+in+long-term+cancer+survivors&rft.au=Forsythe%2C+Laura+P%3BAlfano%2C+Catherine+M%3BKent%2C+Erin+E%3BWeaver%2C+Kathryn+E%3BBellizzi%2C+Keith%3BArora%2C+Neeraj%3BAziz%2C+Noreen%3BKeel%2C+Gretchen%3BRowland%2C+Julia+H&rft.aulast=Forsythe&rft.aufirst=Laura&rft.date=2014-07-01&rft.volume=23&rft.issue=7&rft.spage=788&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3480 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-08-17 DO - http://dx.doi.org/10.1002/pon.3480 ER - TY - JOUR T1 - Harmonization of Neuroticism and Extraversion phenotypes across inventories and cohorts in the Genetics of Personality Consortium: an application of Item Response Theory AN - 1665150623 AB - Mega- or meta-analytic studies (e.g. genome-wide association studies) are increasingly used in behavior genetics. An issue in such studies is that phenotypes are often measured by different instruments across study cohorts, requiring harmonization of measures so that more powerful fixed effect meta-analyses can be employed. Within the Genetics of Personality Consortium, we demonstrate for two clinically relevant personality traits, Neuroticism and Extraversion, how Item-Response Theory (IRT) can be applied to map item data from different inventories to the same underlying constructs. Personality item data were analyzed in >160,000 individuals from 23 cohorts across Europe, USA and Australia in which Neuroticism and Extraversion were assessed by nine different personality inventories. Results showed that harmonization was very successful for most personality inventories and moderately successful for some. Neuroticism and Extraversion inventories were largely measurement invariant across cohorts, in particular when comparing cohorts from countries where the same language is spoken. The IRT-based scores for Neuroticism and Extraversion were heritable (48 and 49 %, respectively, based on a meta-analysis of six twin cohorts, total N = 29,496 and 29,501 twin pairs, respectively) with a significant part of the heritability due to non-additive genetic factors. For Extraversion, these genetic factors qualitatively differ across sexes. We showed that our IRT method can lead to a large increase in sample size and therefore statistical power. The IRT approach may be applied to any mega- or meta-analytic study in which item-based behavioral measures need to be harmonized. JF - Behavior Genetics AU - Berg, Stéphanie M AU - Moor, Marleen H M AU - McGue, Matt AU - Pettersson, Erik AU - Terracciano, Antonio AU - Verweij, Karin J H AU - Amin, Najaf AU - Derringer, Jaime AU - Esko, Tõnu AU - Grootheest, Gerard AU - Hansell, Narelle K AU - Huffman, Jennifer AU - Konte, Bettina AU - Lahti, Jari AU - Luciano, Michelle AU - Matteson, Lindsay K AU - Viktorin, Alexander AU - Wouda, Jasper AU - Agrawal, Arpana AU - Allik, Jüri AU - Bierut, Laura AU - Broms, Ulla AU - Campbell, Harry AU - Smith, George Davey AU - Eriksson, Johan G AU - Ferrucci, Luigi AU - Franke, Barbera AU - Fox, Jean-Paul AU - Geus, Eco J C AU - Giegling, Ina AU - Gow, Alan J AU - Grucza, Richard AU - Hartmann, Annette M AU - Heath, Andrew C AU - Heikkilä, Kauko AU - Iacono, William G AU - Janzing, Joost AU - Jokela, Markus AU - Kiemeney, Lambertus AU - Lehtimäki, Terho AU - Madden, Pamela A F AU - Magnusson, Patrik K E AU - Northstone, Kate AU - Nutile, Teresa AU - Ouwens, Klaasjan G AU - Palotie, Aarno AU - Pattie, Alison AU - Pesonen, Anu-Katriina AU - Polasek, Ozren AU - Pulkkinen, Lea AD - Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Institute of Public Health, University of Southern Denmark, Odense, Denmark ; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden ; National Institute on Aging, NIH, Baltimore, MD, USA, College of Medicine, Florida State University, Tallahassee, FL, USA ; QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia, Department of Developmental Psychology and EMGO Institute for Health and Care Research, VU University Amsterdam, Amsterdam, The Netherlands ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychology, University of Illinois at Urbana-Champaign, Champaign, IL, USA ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Estonian Genome Center, University of Tartu, Tartu, Estonia ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychiatry, EMGO+ Institute, Neuroscience Campus Amsterdam, VU University Medical Center Amsterdam, Amsterdam, The Netherlands ; QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, MRC Human Genetics, MRC IGMM, Western General Hospital, University of Edinburgh, Edinburgh, Scotland, UK ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychiatry, University of Halle, Halle, Germany ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland, Folkhälsan Research Center, Helsinki, Finland ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychology, University of Edinburgh, Edinburgh, UK, Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Department of Psychology, University of Tartu, Tartu, Estonia, Estonian Academy of Sciences, Tallinn, Estonia ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Department of Public Health, Hjelt Institute, University of Helsinki, Helsinki, Finland, National Institute for Health and Welfare (THL), Helsinki, Finland ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Centre for Population Health Sciences, Medical School, University of Edinburgh, Edinburgh, UK ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, MRC Integrative Epidemiology Unit, School of Social and Community Medicine, University of Bristol, Bristol, UK ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Folkhälsan Research Center, Helsinki, Finland, Vasa Central Hospital, Vaasa, Finland ; National Institute on Aging, NIH, Baltimore, MD, USA ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Donders Institute for Cognitive Neuroscience, Radboud University Nijmegen, Nijmegen, The Netherlands, Department of Human Genetics, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Department of Psychology, School of Life Sciences, Heriot-Watt University, Edinburgh, UK ; Department of Biological Psychology, VU University, Amsterdam, The Netherlands, Department of Public Health, Hjelt Institute, University of Helsinki, Helsinki, Finland ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Department of Psychiatry, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland, Department of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Department of Health Evidence, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands, Department of Urology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Department of Clinical Chemistry, Fimlab Laboratories and School of Medicine, University of Tampere, Tampere, Finland ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Institute of Genetics and Biophysics “A. Buzzati-Traverso" – CNR, Naples, Italy ; Department of Psychology, University of Minnesota, Elliott Hall, Minneapolis, MN, USA, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, UK, Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands, Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland ; Institute of Public Health, University of Southern Denmark, Odense, Denmark, Department of Public Health, Faculty of Medicine, University of Split, Split, Croatia ; Institute of Public Health, University of Southern Denmark, Odense, Denmark, Department of Psychology, University of Jyväskylä, Jyväskylä, Finland ; Department of Research Methodology, Measurement and Data-Analysis, University of Twente, Enschede, The Netherlands; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 295 EP - 313 CY - New York PB - Springer Science & Business Media VL - 44 IS - 4 SN - 0001-8244 KW - Biology KW - Behaviour genetics KW - Extraversion KW - Genetic factors KW - Harmonization KW - Heritability KW - Item response theory KW - Measurement KW - Neuroticism KW - Personality KW - Phenotypes KW - Power KW - Statistical power UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665150623?accountid=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=Behavior+Genetics&rft.atitle=Harmonization+of+Neuroticism+and+Extraversion+phenotypes+across+inventories+and+cohorts+in+the+Genetics+of+Personality+Consortium%3A+an+application+of+Item+Response+Theory&rft.au=Berg%2C+St%C3%A9phanie+M%3BMoor%2C+Marleen+H+M%3BMcGue%2C+Matt%3BPettersson%2C+Erik%3BTerracciano%2C+Antonio%3BVerweij%2C+Karin+J+H%3BAmin%2C+Najaf%3BDerringer%2C+Jaime%3BEsko%2C+T%C3%B5nu%3BGrootheest%2C+Gerard%3BHansell%2C+Narelle+K%3BHuffman%2C+Jennifer%3BKonte%2C+Bettina%3BLahti%2C+Jari%3BLuciano%2C+Michelle%3BMatteson%2C+Lindsay+K%3BViktorin%2C+Alexander%3BWouda%2C+Jasper%3BAgrawal%2C+Arpana%3BAllik%2C+J%C3%BCri%3BBierut%2C+Laura%3BBroms%2C+Ulla%3BCampbell%2C+Harry%3BSmith%2C+George+Davey%3BEriksson%2C+Johan+G%3BFerrucci%2C+Luigi%3BFranke%2C+Barbera%3BFox%2C+Jean-Paul%3BGeus%2C+Eco+J+C%3BGiegling%2C+Ina%3BGow%2C+Alan+J%3BGrucza%2C+Richard%3BHartmann%2C+Annette+M%3BHeath%2C+Andrew+C%3BHeikkil%C3%A4%2C+Kauko%3BIacono%2C+William+G%3BJanzing%2C+Joost%3BJokela%2C+Markus%3BKiemeney%2C+Lambertus%3BLehtim%C3%A4ki%2C+Terho%3BMadden%2C+Pamela+A+F%3BMagnusson%2C+Patrik+K+E%3BNorthstone%2C+Kate%3BNutile%2C+Teresa%3BOuwens%2C+Klaasjan+G%3BPalotie%2C+Aarno%3BPattie%2C+Alison%3BPesonen%2C+Anu-Katriina%3BPolasek%2C+Ozren%3BPulkkinen%2C+Lea&rft.aulast=Berg&rft.aufirst=St%C3%A9phanie&rft.date=2014-07-01&rft.volume=44&rft.issue=4&rft.spage=295&rft.isbn=&rft.btitle=&rft.title=Behavior+Genetics&rft.issn=00018244&rft_id=info:doi/10.1007%2Fs10519-014-9654-x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2015-12-14 DO - http://dx.doi.org/10.1007/s10519-014-9654-x ER - TY - JOUR T1 - Inhibition of phosphoinositol 3 kinase contributes to nanoparticle-mediated exaggeration of endotoxin-induced leukocyte procoagulant activity AN - 1660423612; PQ0001124109 AB - Aim: Disseminated intravascular coagulation is an increasing concern for certain types of engineered nanomaterials. Recent studies have shed some light on the nanoparticle physicochemical properties contributing to this toxicity; however, the mechanisms are poorly understood. Leukocyte procoagulant activity (PCA) is a key factor contributing to the initiation of this toxicity. We have previously reported on the exaggeration of endotoxin-induced PCA by cationic dendrimers. Herein, we report an effort to discern the mechanism. Materials & methods: Poly(amidoamine) dendrimers with various sizes and surface functionalities were studied in vitro by the recalcification test, flow cytometry and other relevant assays. Results & conclusion: Cationic dendrimers exaggerated endotoxin-induced PCA, but their anionic or neutral counterparts did not; the cationic charge prompts this phenomenon, but different cationic surface chemistries do not influence it. Cationic dendrimers and endotoxin differentially affect the PCA complex. The inhibition of phosphoinositol 3 kinase by dendrimers contributes to the exaggeration of the endotoxin-induced PCA. Original submitted: 4 February 2013; Revised submitted: 2 June 2013 JF - Nanomedicine AU - Ilinskaya, Anna N AU - Man, Sonny AU - Patri, Anil K AU - Clogston, Jeffrey D AU - Crist, Rachael M AU - Cachau, Raul E AU - McNeil, Scott E AU - Dobrovolskaia, Marina A AD - super(1)Nanotechnology Characterization Laboratory, Advanced Technology Program, SAIC-Frederick Inc., NCI-Frederick, 1050 Boyles Street, Building 469, Frederick, MD 21702, USA Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 1311 EP - 1326 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 9 IS - 9 SN - 1743-5889, 1743-5889 KW - Biotechnology and Bioengineering Abstracts KW - coagulopathy KW - dendrimer KW - disseminated intravascular coagulation KW - leukocyte KW - nanoparticle KW - procoagulant activity KW - thrombosis KW - Flow cytometry KW - Endotoxins KW - Disseminated intravascular coagulation KW - Leukocytes KW - Physicochemical properties KW - Toxicity KW - nanoparticles KW - nanotechnology KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660423612?accountid=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=Inhibition+of+phosphoinositol+3+kinase+contributes+to+nanoparticle-mediated+exaggeration+of+endotoxin-induced+leukocyte+procoagulant+activity&rft.au=Ilinskaya%2C+Anna+N%3BMan%2C+Sonny%3BPatri%2C+Anil+K%3BClogston%2C+Jeffrey+D%3BCrist%2C+Rachael+M%3BCachau%2C+Raul+E%3BMcNeil%2C+Scott+E%3BDobrovolskaia%2C+Marina+A&rft.aulast=Ilinskaya&rft.aufirst=Anna&rft.date=2014-07-01&rft.volume=9&rft.issue=9&rft.spage=1311&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 60 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Endotoxins; Flow cytometry; Disseminated intravascular coagulation; Physicochemical properties; Leukocytes; Toxicity; nanoparticles; nanotechnology ER - TY - JOUR T1 - Depressive Symptoms in Young, Urban Schoolchildren: Environmental, Social, and Cognitive Risk AN - 1660018774; 201501242 AB - This study examined relations among stressors, perceived social competence, attributional style, and depressive symptoms in young urban schoolchildren. Data were collected from 85 5- to 11-year-olds, mostly African American, who attended a public elementary school in a low-income urban area. Social competence was examined as a potential mediator, and attributional style was examined as a potential moderator of the relation between stressful life events and depressive symptoms. Separate analyses were conducted by age and gender. For older children and girls, main effects were found for stressful life events as predictors of depressive symptoms. Mediational analyses indicated that perceived peer acceptance served as a mediator of the relation between stressful life events and depressive symptoms for girls. In addition, attributional style moderated the relation between stressors and depressive symptoms in the older children. Together, findings suggest that significant relations exist among stressful life events, social and cognitive processes, and depressive symptoms in young urban children and that these relations are influenced by gender and development. Adapted from the source document. JF - Journal of Prevention & Intervention in the Community AU - Thurm, Audrey E AU - Carlson, Ginger A AU - Lyons, Aoife L AU - Grant, Kathryn E AU - Wagstaff, Amanda E AD - Pediatrics and Developmental Neuroscience, National Institute of Mental Health, Bethesda, Maryland, USA athurm@mail.nih.gov Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 169 EP - 182 PB - Taylor & Francis, Philadelphia PA VL - 42 IS - 3 SN - 1085-2352, 1085-2352 KW - Depression (Psychology) KW - Urban Areas KW - Life Events KW - Stress KW - Social Competence KW - Females KW - Children KW - Cognition KW - Sex KW - article KW - 6143: child & family welfare UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660018774?accountid=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+Prevention+%26+Intervention+in+the+Community&rft.atitle=Depressive+Symptoms+in+Young%2C+Urban+Schoolchildren%3A+Environmental%2C+Social%2C+and+Cognitive+Risk&rft.au=Thurm%2C+Audrey+E%3BCarlson%2C+Ginger+A%3BLyons%2C+Aoife+L%3BGrant%2C+Kathryn+E%3BWagstaff%2C+Amanda+E&rft.aulast=Thurm&rft.aufirst=Audrey&rft.date=2014-07-01&rft.volume=42&rft.issue=3&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=Journal+of+Prevention+%26+Intervention+in+the+Community&rft.issn=10852352&rft_id=info:doi/10.1080%2F10852352.2014.916574 LA - English DB - Social Services Abstracts N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-09-28 N1 - SubjectsTermNotLitGenreText - Depression (Psychology); Urban Areas; Children; Social Competence; Females; Stress; Cognition; Sex; Life Events DO - http://dx.doi.org/10.1080/10852352.2014.916574 ER - TY - JOUR T1 - Testicular Swelling Due to Lymphatic Filariasis After Brief Travel to Haiti AN - 1647023029; 21189963 AB - After 6 months of a trip to Haiti, a 25-year-old healthy man presented with a 6-week history of a very slow progressive intermittent bilateral testicular pain and swelling. The biopsies in both testicles revealed the presence of a dead filarial parasite. Polymerase chain reaction products of the DNA from the biopsy were shown to have a 100% identity to Wuchereria bancrofti. Despite being uncommon in travelers, this presentation of W. bancrofti highlights the possibility of acquiring W. bancrofti during short-term trips to highly endemic regions of the world (i.e., Haiti). JF - American Journal of Tropical Medicine and Hygiene AU - Marcos, Luis A AU - Shapley, Nathan P AU - Eberhard, Mark AU - Epstein, Jonathan I AU - Fox, LeAnne M AU - Magill, Alan AU - Nutman, Thomas B AD - Infectious Diseases, Hattiesburg Clinic, Hattiesburg, Mississippi; Urology Clinic, Wesley Medical Center, Hattiesburg, Mississippi; Division of Parasitic Diseases and Malaria, CDC, Atlanta, Georgia; Pathology Department, Johns Hopkins University, Baltimore, Maryland; Malaria, Global Health Program, Bill and Melinda Gates Foundation, Seattle, Washington; Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda, Maryland, marcoslrz@yahoo.com Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 89 EP - 91 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 91 IS - 1 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology KW - Testes KW - Travel KW - Parasites KW - Wuchereria bancrofti KW - Filariasis KW - Polymerase chain reaction KW - Biopsy KW - Pain KW - K 03400:Human Diseases KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647023029?accountid=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=Testicular+Swelling+Due+to+Lymphatic+Filariasis+After+Brief+Travel+to+Haiti&rft.au=Marcos%2C+Luis+A%3BShapley%2C+Nathan+P%3BEberhard%2C+Mark%3BEpstein%2C+Jonathan+I%3BFox%2C+LeAnne+M%3BMagill%2C+Alan%3BNutman%2C+Thomas+B&rft.aulast=Marcos&rft.aufirst=Luis&rft.date=2014-07-01&rft.volume=91&rft.issue=1&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.14-0030 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Travel; Testes; Parasites; Filariasis; Polymerase chain reaction; Pain; Biopsy; Wuchereria bancrofti DO - http://dx.doi.org/10.4269/ajtmh.14-0030 ER - TY - JOUR T1 - Does Social Capital Protect Against the Adverse Behavioural Outcomes of Child Neglect? AN - 1627735339 AB - LONGSCAN was a longitudinal study of the risks and consequences of child abuse and neglect conducted between 1992 and 2012 among five sites across the US. Interviews with mothers of at-risk children began when the children were four years of age, and mothers and children from age six to age 18 years were interviewed every other year. Maltreatment reports were obtained from departments of social services, and subjects’ self-reported abuse was obtained at age 12. Generalised estimating equations were used to investigate the impact of informal social control, social cohesion and trust (SCT), and caregiver depression at ages 12, 14 and 16 years on externalising behaviours, smoking and alcohol use among 18-year olds who had been neglected prior to age 12. In models controlling for child age and gender, maltreatment types other than neglect, maternal education and study site, SCT significantly reduced the impact of caregiver depression on externalising behaviour and alcohol use among the neglected children at age 18. This moderating effect was not seen among non-neglected 18-year-old children. Copyright © 2014 John Wiley & Sons, Ltd. Key Practitioner Messages: * Child neglect is a significant predictor of adolescent health risk behaviours. * Caregiver depression increases the risk of neglect and increases the adverse behavioural outcomes of neglect. * Among children neglected before age 12, in the presence of caregiver depression, SCT reduce externalising behaviours and alcohol use at age 18. * Identification and treatment of caregiver depression, along with supporting community cohesion and neighbourhood trust, can ameliorate some of the negative outcomes associated with child neglect. ‘Child neglect is a significant predictor of adolescent health risk behaviours’ JF - Child Abuse Review AU - Kotch, Jonathan B AU - Smith, Jamie AU - Margolis, Benyamin AU - Black, Maureen M AU - English, Diana AU - Thompson, Richard AU - Lee, Li-Ching AU - Taneja, Gitanjali AU - Bangdiwala, Shrikant I AD - Department of Maternal and Child Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Injury Prevention Research Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Maternal and Child Health Bureau, Health Resources and Services Administration, US Department of Health and Human Services, Rockville, MD, USA. ; Department of Pediatrics, University of Maryland School of Medicine, Baltimore, MD, USA. ; School of Social Work, University of Washington, Seattle, WA, USA. ; Juvenile Protective Association, Chicago, IL, USA. ; Department of Epidemiology, Johns Hopkins University, Baltimore, MD, USA. ; National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA. ; Department of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. ; Department of Maternal and Child Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 246 EP - 261 CY - Hoboken PB - Wiley Subscription Services, Inc. VL - 23 IS - 4 SN - 0952-9136 KW - Social Services And Welfare KW - Neglected children KW - Adolescents KW - Age KW - Alcohol related KW - Child abuse KW - Cohesion KW - Health behaviour KW - Identification KW - Maltreated children KW - Maltreatment KW - Mothers KW - Protective factors KW - Risk behaviour KW - Smoking KW - Social capital KW - Social cohesion KW - Social control KW - Social services KW - Depression KW - Child neglect KW - Child maltreatment KW - Carers KW - At risk KW - Alcohol consumption KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627735339?accountid=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+Review&rft.atitle=Does+Social+Capital+Protect+Against+the+Adverse+Behavioural+Outcomes+of+Child+Neglect%3F&rft.au=Kotch%2C+Jonathan+B%3BSmith%2C+Jamie%3BMargolis%2C+Benyamin%3BBlack%2C+Maureen+M%3BEnglish%2C+Diana%3BThompson%2C+Richard%3BLee%2C+Li-Ching%3BTaneja%2C+Gitanjali%3BBangdiwala%2C+Shrikant+I&rft.aulast=Kotch&rft.aufirst=Jonathan&rft.date=2014-07-01&rft.volume=23&rft.issue=4&rft.spage=246&rft.isbn=&rft.btitle=&rft.title=Child+Abuse+Review&rft.issn=09529136&rft_id=info:doi/10.1002%2Fcar.2345 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA); Social Services Abstracts N1 - Date revised - 2014-11-10 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1002/car.2345 ER - TY - JOUR T1 - Nonresponse Bias in Survey Estimates of Alcohol Consumption and Its Association With Harm AN - 1627731308 AB - Objective: Selective nonresponse represents a major source of potential bias in survey-based estimates of alcohol consumption and its association with harm. This study examined whether consumption differs for respondents and nonrespondents after correcting for their sociodemographic differences. Method: This study compared baseline consumption among initial respondents who did ( n = 34,653) and did not ( n = 5,306) respond to a 3-year follow-up interview in a prospective study of the U.S. general population. Differences in consumption measures were presented before and after adjustment or sociodemographic differences, and interactions of nonresponse with consumption were assessed in models predicting various types of harm. Results: After we adjusted for sociodemographic differences and factored in the overall level of nonresponse (13.3%), the degree to which the prevalence of drinking was underestimated in the total population was only 1.6%, and the extent to which consumption was overestimated among drinkers lay in the range of 1.7% to 2.4%. There was no consistent evidence that nonresponse moderated the association between consumption and alcohol-related harm. Sociodemographic differentials in nonresponse generally matched those reported for cross-sectional studies in the literature. Conclusions: The extent of nonresponse bias in survey estimates of alcohol consumption should not affect drinking guidelines and planning for prevention and treatment programs. The findings of this study are supportive of study designs that have been used to assess nonresponse bias, including the use of registry data on alcohol-related harms and secondary nonresponse data from prospective studies. JF - Journal of Studies on Alcohol and Drugs AU - DAWSON, DEBORAH A AU - GOLDSTEIN, RISE B AU - PICKERING, ROGER P AU - GRANT, BRIDGET F AD - Kelly Government Services, Bethesda, Maryland; Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland ; Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland ; Kelly Government Services, Bethesda, Maryland; Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 695 EP - 703 CY - Piscataway PB - Alcohol Research Documentation, Inc. VL - 75 IS - 4 SN - 1937-1888 KW - Medical Sciences KW - Alcohol consumption KW - Alcohol related KW - Associations KW - Consumption KW - Cross-sectional studies KW - Moderated KW - Nonresponse KW - Preventive programmes KW - Prospective studies KW - Nonresponse bias KW - Treatment methods KW - Sociodemographic aspects KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627731308?accountid=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=Nonresponse+Bias+in+Survey+Estimates+of+Alcohol+Consumption+and+Its+Association+With+Harm&rft.au=DAWSON%2C+DEBORAH+A%3BGOLDSTEIN%2C+RISE+B%3BPICKERING%2C+ROGER+P%3BGRANT%2C+BRIDGET+F&rft.aulast=DAWSON&rft.aufirst=DEBORAH&rft.date=2014-07-01&rft.volume=75&rft.issue=4&rft.spage=695&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 - 2014-10-14 N1 - Last updated - 2016-05-16 N1 - SubjectsTermNotLitGenreText - United States--US ER - TY - JOUR T1 - Multiyear Persistence of 2 Pandemic A/H1N1 Influenza Virus Lineages in West Africa AN - 1618151794; 20800428 AB - Our understanding of the global ecology of influenza viruses is impeded by historically low levels of viral surveillance in Africa. Increased genetic sequencing of African A/H1N1 pandemic Influenza viruses during 2009-2013 revealed multiyear persistence of 2 viral lineages within West Africa, raising questions about the roles of reduced air traffic and the asynchrony of seasonal influenza epidemics among West African countries in the evolution of independent lineages. The potential for novel influenza virus lineages to evolve within Africa warrants Intensified influenza surveillance in Africa and other understudied areas. JF - Journal of Infectious Diseases AU - Nelson, Martha I AU - Njouom, Richard AU - Viboud, Cecile AU - Niang, Mbayame N D AU - Kadjo, Herve AU - Ampofo, William AU - Adebayo, Adedeji AU - Tarnagda, Zekiba AU - Miller, Mark A AU - Holmes, Edward C AU - Diop, Ousmane M AD - Division of International Epidemiology and Population Studies, Fogarty International Center, National Institutes of Health, 16 Center Dr, Room 202, Bethesda, MD 20892, nelsonma@mail.nih.gov Y1 - 2014/07/01/ PY - 2014 DA - 2014 Jul 01 SP - 121 EP - 125 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 210 IS - 1 SN - 0022-1899, 0022-1899 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - human influenza A virus KW - pandemic KW - phylogenetic analysis KW - Africa KW - Historical account KW - Epidemics KW - Air traffic control KW - Viruses KW - Traffic KW - Ecology KW - Influenza KW - pandemics KW - Influenza virus KW - Sulfur dioxide KW - Infectious diseases KW - Seasonal variations KW - Evolution KW - H 0500:General KW - V 22310:Genetics, Taxonomy & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618151794?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Multiyear+Persistence+of+2+Pandemic+A%2FH1N1+Influenza+Virus+Lineages+in+West+Africa&rft.au=Nelson%2C+Martha+I%3BNjouom%2C+Richard%3BViboud%2C+Cecile%3BNiang%2C+Mbayame+N+D%3BKadjo%2C+Herve%3BAmpofo%2C+William%3BAdebayo%2C+Adedeji%3BTarnagda%2C+Zekiba%3BMiller%2C+Mark+A%3BHolmes%2C+Edward+C%3BDiop%2C+Ousmane+M&rft.aulast=Nelson&rft.aufirst=Martha&rft.date=2014-07-01&rft.volume=210&rft.issue=1&rft.spage=121&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiu047 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-10-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Influenza; pandemics; Epidemics; Evolution; Traffic; Ecology; Historical account; Sulfur dioxide; Infectious diseases; Air traffic control; Viruses; Seasonal variations; Influenza virus; Africa DO - http://dx.doi.org/10.1093/infdis/jiu047 ER - TY - JOUR T1 - Cannabinoids in oral fluid by on-site immunoassay and by GC-MS using two different oral fluid collection devices AN - 1567099119; 20555747 AB - Oral fluid (OF) enables non-invasive sample collection for on-site drug testing, but performance of on-site tests with occasional and frequent smokers' OF to identify cannabinoid intake requires further evaluation. Furthermore, as far as we are aware, no studies have evaluated differences between cannabinoid disposition among OF collection devices with authentic OF samples after controlled cannabis administration. Fourteen frequent and 10 occasional adult cannabis smokers smoked one 6.8% delta [sup 9]-tetrahydrocannabinol (THC) cigarette ad libitum over 10 min. OF was collected with the StatSure Saliva Sampler, Oral-Eze, and Draeger DrugTest 5000 test cassette before and up to 30 h after cannabis smoking. Test cassettes were analyzed within 15 min and gas chromatography-mass spectrometry cannabinoid results were obtained within 24 h. The DrugTest 5000 on-site device had high diagnostic sensitivity, specificity, and efficiency for cannabinoids. JF - Analytical and Bioanalytical Chemistry AU - Desrosiers, Nathalie A AU - Milman, Garry AU - Mendu, Damodara R AU - Lee, Dayong AU - Barnes, Allan J AU - Gorelick, David A AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism Section, NIDA IRP, 251 Bayview Boulevard, Baltimore, MD 21224, USA; Program in Toxicology, University of Maryland Baltimore, 655 W. Baltimore Street, Baltimore, MD 21201, USA, mhuestis@intra.nida.nih.gov PY - 2014 SP - 4117 EP - 4128 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 406 IS - 17 SN - 1618-2642, 1618-2642 KW - Aqualine Abstracts; Water Resources Abstracts KW - Cannabinoid KW - Oral fluid KW - On-site test KW - Draeger DrugTest 5000 KW - Testing Procedures KW - Samplers KW - Evaluation KW - On-site Tests KW - Performance Evaluation KW - Administration KW - Drugs KW - AQ 00001:Water Resources and Supplies KW - SW 5040:Data acquisition UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1567099119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+Bioanalytical+Chemistry&rft.atitle=Cannabinoids+in+oral+fluid+by+on-site+immunoassay+and+by+GC-MS+using+two+different+oral+fluid+collection+devices&rft.au=Desrosiers%2C+Nathalie+A%3BMilman%2C+Garry%3BMendu%2C+Damodara+R%3BLee%2C+Dayong%3BBarnes%2C+Allan+J%3BGorelick%2C+David+A%3BHuestis%2C+Marilyn+A&rft.aulast=Desrosiers&rft.aufirst=Nathalie&rft.date=2014-07-01&rft.volume=406&rft.issue=17&rft.spage=4117&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-014-7813-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 27 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Evaluation; Testing Procedures; Performance Evaluation; On-site Tests; Administration; Drugs; Samplers DO - http://dx.doi.org/10.1007/s00216-014-7813-9 ER - TY - JOUR T1 - First Report of Olpidium bornovanus and O. virulentus on Melon in Italy AN - 1560114309; 20500663 AB - A survey for the presence of Olpidium spp. on melon (Cucumis melo L.) was conducted during the beginning of 2013 in central Italy in an unheated greenhouse, located in the melon-producing coastal area of north Latium (central Italy, Viterbo Province) (42 parallel 23'09.31" N, 11 parallel 30'46.10" E) with a history of monosporascus root rot and vine decline (MRRVD). For this aim, 10 soil samples were collected adjacent to the roots of plants symptomatic of MRRVD, represented by root lesions and rots and loss of smaller feeder roots. Olpidium was baited from collected infested soil by growing melon (cv. Dinero) plants for 45 days. Bait plants grown in sterilized soil were used as negative controls. All the baited melon roots were analyzed by morphological and molecular methods. JF - Plant Disease AU - Aleandri, M P AU - Martignoni, D AU - Reda, R AU - Alfaro-Fernandez, A AU - Font, M I AU - Armengol, J AU - Chilosi, G AD - Dipartamento per la Innovazione nei Sistemi Biologici, Agroalimentari e Forestali (DIBAF), Universita degli Studi della Tuscia, Via S. Camillo de Lellis, 01100 Viterbo, Italy PY - 2014 SP - 997 EP - 998 PB - American Phytopathological Society, 3340 Pilot Knob Road St. Paul MN 55121-2097 United States VL - 98 IS - 7 SN - 0191-2917, 0191-2917 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Soil KW - Cucumis melo KW - Plant diseases KW - Vines KW - Root rot KW - Olpidium KW - Greenhouses KW - A 01360:Plant Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560114309?accountid=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=Plant+Disease&rft.atitle=First+Report+of+Olpidium+bornovanus+and+O.+virulentus+on+Melon+in+Italy&rft.au=Aleandri%2C+M+P%3BMartignoni%2C+D%3BReda%2C+R%3BAlfaro-Fernandez%2C+A%3BFont%2C+M+I%3BArmengol%2C+J%3BChilosi%2C+G&rft.aulast=Aleandri&rft.aufirst=M&rft.date=2014-07-01&rft.volume=98&rft.issue=7&rft.spage=997&rft.isbn=&rft.btitle=&rft.title=Plant+Disease&rft.issn=01912917&rft_id=info:doi/10.1094%2FPDIS-10-13-1041-PDN LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2015-12-09 N1 - SubjectsTermNotLitGenreText - Soil; Plant diseases; Vines; Root rot; Greenhouses; Cucumis melo; Olpidium DO - http://dx.doi.org/10.1094/PDIS-10-13-1041-PDN ER - TY - JOUR T1 - Stability of Core Language Skill from Early Childhood to Adolescence: A Latent Variable Approach AN - 1558997949; 201412781 AB - This four-wave prospective longitudinal study evaluated stability of language in 324 children from early childhood to adolescence. Structural equation modeling supported loadings of multiple age-appropriate multisource measures of child language on single-factor core language skills at 20 months and 4, 10, and 14 years. Large stability coefficients (standardized indirect effect = .46) were obtained between language latent variables from early childhood to adolescence even when accounting for child nonverbal intelligence and social competence and maternal verbal intelligence, education, speech, and social desirability. Stability coefficients were similar for girls and boys. Stability of core language skill was stronger from 4 to 10 to 14 years than from 20 months to 4 years, so early intervention to improve lagging language is recommended. Adapted from the source document JF - Child Development AU - Bornstein, Marc H AU - Hahn, Chun-Shin AU - Putnick, Diane L AU - Suwalsky, Joan T D AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 1346 EP - 1356 VL - 85 IS - 4 SN - 0009-3920, 0009-3920 KW - Education (20900) KW - Child Language (11800) KW - Longitudinal Studies (49900) KW - Intelligence (36450) KW - Children (11850) KW - article KW - 4015: psycholinguistics; child language acquisition UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558997949?accountid=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=Child+Development&rft.atitle=Stability+of+Core+Language+Skill+from+Early+Childhood+to+Adolescence%3A+A+Latent+Variable+Approach&rft.au=Bornstein%2C+Marc+H%3BHahn%2C+Chun-Shin%3BPutnick%2C+Diane+L%3BSuwalsky%2C+Joan+T+D&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2014-07-01&rft.volume=85&rft.issue=4&rft.spage=1346&rft.isbn=&rft.btitle=&rft.title=Child+Development&rft.issn=00093920&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2014-09-01 N1 - Last updated - 2016-09-27 N1 - CODEN - CHDEAW N1 - SubjectsTermNotLitGenreText - Children (11850); Intelligence (36450); Child Language (11800); Education (20900); Longitudinal Studies (49900) ER - TY - JOUR T1 - Prioritizing practice in Ombudsman and ADR programs AN - 1556292913; 4591999 AB - This article examines ways in which the Office of the Ombudsman/Center for Cooperative Resolution (OO/CCR) at the National Institutes of Health pursues activities that comprise an orientation toward practice and supports development of an 'activist' ombudsman orientation. The article opens by describing challenges that alternative dispute resolution (ADR) organizations face, contrasts them with the experience of OO/CCR, details elements of a practice orientation as experienced at OO/CCR, and suggests ways in which ADR and ombudsman organizations may address their own challenges and pursue a practice orientation. JF - Conflict resolution quarterly AU - Michael, David E AD - National Institutes of Health Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 463 EP - 476 VL - 31 IS - 4 SN - 1536-5581, 1536-5581 KW - Political Science KW - Activists KW - Co-operatives KW - Ombudsman KW - Conflict theory KW - Alternation KW - Conflict resolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556292913?accountid=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=Conflict+resolution+quarterly&rft.atitle=Prioritizing+practice+in+Ombudsman+and+ADR+programs&rft.au=Michael%2C+David+E&rft.aulast=Michael&rft.aufirst=David&rft.date=2014-07-01&rft.volume=31&rft.issue=4&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=Conflict+resolution+quarterly&rft.issn=15365581&rft_id=info:doi/10.1002%2Fcrq.21098 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-08-26 N1 - Last updated - 2014-08-27 N1 - SubjectsTermNotLitGenreText - 2703 2698; 8925 10742; 934; 2704 9798; 2409; 553 9637 DO - http://dx.doi.org/10.1002/crq.21098 ER - TY - JOUR T1 - A tiered framework for risk-relevant characterization and ranking of chemical exposures: applications to the National Children's Study (NCS) AN - 1556292738; 4591484 AB - A challenge for large-scale environmental health investigations such as the National Children's Study (NCS), is characterizing exposures to multiple, co-occurring chemical agents with varying spatiotemporal concentrations and consequences modulated by biochemical, physiological, behavioral, socioeconomic, and environmental factors. Such investigations can benefit from systematic retrieval, analysis, and integration of diverse extant information on both contaminant patterns and exposure-relevant factors. This requires development, evaluation, and deployment of informatics methods that support flexible access and analysis of multiattribute data across multiple spatiotemporal scales. A new 'Tiered Exposure Ranking' (TiER) framework, developed to support various aspects of risk-relevant exposure characterization, is described here, with examples demonstrating its application to the NCS. TiER utilizes advances in informatics computational methods, extant database content and availability, and integrative environmental/exposure/biological modeling to support both 'discovery-driven' and 'hypothesis-driven' analyses. 'Tier 1' applications focus on 'exposomic' pattern recognition for extracting information from multidimensional data sets, whereas second and higher tier applications utilize mechanistic models to develop risk-relevant exposure metrics for populations and individuals. In this article, 'tier 1' applications of TiER explore identification of potentially causative associations among risk factors, for prioritizing further studies, by considering publicly available demographic/socioeconomic, behavioral, and environmental data in relation to two health endpoints (preterm birth and low birth weight). A 'tier 2' application develops estimates of pollutant mixture inhalation exposure indices for NCS counties, formulated to support risk characterization for these endpoints. Applications of TiER demonstrate the feasibility of developing risk-relevant exposure characterizations for pollutants using extant environmental and demographic/socioeconomic data. Reprinted by permission of Blackwell Publishers JF - Risk analysis AU - Dellarco, Michael AU - Landrigan, Philip J AU - Lioy, Paul J AU - Georgopoulos, Panos G AU - Brinkerhoff, Christopher J AU - Isukapalli, Sastry AD - Rutgers, The State University of New Jersey ; National Institutes of Health ; Icahn School of Medicine at Mount Sinai Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 1299 EP - 1316 VL - 34 IS - 7 SN - 0272-4332, 0272-4332 KW - Economics KW - Pollutants KW - Health care KW - Computational methods KW - Population KW - Data analysis KW - Risk theory UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556292738?accountid=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=Risk+analysis&rft.atitle=A+tiered+framework+for+risk-relevant+characterization+and+ranking+of+chemical+exposures%3A+applications+to+the+National+Children%27s+Study+%28NCS%29&rft.au=Dellarco%2C+Michael%3BLandrigan%2C+Philip+J%3BLioy%2C+Paul+J%3BGeorgopoulos%2C+Panos+G%3BBrinkerhoff%2C+Christopher+J%3BIsukapalli%2C+Sastry&rft.aulast=Dellarco&rft.aufirst=Michael&rft.date=2014-07-01&rft.volume=34&rft.issue=7&rft.spage=1299&rft.isbn=&rft.btitle=&rft.title=Risk+analysis&rft.issn=02724332&rft_id=info:doi/10.1111%2Frisa.12165 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-08-26 N1 - Last updated - 2014-08-27 N1 - SubjectsTermNotLitGenreText - 2671 10919; 11040 11035; 5775 13521; 9814; 3279 971 3286; 9846 DO - http://dx.doi.org/10.1111/risa.12165 ER - TY - JOUR T1 - Two perspectives on learning the organizational ombudsman role AN - 1556291728; 4591998 AB - This article explores the challenges in learning the role of the organizational ombudsman from the perspectives of two practitioners-one an experienced workplace mediator, the other a student of conflict resolution. The discussion of the shift in thinking, as well as skills needed to transition into the various facets of organizational ombudsman work, combines concepts from ombudsman theory with insights on enhancing ombudsman practice. The authors provide observations and recommendations based on their own experiences assuming the roles of a new ombudsman, including reflective practice and partnering, coaching with employees, and expanding systemic engagements with and cultural knowledge of organizations. JF - Conflict resolution quarterly AU - Witzler, Lisa AU - Myers, Linda AD - National Institutes of Health Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 447 EP - 462 VL - 31 IS - 4 SN - 1536-5581, 1536-5581 KW - Sociology KW - Learning KW - Organizations KW - Engagement KW - Students KW - Knowledge KW - Work place UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556291728?accountid=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=Conflict+resolution+quarterly&rft.atitle=Two+perspectives+on+learning+the+organizational+ombudsman+role&rft.au=Witzler%2C+Lisa%3BMyers%2C+Linda&rft.aulast=Witzler&rft.aufirst=Lisa&rft.date=2014-07-01&rft.volume=31&rft.issue=4&rft.spage=447&rft.isbn=&rft.btitle=&rft.title=Conflict+resolution+quarterly&rft.issn=15365581&rft_id=info:doi/10.1002%2Fcrq.21096 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-08-26 N1 - Last updated - 2014-08-27 N1 - SubjectsTermNotLitGenreText - 7278 12929 7073; 9030; 12334 4049; 7073; 4278; 13673 4214 DO - http://dx.doi.org/10.1002/crq.21096 ER - TY - JOUR T1 - The reflective observer model AN - 1556285924; 4591995 AB - The reflective observer (RO) model is a unique process that incorporates live observation by a trained observer of an ombudsman during a mediation session, followed by an in-depth debriefing between the ombudsman and the RO. The clinical goal is to explore cognitive schema used by the ombudsman in decision making during critical moments of the mediation and to describe the underrecognized rationale behind seemingly intuitive expertise. During the debriefing, the exploration is guided by a protocol specifically designed to elicit personal associations, as well as tactical decisions of the ombudsman not frequently addressed in ombudsman practice or training. While research on reflective practice is common among mediators (Bronson ), less research has focused on the impact of reflective practice on the work of ombudsmen. The RO model shows promise as a personal and professional developmental tool for ombudsmen and is a novel approach for both deeper learning as well as developing higher-order clinical interviewing skills. JF - Conflict resolution quarterly AU - Kathleen moore, J AD - US National Institutes of Health Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 403 EP - 419 VL - 31 IS - 4 SN - 1536-5581, 1536-5581 KW - Political Science KW - Decision making KW - Skills KW - Research methods KW - Training KW - Tactics KW - Conflict resolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556285924?accountid=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=Conflict+resolution+quarterly&rft.atitle=The+reflective+observer+model&rft.au=Kathleen+moore%2C+J&rft.aulast=Kathleen+moore&rft.aufirst=J&rft.date=2014-07-01&rft.volume=31&rft.issue=4&rft.spage=403&rft.isbn=&rft.btitle=&rft.title=Conflict+resolution+quarterly&rft.issn=15365581&rft_id=info:doi/10.1002%2Fcrq.21094 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-08-26 N1 - Last updated - 2014-08-27 N1 - SubjectsTermNotLitGenreText - 11713; 12483; 12894; 3322 6071 1542 11325; 10919; 2703 2698 DO - http://dx.doi.org/10.1002/crq.21094 ER - TY - JOUR T1 - Toward the activist ombudsman: an introduction AN - 1556284891; 4591994 AB - This introduction frames the articles in this mini-colloquy on the work of the Office of the Ombudsman at the National Institutes of Health, Center for Cooperative Resolution (OO/CCR). This office is unique in its size, experience, and approach to the work of the organizational ombudsman. Through this series of articles, we share our understandings of the potential for the role of the organizational conflict management specialists called ombudsmen and to assist other organizations and practitioners as they consider and enact similar roles within their workplaces. JF - Conflict resolution quarterly AU - Gadlin, Howard AD - National Institutes of Health Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 387 EP - 402 VL - 31 IS - 4 SN - 1536-5581, 1536-5581 KW - Political Science KW - Organizations KW - Cooperation KW - Conflict resolution KW - Institutions KW - Framing KW - Work place UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1556284891?accountid=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=Conflict+resolution+quarterly&rft.atitle=Toward+the+activist+ombudsman%3A+an+introduction&rft.au=Gadlin%2C+Howard&rft.aulast=Gadlin&rft.aufirst=Howard&rft.date=2014-07-01&rft.volume=31&rft.issue=4&rft.spage=387&rft.isbn=&rft.btitle=&rft.title=Conflict+resolution+quarterly&rft.issn=15365581&rft_id=info:doi/10.1002%2Fcrq.21099 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-08-26 N1 - Last updated - 2014-08-27 N1 - SubjectsTermNotLitGenreText - 2703 2698; 13673 4214; 9030; 2859; Framing; 6590 DO - http://dx.doi.org/10.1002/crq.21099 ER - TY - JOUR T1 - Phenol-soluble modulins - critical determinants of staphylococcal virulence AN - 1551645557; 20317181 AB - Phenol-soluble modulins (PSMs) are a recently discovered family of amphipathic, alpha-helical peptides that have multiple roles in staphylococcal pathogenesis and contribute to a large extent to the pathogenic success of virulent staphylococci, such as Staphylococcus aureus. PSMs may cause lysis of many human cell types including leukocytes and erythrocytes, stimulate inflammatory responses, and contribute to biofilm development. PSMs appear to have an original role in the commensal lifestyle of staphylococci, where they facilitate growth and spreading on epithelial surfaces. Aggressive, cytolytic PSMs seem to have evolved from that original role and are mainly expressed in highly virulent S. aureus. Here, we will review the biochemistry, genetics, and role of PSMs in the commensal and pathogenic lifestyles of staphylococci, discuss how diversification of PSMs defines the aggressiveness of staphylococcal species, and evaluate potential avenues to target PSMs for drug development against staphylococcal infections. Phenol-soluble modulins are newly recognized peptide toxins that define the virulence potential of Staphylococcus aureus and other staphylococci. JF - FEMS Microbiology Reviews AU - Cheung, Gordon YC AU - Joo, Hwang-Soo AU - Chatterjee, Som S AU - Otto, Michael AD - Pathogen Molecular Genetics Section Laboratory of Human Bacterial Pathogenesis. National Institute of Allergy and Infectious DiseasesThe National Institutes of Health Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 698 EP - 719 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 38 IS - 4 SN - 0168-6445, 0168-6445 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - Virulence KW - Spreading KW - Erythrocytes KW - Leukocytes KW - Commensals KW - Drug development KW - Biofilms KW - Staphylococcus aureus KW - Infection KW - Toxins KW - Inflammation KW - A 01450:Environmental Pollution & Waste Treatment KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551645557?accountid=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=Phenol-soluble+modulins+-+critical+determinants+of+staphylococcal+virulence&rft.au=Cheung%2C+Gordon+YC%3BJoo%2C+Hwang-Soo%3BChatterjee%2C+Som+S%3BOtto%2C+Michael&rft.aulast=Cheung&rft.aufirst=Gordon&rft.date=2014-07-01&rft.volume=38&rft.issue=4&rft.spage=698&rft.isbn=&rft.btitle=&rft.title=FEMS+Microbiology+Reviews&rft.issn=01686445&rft_id=info:doi/10.1111%2F1574-6976.12057 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Virulence; Spreading; Leukocytes; Erythrocytes; Commensals; Drug development; Biofilms; Infection; Toxins; Inflammation; Staphylococcus aureus DO - http://dx.doi.org/10.1111/1574-6976.12057 ER - TY - JOUR T1 - Clinicopathological correlates of Gli1 expression in a population-based cohort of patients with newly diagnosed bladder cancer. AN - 1549199396; 24856810 AB - Dysregulation of the hedgehog signaling pathway has been linked to the development and progression of a variety of different human tumors including cancers of the skin, brain, colon, prostate, blood, and pancreas. We assessed the clinicopathological factors that are potentially related to expression of Gli1, the transcription factor that is thought to be the most reliable marker of hedgehog pathway activation in bladder cancer. Bladder cancer cases were identified from the New Hampshire State Cancer Registry as histologically confirmed primary bladder cancer diagnosed between January 1, 2002, and July 31, 2004. Immunohistochemical analysis was performed on a tissue microarray to detect Gli1 and p53 expression in these bladder tumors. We computed odds ratios (ORs) and their 95% CIs for Gli1 positivity for pathological category using T category (from TNM), invasiveness, and grade with both the World Health Organization 1973 and World Health Organization International Society of Urological Pathology criteria. We calculated hazard ratios and their 95% CI for Gli1 positivity and recurrence for both Ta-category and invasive bladder tumors (T1+). A total of 194 men and 67 women, whose tumors were assessable for Gli1 staining, were included in the study. No appreciable differences in Gli1 staining were noted by sex, age, smoking status, or high-risk occupation. Ta-category tumors were more likely to stain for Gli1 as compared with T1-category tumors (adjusted OR = 0.38, CI: 0.17-0.87). Similarly, low-grade (grades 1-2) tumors were more likely to stain for Gli1 as compared with high-grade tumors (grade 3) (adjusted OR = 0.44, CI: 0.21-0.93). In a Cox proportional hazards regression analysis, non-muscle-invasive bladder tumors expressing Gli1 were less likely to recur (adjusted hazard ratio = 0.48; CI: 0.28-0.82; P<0.05) than those in which Gli1 was absent. Our findings indicate that Gli1 expression may be a marker of low-stage, low-grade bladder tumors and an indicator of a reduced risk of recurrence in this group. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Urologic oncology AU - Sverrisson, Einar F AU - Zens, Michael S AU - Fei, Dennis Liang AU - Andrews, Angeline AU - Schned, Alan AU - Robbins, David AU - Kelsey, Karl T AU - Li, Hua AU - DiRenzo, James AU - Karagas, Margaret R AU - Seigne, John D AD - Department of Surgery (Urology), Dartmouth-Hitchcock Medical Center, Lebanon, NH. ; Department of Community and Family Medicine, Geisel School of Medicine at Dartmouth, Hanover, NH. ; Cancer Biology Section, National Institutes of Health, Bethesda, MD. ; Department of Pathology (Urology), Dartmouth-Hitchcock Medical Center, Lebanon, NH. ; Molecular Oncology Program, Department of Surgery, University of Miami, Miami, FL. ; Department of Community Health, Brown University, Providence, RI. ; Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, MD. ; Department of Pharmacology and Toxicology, Geisel School of Medicine at Dartmouth, Hanover, NH. ; Department of Surgery (Urology), Dartmouth-Hitchcock Medical Center, Lebanon, NH. Electronic address: john.d.seigne@hitchcock.org. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 539 EP - 545 VL - 32 IS - 5 KW - GLI1 protein, human KW - 0 KW - Hedgehog Proteins KW - TP53 protein, human KW - Transcription Factors KW - Tumor Suppressor Protein p53 KW - Zinc Finger Protein GLI1 KW - Index Medicus KW - Gli1 KW - Bladder neoplasm KW - Odds Ratio KW - Humans KW - Aged KW - Tumor Suppressor Protein p53 -- metabolism KW - Registries KW - Hedgehog Proteins -- metabolism KW - Tissue Array Analysis KW - Adult KW - Cohort Studies KW - Treatment Outcome KW - Middle Aged KW - Neoplasm Recurrence, Local KW - Time Factors KW - Immunohistochemistry KW - Female KW - Male KW - Proportional Hazards Models KW - Gene Expression Regulation, Neoplastic KW - Transcription Factors -- metabolism KW - Urinary Bladder Neoplasms -- metabolism KW - Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549199396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Urologic+oncology&rft.atitle=Clinicopathological+correlates+of+Gli1+expression+in+a+population-based+cohort+of+patients+with+newly+diagnosed+bladder+cancer.&rft.au=Sverrisson%2C+Einar+F%3BZens%2C+Michael+S%3BFei%2C+Dennis+Liang%3BAndrews%2C+Angeline%3BSchned%2C+Alan%3BRobbins%2C+David%3BKelsey%2C+Karl+T%3BLi%2C+Hua%3BDiRenzo%2C+James%3BKaragas%2C+Margaret+R%3BSeigne%2C+John+D&rft.aulast=Sverrisson&rft.aufirst=Einar&rft.date=2014-07-01&rft.volume=32&rft.issue=5&rft.spage=539&rft.isbn=&rft.btitle=&rft.title=Urologic+oncology&rft.issn=1873-2496&rft_id=info:doi/10.1016%2Fj.urolonc.2014.03.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-23 N1 - Date created - 2014-06-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer. 2002 May 1;94(9):2511-6 [12015777] Oncogene. 2002 Jul 25;21(32):4894-9 [12118368] Oncogene. 2003 May 15;22(19):2967-71 [12771948] Development. 1997 Jul;124(13):2537-52 [9216996] Am J Surg Pathol. 1998 Dec;22(12):1435-48 [9850170] J Cell Physiol. 2005 May;203(2):372-7 [15521068] Oncogene. 2005 Jun 9;24(25):4026-36 [15806168] J Urol. 2007 Dec;178(6):2314-30 [17993339] Cancer Res. 2010 Mar 1;70(5):1981-8 [20179202] J Mol Cell Biol. 2010 Apr;2(2):84-95 [20083481] J Urol. 2010 Jul;184(1):344-51 [20488474] Cancer Prev Res (Phila). 2010 Oct;3(10):1235-45 [20858759] Cell. 2011 Mar 4;144(5):646-74 [21376230] Br J Cancer. 2012 Mar 13;106(6):1177-86 [22361633] Pathol Oncol Res. 2012 Apr;18(2):349-55 [21861243] Cancer Res. 2012 Sep 1;72(17):4449-58 [22815529] Eur Urol. 2013 Jan;63(1):4-15 [23083902] Nat Rev Mol Cell Biol. 2013 Jul;14(7):416-29 [23719536] Urol Oncol. 2013 Aug;31(6):802-11 [21924649] Comment In: Urol Oncol. 2014 Jul;32(5):546-8 [24814405] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.urolonc.2014.03.006 ER - TY - JOUR T1 - Parenting in Fukushima City in the post-disaster period: short-term strategies and long-term perspectives AN - 1548777860; 4579960 AB - Growing evidence indicates the adverse psychological and welfare consequences of nuclear power accidents particularly among parents of small children. However, little has been published about the public health experiences of and practical countermeasures to deal with such consequences for parents of small children in the aftermath of disasters. Based on our past research efforts to develop parenting support programmes in Fukushima City, we describe here the discussions and resulting strategies that developed from collaborative efforts between university researchers and public health nurses after the Fukushima nuclear plant accident caused by the Great East Japan Earthquake. The processes presented here may be useful to improve national and international preparedness to protect the health of parents and children in future nuclear disasters. Reprinted by permission of Blackwell Publishers JF - Disasters AU - Goto, Aya AU - Reich, Michael R AU - Suzuki, Yuriko AU - Tsutomi, Hiroshi AU - Watanabe, Eiko AU - Yasumura, Seiji AD - Fukushima Medical University ; Harvard University ; National Institute of Mental Health ; University of Shizuoka Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - s179 EP - s189 VL - 38 IS - s2 SN - 0361-3666, 0361-3666 KW - Sociology KW - Parenting KW - Nurses KW - Nuclear accidents KW - Nuclear energy KW - Children KW - Japan KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548777860?accountid=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=Disasters&rft.atitle=Parenting+in+Fukushima+City+in+the+post-disaster+period%3A+short-term+strategies+and+long-term+perspectives&rft.au=Goto%2C+Aya%3BReich%2C+Michael+R%3BSuzuki%2C+Yuriko%3BTsutomi%2C+Hiroshi%3BWatanabe%2C+Eiko%3BYasumura%2C+Seiji&rft.aulast=Goto&rft.aufirst=Aya&rft.date=2014-07-01&rft.volume=38&rft.issue=s2&rft.spage=s179&rft.isbn=&rft.btitle=&rft.title=Disasters&rft.issn=03613666&rft_id=info:doi/10.1111%2Fdisa.12070 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-07-21 N1 - Last updated - 2014-07-29 N1 - SubjectsTermNotLitGenreText - 9183; 8759 4246; 8758 524; 2212; 10449 5772; 8806; 191 300 30 DO - http://dx.doi.org/10.1111/disa.12070 ER - TY - JOUR T1 - Web-based computational chemistry education with CHARMMing III: Reduction potentials of electron transfer proteins. AN - 1548638615; 25058418 AB - A module for fast determination of reduction potentials, E°, of redox-active proteins has been implemented in the CHARMM INterface and Graphics (CHARMMing) web portal (www.charmming.org). The free energy of reduction, which is proportional to E°, is composed of an intrinsic contribution due to the redox site and an environmental contribution due to the protein and solvent. Here, the intrinsic contribution is selected from a library of pre-calculated density functional theory values for each type of redox site and redox couple, while the environmental contribution is calculated from a crystal structure of the protein using Poisson-Boltzmann continuum electrostatics. An accompanying lesson demonstrates a calculation of E°. In this lesson, an ionizable residue in a [4Fe-4S]-protein that causes a pH-dependent E° is identified, and the E° of a mutant that would test the identification is predicted. This demonstration is valuable to both computational chemistry students and researchers interested in predicting sequence determinants of E° for mutagenesis. JF - PLoS computational biology AU - Perrin, B Scott AU - Miller, Benjamin T AU - Schalk, Vinushka AU - Woodcock, H Lee AU - Brooks, Bernard R AU - Ichiye, Toshiko AD - Laboratory of Computational Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Natural Sciences, New College of Florida, Sarasota, Florida, United States of America. ; Department of Chemistry, University of South Florida, Tampa, Florida, United States of America. ; Department of Chemistry, Georgetown University, Washington, D.C., United States of America. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 1 VL - 10 IS - 7 KW - Proteins KW - 0 KW - Index Medicus KW - Oxidation-Reduction KW - Thermodynamics KW - Computational Biology -- education KW - Proteins -- chemistry KW - Electron Transport KW - Computational Biology -- methods KW - Proteins -- metabolism KW - Internet UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548638615?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+computational+biology&rft.atitle=Web-based+computational+chemistry+education+with+CHARMMing+III%3A+Reduction+potentials+of+electron+transfer+proteins.&rft.au=Perrin%2C+B+Scott%3BMiller%2C+Benjamin+T%3BSchalk%2C+Vinushka%3BWoodcock%2C+H+Lee%3BBrooks%2C+Bernard+R%3BIchiye%2C+Toshiko&rft.aulast=Perrin&rft.aufirst=B&rft.date=2014-07-01&rft.volume=10&rft.issue=7&rft.spage=e1003739&rft.isbn=&rft.btitle=&rft.title=PLoS+computational+biology&rft.issn=1553-7358&rft_id=info:doi/10.1371%2Fjournal.pcbi.1003739 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-02 N1 - Date created - 2014-07-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10037-41 [11517324] Biophys J. 2001 Aug;81(2):601-13 [11463610] Biophys J. 2003 Nov;85(5):2818-29 [14581187] Biochemistry. 1986 Apr 8;25(7):1675-81 [3011070] Proc Natl Acad Sci U S A. 1991 Oct 15;88(20):9151-5 [1924378] J Biol Chem. 1991 Nov 15;266(32):21563-71 [1657971] Biophys J. 1996 Dec;71(6):2958-69 [8968568] J Chem Inf Model. 2008 Sep;48(9):1920-9 [18698840] J Comput Chem. 2009 Jul 30;30(10):1545-614 [19444816] Biophys J. 2010 Feb 17;98(4):560-8 [20159152] Proteins. 2010 Oct;78(13):2798-808 [20635418] J Comput Chem. 2013 Mar 15;34(7):576-82 [23115132] Biochemistry. 2013 May 7;52(18):3022-4 [23607577] J Biol Inorg Chem. 2013 Aug;18(6):599-608 [23690205] Acta Crystallogr D Biol Crystallogr. 1999 Nov;55(Pt 11):1773-84 [10531472] Biochemistry. 1999 Nov 9;38(45):14803-9 [10555962] Nucleic Acids Res. 2000 Jan 1;28(1):235-42 [10592235] Biochemistry. 2003 Aug 26;42(33):9829-40 [12924932] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pcbi.1003739 ER - TY - JOUR T1 - A Conserved Hydrogen-Bonding Network of P2 bis-Tetrahydrofuran-Containing HIV-1 Protease Inhibitors (PIs) with a Protease Active-Site Amino Acid Backbone Aids in Their Activity against PI-Resistant HIV AN - 1547866920; 20207758 AB - In the present study, GRL008, a novel nonpeptidic human immunodeficiency virus type 1 (HIV-1) protease inhibitor (PI), and darunavir (DRV), both of which contain a P2-bis-tetrahydrofuranyl urethane (bis-THF) moiety, were found to exert potent antiviral activity (50% effective concentrations [EC50s], 0.029 and 0.002 mu M, respectively) against a multidrug-resistant clinical isolate of HIV-1 (HIVA02) compared to ritonavir (RTV; EC50, >1.0 mu M) and tipranavir (TPV; EC50, 0.364 mu M). Additionally, GRL008 showed potent antiviral activity against an HIV-1 variant selected in the presence of DRV over 20 passages (HIVDRVRP20), with a 2.6-fold increase in its EC50 (0.097 mu M) compared to its corresponding EC50 (0.038 mu M) against wild-type HIV-1NL4-3 (HIVWT). Based on X-ray crystallographic analysis, both GRL008 and DRV showed strong hydrogen bonds (H-bonds) with the backbone-amide nitrogen/carbonyl oxygen atoms of conserved active-site amino acids G27, D29, D30, and D30' of HIVA02 protease (PRA02) and wild-type PR in their corresponding crystal structures, while TPV lacked H-bonds with G27 and D30' due to an absence of polar groups. The P2' thiazolyl moiety of RTV showed two conformations in the crystal structure of the PRA02-RTV complex, one of which showed loss of contacts in the S2' binding pocket of PRA02, supporting RTV's compromised antiviral activity (EC50, >1 mu M). Thus, the conserved H-bonding network of P2-bis-THF-containing GRL008 with the backbone of G27, D29, D30, and D30' most likely contributes to its persistently greater antiviral activity against HIVWT, HIVA02, and HIVDRVRP20. JF - Antimicrobial Agents & Chemotherapy AU - Yedidi, Ravikiran S AU - Garimella, Harisha AU - Aoki, Manabu AU - Aoki-Ogata, Hiromi AU - Desai, Darshan V AU - Chang, Simon B AU - Davis, David A AU - Fyvie, W Sean AU - Kaufman, Joshua D AU - Smith, David W AD - Experimental Retrovirology Section, HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA, mitsuyah@helix.nih.gov. Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 3679 EP - 3688 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 58 IS - 7 SN - 0066-4804, 0066-4804 KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Clinical isolates KW - Amino acids KW - Drug resistance KW - Proteinase inhibitors KW - Antiviral activity KW - Oxygen KW - Ritonavir KW - Hydrogen bonding KW - Ionizing radiation KW - Human immunodeficiency virus 1 KW - Crystal structure KW - carbonyls KW - urethane KW - Conformation KW - Nitrogen KW - A 01340:Antibiotics & Antimicrobials KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547866920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=A+Conserved+Hydrogen-Bonding+Network+of+P2+bis-Tetrahydrofuran-Containing+HIV-1+Protease+Inhibitors+%28PIs%29+with+a+Protease+Active-Site+Amino+Acid+Backbone+Aids+in+Their+Activity+against+PI-Resistant+HIV&rft.au=Yedidi%2C+Ravikiran+S%3BGarimella%2C+Harisha%3BAoki%2C+Manabu%3BAoki-Ogata%2C+Hiromi%3BDesai%2C+Darshan+V%3BChang%2C+Simon+B%3BDavis%2C+David+A%3BFyvie%2C+W+Sean%3BKaufman%2C+Joshua+D%3BSmith%2C+David+W&rft.aulast=Yedidi&rft.aufirst=Ravikiran&rft.date=2014-07-01&rft.volume=58&rft.issue=7&rft.spage=3679&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.00107-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-07-01 N1 - Number of references - 36 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Clinical isolates; Amino acids; Drug resistance; Proteinase inhibitors; Antiviral activity; Oxygen; Hydrogen bonding; Ritonavir; Ionizing radiation; Crystal structure; urethane; carbonyls; Nitrogen; Conformation; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1128/AAC.00107-14 ER - TY - JOUR T1 - Breast cancer risk in older women: results from the NIH-AARP Diet and Health Study AN - 1547866051; 20116971 AB - Background: Divergent risk factors exist for premenopausal and postmenopausal breast cancers, but it is unclear whether differences by age exist among postmenopausal women. Methods: We examined relationships among 190,872 postmenopausal women, ages 50-71 years recruited during 1995-1996 for the NIH-AARP Diet and Health Study, in whom 7,384 incident invasive breast carcinomas were identified through 2006. Multivariable Cox regression hazard ratios (HRs) and 95 % confidence intervals (CIs) were estimated for breast cancer risk factors by age (50-59, 60-69, greater than or equal to 70 years). Results: The only factor showing significant statistical heterogeneity by age (p sub(het) = 0.001) was menopausal hormone therapy duration, but trends were apparent across all ages and the strongest association prevailed among women 60-69 years. Although other risk factors did not show statistically significant heterogeneity by age, we did observe attenuated relations for parity and late age at first birth among older women [e.g., HR for age at first birth greater than or equal to 30 vs. 20-24 = 1.62 (95 % CI 1.23-2.14) for women 50-59 years vs. 1.12 (0.96-1.31) for greater than or equal to 70 years]. In contrast, risk estimates associated with alcohol consumption and BMI tended to be slightly stronger among the oldest subjects [e.g., HR for BMI greater than or equal to 35 vs. 18.5-24.9 = 1.24 (95 % CI 0.97-1.58) for 50-59 years vs. 1.46 (1.26-1.70) for greater than or equal to 70 years]. These differences were somewhat more pronounced for estrogen receptor positive and ductal cancers, tumors predominating among older women. Breast cancer family history, physical activity, and previous breast biopsies did not show divergent associations by age. Conclusion: Although breast cancer risk factor differences among older women were not large, they may merit further consideration with respect to individualized risk prediction. JF - Cancer Causes & Control AU - Brinton, Louise A AU - Smith, Llewellyn AU - Gierach, Gretchen L AU - Pfeiffer, Ruth M AU - Nyante, Sarah J AU - Sherman, Mark E AU - Park, Yikyung AU - Hollenbeck, Albert R AU - Dallal, Cher M AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, 20892, USA, brinton@nih.gov Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 843 EP - 857 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 25 IS - 7 SN - 0957-5243, 0957-5243 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Prediction KW - Diets KW - Alcohol KW - Estrogens KW - Age KW - Physical activity KW - Body mass KW - Hormones KW - Genetics KW - Health risks KW - Post-menopause KW - Risk factors KW - Breast cancer KW - Females 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/1547866051?accountid=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+risk+in+older+women%3A+results+from+the+NIH-AARP+Diet+and+Health+Study&rft.au=Brinton%2C+Louise+A%3BSmith%2C+Llewellyn%3BGierach%2C+Gretchen+L%3BPfeiffer%2C+Ruth+M%3BNyante%2C+Sarah+J%3BSherman%2C+Mark+E%3BPark%2C+Yikyung%3BHollenbeck%2C+Albert+R%3BDallal%2C+Cher+M&rft.aulast=Brinton&rft.aufirst=Louise&rft.date=2014-07-01&rft.volume=25&rft.issue=7&rft.spage=843&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-014-0385-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-07-01 N1 - Number of references - 45 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Diets; Prediction; Alcohol; Age; Estrogens; Body mass; Physical activity; Hormones; Health risks; Genetics; Post-menopause; Risk factors; Breast cancer; Females DO - http://dx.doi.org/10.1007/s10552-014-0385-3 ER - TY - JOUR T1 - African Green Monkeys Recapitulate the Clinical Experience with Replication of Live Attenuated Pandemic Influenza Virus Vaccine Candidates AN - 1547865520; 20207856 AB - Live attenuated cold-adapted (ca) H5N1, H7N3, H6N1, and H9N2 influenza vaccine viruses replicated in the respiratory tract of mice and ferrets, and 2 doses of vaccines were immunogenic and protected these animals from challenge infection with homologous and heterologous wild-type (wt) viruses of the corresponding subtypes. However, when these vaccine candidates were evaluated in phase I clinical trials, there were inconsistencies between the observations in animal models and in humans. The vaccine viruses did not replicate well and immune responses were variable in humans, even though the study subjects were seronegative with respect to the vaccine viruses before vaccination. Therefore, we sought a model that would better reflect the findings in humans and evaluated African green monkeys (AGMs) as a nonhuman primate model. The distribution of sialic acid (SA) receptors in the respiratory tract of AGMs was similar to that in humans. We evaluated the replication of wt and ca viruses of avian influenza (AI) virus subtypes H5N1, H6N1, H7N3, and H9N2 in the respiratory tract of AGMs. All of the wt viruses replicated efficiently, while replication of the ca vaccine viruses was restricted to the upper respiratory tract. Interestingly, the patterns and sites of virus replication differed among the different subtypes. We also evaluated the immunogenicity and protective efficacy of H5N1, H6N1, H7N3, and H9N2 ca vaccines. Protection from wt virus challenge correlated well with the level of serum neutralizing antibodies. Immune responses were slightly better when vaccine was delivered by both intranasal and intratracheal delivery than when it was delivered intranasally by sprayer. We conclude that live attenuated pandemic influenza virus vaccines replicate similarly in AGMs and human subjects and that AGMs may be a useful model to evaluate the replication of ca vaccine candidates. IMPORTANCE Ferrets and mice are commonly used for preclinical evaluation of influenza vaccines. However, we observed significant inconsistencies between observations in humans and in these animal models. We used African green monkeys (AGMs) as a nonhuman primate (NHP) model for a comprehensive and comparative evaluation of pairs of wild-type and pandemic live attenuated influenza virus vaccines (pLAIV) representing four subtypes of avian influenza viruses and found that pLAIVs replicate similarly in AGMs and humans and that AGMs can be useful for evaluation of the protective efficacy of pLAIV. JF - Journal of Virology AU - Matsuoka, Yumiko AU - Suguitan, Amorsolo Jr AU - Orandle, Marlene AU - Paskel, Myeisha AU - Boonnak, Kobporn AU - Gardner, Donald J AU - Feldmann, Friederike AU - Feldmann, Heinz AU - Marino, Michael AU - Jin, Hong AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, ksubbarao@niaid.nih.gov. Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 8139 EP - 8152 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 88 IS - 14 SN - 0022-538X, 0022-538X KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - Viruses KW - Animal models KW - Infection KW - Clinical trials KW - Influenza KW - pandemics KW - Mustela KW - Trachea KW - Respiratory tract KW - Replication KW - Sprays KW - Mice KW - Primates KW - Fowl plague KW - Antibodies KW - Influenza virus KW - Immunogenicity KW - Africa KW - Immune response KW - Vaccines KW - Sialic acids KW - V 22350:Immunology KW - H 1000:Occupational Safety and Health KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547865520?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=African+Green+Monkeys+Recapitulate+the+Clinical+Experience+with+Replication+of+Live+Attenuated+Pandemic+Influenza+Virus+Vaccine+Candidates&rft.au=Matsuoka%2C+Yumiko%3BSuguitan%2C+Amorsolo+Jr%3BOrandle%2C+Marlene%3BPaskel%2C+Myeisha%3BBoonnak%2C+Kobporn%3BGardner%2C+Donald+J%3BFeldmann%2C+Friederike%3BFeldmann%2C+Heinz%3BMarino%2C+Michael%3BJin%2C+Hong&rft.aulast=Matsuoka&rft.aufirst=Yumiko&rft.date=2014-07-01&rft.volume=88&rft.issue=14&rft.spage=8139&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.00425-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-07-01 N1 - Number of references - 64 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Replication; Animal models; Infection; Clinical trials; Fowl plague; pandemics; Antibodies; Immunogenicity; Vaccines; Immune response; Trachea; Sialic acids; Respiratory tract; Influenza; Sprays; Viruses; Mice; Primates; Influenza virus; Mustela; Africa DO - http://dx.doi.org/10.1128/JVI.00425-14 ER - TY - JOUR T1 - Inclusion of a universal tetanus toxoid CD4+ T cell epitope P2 significantly enhanced the immunogenicity of recombinant rotavirus Delta VP8* subunit parenteral vaccines AN - 1547856102; 20297679 AB - Currently available live oral rotavirus vaccines, Rotarix registered and RotaTeq registered , are highly efficacious in developed countries. However, the immunogenicity and efficacy of such vaccines in some developing countries are low. We reported previously that bacterially-expressed rotavirus Delta VP8* subunit vaccine candidates with P[8], P[4] or P[6] specificity elicited high-titer virus neutralizing antibodies in animals immunized intramuscularly. Of note was the finding that antibodies induced with the P[8] Delta VP8* vaccine neutralized both homotypic P[8] and heterotypic P[4] rotavirus strains to high titer. To further improve its vaccine potential, a tetanus toxoid universal CD4+ T cell epitope P2 was introduced into P[8] or P[6] Delta VP8* construct. The resulting recombinant fusion proteins expressed in were of high solubility and were produced with high yield. Two doses (10 or 20 mu g/dose) of the P2-P[8] Delta VP8* vaccine or P2-P[6] Delta VP8* vaccine with aluminum phosphate adjuvant elicited significantly higher geometric mean homologous neutralizing antibody titers than the vaccines without P2 in intramuscularly immunized guinea pigs. Interestingly, high levels of neutralizing antibody responses induced in guinea pigs with 3 doses of the P2-P[8] Delta VP8* vaccine persisted for at least 6 months. Furthermore, in the gnotobiotic piglet challenge study, three intramuscular doses (50 mu g/dose) of the P2-P[8] Delta VP8* vaccine with aluminum phosphate adjuvant significantly delayed the onset of diarrhea and significantly reduced the duration of diarrhea and the cumulative diarrhea score after oral challenge with virulent human rotavirus Wa (G1P[8]) strain. The P2-P[8] Delta VP8* vaccine induced serum virus neutralizing antibody and VP4-specific IgG antibody production prechallenge, and primed the pigs for higher antibody and intestinal and systemic virus-specific IFN- gamma producing CD4+ T cell responses postchallenge. These two subunit vaccines could be used at a minimum singly or preferably in bivalent formulation to provide antigenic coverage of most of the G types of global importance. JF - Vaccine AU - Wen, Xiaobo AU - Wen, Ke AU - Cao, Dianjun AU - Li, Guohua AU - Jones, Ronald W AU - Li, Jianping AU - Szu, Shousun AU - Hoshino, Yasutaka AU - Yuan, Lijuan AD - Rotavirus Vaccine Development Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 4420 EP - 4427 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 32 IS - 35 SN - 0264-410X, 0264-410X KW - Virology & AIDS Abstracts; Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Human rotavirus KW - Subunit vaccine KW - T cell epitope KW - Immunogenicity KW - Protective efficacy KW - Diarrhea KW - Gnotobiotic pigs KW - gamma -Interferon KW - Solubility KW - Adjuvants KW - Tetanus KW - CD4 antigen KW - Phosphate KW - Aluminum KW - Lymphocytes T KW - Intestine KW - Gnotobiotics KW - Immunoglobulin G KW - Fusion protein KW - Vaccines KW - Developing countries KW - Epitopes KW - V 22350:Immunology KW - F 06905:Vaccines KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547856102?accountid=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=Vaccine&rft.atitle=Inclusion+of+a+universal+tetanus+toxoid+CD4%2B+T+cell+epitope+P2+significantly+enhanced+the+immunogenicity+of+recombinant+rotavirus+Delta+VP8*+subunit+parenteral+vaccines&rft.au=Wen%2C+Xiaobo%3BWen%2C+Ke%3BCao%2C+Dianjun%3BLi%2C+Guohua%3BJones%2C+Ronald+W%3BLi%2C+Jianping%3BSzu%2C+Shousun%3BHoshino%2C+Yasutaka%3BYuan%2C+Lijuan&rft.aulast=Wen&rft.aufirst=Xiaobo&rft.date=2014-07-01&rft.volume=32&rft.issue=35&rft.spage=4420&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2014.06.060 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-07-01 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - gamma -Interferon; Diarrhea; Solubility; Adjuvants; Tetanus; CD4 antigen; Phosphate; Immunogenicity; Aluminum; Immunoglobulin G; Gnotobiotics; Intestine; Lymphocytes T; Vaccines; Fusion protein; Developing countries; Epitopes; Human rotavirus DO - http://dx.doi.org/10.1016/j.vaccine.2014.06.060 ER - TY - JOUR T1 - Chlamydia trachomatis Polymorphic Membrane Protein D Is a Virulence Factor Involved in Early Host-Cell Interactions AN - 1547852776; 20296413 AB - Chlamydia trachomatis is an obligate intracellular mucosotropic pathogen of significant medical importance. It is the etiological agent of blinding trachoma and bacterial sexually transmitted diseases, infections that afflict hundreds of millions of people globally. The C. trachomatis polymorphic membrane protein D (PmpD) is a highly conserved autotransporter and the target of broadly cross-reactive neutralizing antibodies; however, its role in host-pathogen interactions is unknown. Here we employed a targeted reverse genetics approach to generate a pmpD null mutant that was used to define the role of PmpD in the pathogenesis of chlamydial infection. We show that pmpD is not an essential chlamydial gene and the pmpD null mutant has no detectable deficiency in cultured murine cells or in a murine mucosal infection model. Notably, however, the pmpD null mutant was significantly attenuated for macaque eyes and cultured human cells. A reduction in pmpD null infection of human endocervical cells was associated with a deficiency in chlamydial attachment to cells. Collectively, our results show that PmpD is a chlamydial virulence factor that functions in early host-cell interactions. This study is the first of its kind using reverse genetics to evaluate the contribution of a C. trachomatis gene to disease pathogenesis. JF - Infection and Immunity AU - Kari, Laszlo AU - Southern, Timothy R AU - Downey, Carey J AU - Watkins, Heather S AU - Randall, Linnell B AU - Taylor, Lacey D AU - Sturdevant, Gail L AU - Whitmire, William M AU - Caldwell, Harlan D Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 2756 EP - 2762 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 82 IS - 7 SN - 0019-9567, 0019-9567 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - virulence factors KW - Sexually-transmitted diseases KW - Macaca KW - Mucosa KW - Animal models KW - Chlamydia trachomatis KW - Medical importance KW - Membrane proteins KW - Pathogens KW - Infection KW - Trachoma KW - Antibodies KW - Host-pathogen interactions KW - J 02410:Animal Diseases KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547852776?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Chlamydia+trachomatis+Polymorphic+Membrane+Protein+D+Is+a+Virulence+Factor+Involved+in+Early+Host-Cell+Interactions&rft.au=Kari%2C+Laszlo%3BSouthern%2C+Timothy+R%3BDowney%2C+Carey+J%3BWatkins%2C+Heather+S%3BRandall%2C+Linnell+B%3BTaylor%2C+Lacey+D%3BSturdevant%2C+Gail+L%3BWhitmire%2C+William+M%3BCaldwell%2C+Harlan+D&rft.aulast=Kari&rft.aufirst=Laszlo&rft.date=2014-07-01&rft.volume=82&rft.issue=7&rft.spage=2756&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.01686-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-07-01 N1 - Number of references - 34 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Antibodies; Sexually-transmitted diseases; virulence factors; Host-pathogen interactions; Mucosa; Animal models; Medical importance; Pathogens; Membrane proteins; Infection; Trachoma; Macaca; Chlamydia trachomatis DO - http://dx.doi.org/10.1128/IAI.01686-14 ER - TY - JOUR T1 - Structural insight into exosite binding and discovery of novel exosite inhibitors of botulinum neurotoxin serotype A through in silico screening. AN - 1545417329; 24958623 AB - Botulinum neurotoxin serotype A (BoNT/A) is the most lethal toxin among the Tier 1 Select Agents. Development of potent and selective small molecule inhibitors against BoNT/A zinc metalloprotease remains a challenging problem due to its exceptionally large substrate binding surface and conformational plasticity. The exosites of the catalytic domain of BoNT/A are intriguing alternative sites for small molecule intervention, but their suitability for inhibitor design remains largely unexplored. In this study, we employed two recently identified exosite inhibitors, D-chicoric acid and lomofungin, to probe the structural features of the exosites and molecular mechanisms of synergistic inhibition. The results showed that D-chicoric acid favors binding at the α-exosite, whereas lomofungin preferentially binds at the β-exosite by mimicking the substrate β-sheet binding interaction. Molecular dynamics simulations and binding interaction analysis of the exosite inhibitors with BoNT/A revealed key elements and hotspots that likely contribute to the inhibitor binding and synergistic inhibition. Finally, we performed database virtual screening for novel inhibitors of BoNT/A targeting the exosites. Hits C1 and C2 showed non-competitive inhibition and likely target the α- and β-exosites, respectively. The identified exosite inhibitors may provide novel candidates for structure-based development of therapeutics against BoNT/A intoxication. JF - Journal of computer-aided molecular design AU - Hu, Xin AU - Legler, Patricia M AU - Southall, Noel AU - Maloney, David J AU - Simeonov, Anton AU - Jadhav, Ajit AD - NIH Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, MD, 20850, USA, hux61@mail.nih.gov. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 765 EP - 778 VL - 28 IS - 7 KW - Caffeic Acids KW - 0 KW - Phenazines KW - Succinates KW - lomofungin KW - 26786-84-5 KW - chicoric acid KW - 70831-56-0 KW - Botulinum Toxins, Type A KW - EC 3.4.24.69 KW - Index Medicus KW - Computer Simulation KW - Humans KW - Molecular Dynamics Simulation KW - Molecular Conformation KW - Protein Binding KW - Binding Sites KW - Caffeic Acids -- chemistry KW - Botulinum Toxins, Type A -- toxicity KW - Botulinum Toxins, Type A -- antagonists & inhibitors KW - Phenazines -- chemistry KW - Succinates -- chemistry KW - Structure-Activity Relationship KW - Botulinum Toxins, Type A -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1545417329?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+computer-aided+molecular+design&rft.atitle=Structural+insight+into+exosite+binding+and+discovery+of+novel+exosite+inhibitors+of+botulinum+neurotoxin+serotype+A+through+in+silico+screening.&rft.au=Hu%2C+Xin%3BLegler%2C+Patricia+M%3BSouthall%2C+Noel%3BMaloney%2C+David+J%3BSimeonov%2C+Anton%3BJadhav%2C+Ajit&rft.aulast=Hu&rft.aufirst=Xin&rft.date=2014-07-01&rft.volume=28&rft.issue=7&rft.spage=765&rft.isbn=&rft.btitle=&rft.title=Journal+of+computer-aided+molecular+design&rft.issn=1573-4951&rft_id=info:doi/10.1007%2Fs10822-014-9758-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-30 N1 - Date created - 2014-07-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Rev Drug Discov. 2005 Apr;4(4):281-97 [15803193] Nature. 2004 Dec 16;432(7019):925-9 [15592454] J Biol Chem. 2007 Mar 30;282(13):9621-7 [17244603] Chem Biol. 2007 May;14(5):533-42 [17524984] Bioorg Med Chem Lett. 2007 Dec 1;17(23):6463-6 [17951059] Crit Rev Immunol. 2007;27(4):303-18 [18197811] J Biol Chem. 2008 Jul 4;283(27):18883-91 [18434312] Protein J. 2008 Apr;27(3):151-62 [18213512] PLoS Pathog. 2008;4(9):e1000165 [18818739] Antimicrob Agents Chemother. 2009 Aug;53(8):3478-86 [19528275] Toxicon. 2009 Oct;54(5):550-60 [19268493] J Comput Chem. 2009 Dec;30(16):2785-91 [19399780] Arch Biochem Biophys. 2009 Nov;491(1-2):75-84 [19772855] Infect Immun. 2010 Feb;78(2):756-63 [19917718] J Am Chem Soc. 2010 Mar 10;132(9):2868-9 [20158239] J Mol Biol. 2010 Apr 9;397(4):1106-18 [20138889] PLoS One. 2010;5(4):e10129 [20405003] Biochemistry. 2011 May 17;50(19):4019-28 [21434688] FEBS J. 2011 Dec;278(23):4467-85 [21592305] Physiol Rev. 2000 Apr;80(2):717-66 [10747206] Biochimie. 2000 Sep-Oct;82(9-10):955-66 [11086225] Acc Chem Res. 2000 Dec;33(12):889-97 [11123888] JAMA. 2001 Feb 28;285(8):1059-70 [11209178] Biochemistry. 2002 Feb 12;41(6):1717-23 [11827515] Biochem Biophys Res Commun. 2003 Oct 10;310(1):84-93 [14511652] Annu Rev Pharmacol Toxicol. 2004;44:167-93 [14744243] Q Rev Biophys. 1995 Nov;28(4):423-72 [8771234] Biopolymers. 1996 Mar;38(3):305-20 [8906967] Nat Struct Biol. 1998 Oct;5(10):898-902 [9783750] Bioorg Med Chem. 2005 Jan 17;13(2):333-41 [15598556] Bioorg Med Chem. 2006 May 15;14(10):3583-91 [16458011] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10822-014-9758-7 ER - TY - JOUR T1 - Dietary intake of a plant phospholipid/lipid conjugate reduces lung cancer growth and tumor angiogenesis. AN - 1542652174; 24510111 AB - It is well recognized that early detection and cancer prevention are significant armaments in the 'war against cancer'. Changes in lifestyle and diet have significant impact on the global incidence of cancer. For over 30 years, many investigators have studied the concept of chemoprevention. More recently, with the demonstration that antiangiogenic activity reduces tumor growth, the concept of angioprevention has emerged as a novel strategy in the deterrence of cancer development (carcinogenesis). In this study, we utilized a fast growing, highly aggressive murine Lewis lung cancer model to examine the in vivo antitumor effects of a novel, dietary supplement, known as plant phospholipid/lipid conjugate (pPLC). Our goal was to determine if pPLC possessed direct antitumor activity with relatively little toxicity that could be developed as a chemoprevention therapy. We used pPLC directly in this in vivo model due to the lack of aqueous solubility of this novel formulation, which precludes in vitro experimentation. pPLC contains known antioxidants, ferulic acid and lipoic acid, as well as soy sterols, formulated in a unique aqueous-insoluble matrix. The pPLC dietary supplement was shown to suppress in vivo growth of this tumor model by 30%. We also demonstrated a significant decrease in tumor angiogenesis accompanied by increased apoptosis and present preliminary evidence of enhanced expression of the hypoxia-related genes pentraxin-3 and metallothionein-3, by 24.9-fold and 10.9-fold, respectively, compared with vehicle control. These findings lead us to propose using this plant phosolipid/lipid conjugate as a dietary supplement that may be useful in cancer prevention. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Shuman Moss, Laurie A AU - Jensen-Taubman, Sandra AU - Rubinstein, Danielle AU - Viole, Gary AU - Stetler-Stevenson, William G AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20895, USA, sstevenw@mail.nih.gov laurie.shumanmoss@nih.gov. ; Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20895, USA. ; Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20895, USA, Gettysburg College, Gettysburg, PA 17325, USA and. ; Conjugated Functional Foods, Hackensack, NJ 07601, USA. ; Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20895, USA, sstevenw@mail.nih.gov. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 1556 EP - 1563 VL - 35 IS - 7 KW - Biomarkers, Tumor KW - 0 KW - Lipids KW - Phospholipids KW - Plant Preparations KW - RNA, Messenger KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Animals KW - Biomarkers, Tumor -- genetics KW - Apoptosis KW - Oligonucleotide Array Sequence Analysis KW - Humans KW - Mice KW - Reverse Transcriptase Polymerase Chain Reaction KW - RNA, Messenger -- genetics KW - Cell Proliferation KW - Biomarkers, Tumor -- metabolism KW - Gene Expression Profiling KW - Blotting, Western KW - Tumor Cells, Cultured KW - Mice, Inbred C57BL KW - Female KW - Immunoenzyme Techniques KW - Phytotherapy KW - Plant Preparations -- therapeutic use KW - Phospholipids -- chemistry KW - Lipids -- chemistry KW - Carcinoma, Lewis Lung -- diet therapy KW - Carcinoma, Lewis Lung -- blood supply KW - Carcinoma, Lewis Lung -- pathology KW - Neovascularization, Pathologic -- prevention & control KW - Diet UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542652174?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dietary+intake+of+a+plant+phospholipid%2Flipid+conjugate+reduces+lung+cancer+growth+and+tumor+angiogenesis.&rft.au=Shuman+Moss%2C+Laurie+A%3BJensen-Taubman%2C+Sandra%3BRubinstein%2C+Danielle%3BViole%2C+Gary%3BStetler-Stevenson%2C+William+G&rft.aulast=Shuman+Moss&rft.aufirst=Laurie&rft.date=2014-07-01&rft.volume=35&rft.issue=7&rft.spage=1556&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu039 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-25 N1 - Date created - 2014-07-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Clin Nutr. 2008 Apr;87(4):993-1001 [18400724] Br J Nutr. 2007 Sep;98(3):550-5 [17459188] Clin Dermatol. 2008 Jul-Aug;26(4):358-63 [18691515] Nutr J. 2008;7:29 [18826565] Nutr Rev. 2008 Nov;66(11):646-57 [19019027] Eur J Immunol. 2009 Mar;39(3):843-57 [19224633] Eur J Clin Nutr. 2009 Jul;63(7):813-20 [19491917] Int J Cancer. 2009 Nov 1;125(9):1997-2003 [19551861] Blood. 2009 Sep 10;114(11):2359-60 [19745081] Biochim Biophys Acta. 2009 Oct;1790(10):1149-60 [19664690] J Cardiovasc Pharmacol. 2009 Nov;54(5):391-8 [19998523] Curr Pharm Des. 2010;16(7):877-83 [20388101] Neuroscience. 2010 Sep 15;169(4):1575-88 [20600667] Clin Cancer Res. 2011 Apr 15;17(8):2395-9 [21257721] Cancer Lett. 2011 Sep 28;308(2):172-80 [21624767] Mol Cancer Res. 2011 Jul;9(7):815-23 [21642390] Pharmacol Rep. 2011;63(4):849-58 [22001972] Odontology. 2012 Jul;100(2):215-21 [21932007] Nat Rev Clin Oncol. 2012 Sep;9(9):498-509 [22850752] Nutr Clin Pract. 2012 Oct;27(5):599-612 [22878362] Anticancer Res. 2013 Mar;33(3):965-74 [23482768] Nutr Cancer. 2000;37(2):140-4 [11142085] Blood. 2002 Sep 1;100(5):1551-8 [12176869] Behav Genet. 2002 Nov;32(6):435-43 [12467341] Carcinogenesis. 2003 Jan;24(1):25-9 [12538345] J Cell Physiol. 2003 Mar;194(3):325-40 [12548552] J Lipid Res. 2003 May;44(5):994-1000 [12611905] J Nutr. 2003 Jun;133(6):1937-42 [12771342] J Lab Clin Med. 2004 Apr;143(4):255-62 [15085084] J Nutr. 2004 May;134(5):1145-51 [15113961] Blood. 2004 Jul 1;104(1):92-9 [15031207] Nat Med. 2004 Jul;10(7):727-33 [15195087] Fed Proc. 1976 May 1;35(6):1332-8 [770206] Cancer Res. 1976 Jul;36(7 PT 2):2699-702 [1277177] Drug Metab Rev. 1998 May;30(2):245-75 [9606603] Lung Cancer. 1998 Jul;21(1):37-45 [9792052] J Agric Food Chem. 2006 Jul 26;54(15):5375-81 [16848520] Transl Res. 2007 Jan;149(1):22-30 [17196519] Mol Nutr Food Res. 2007 Feb;51(2):161-70 [17266177] Am J Physiol Cell Physiol. 2007 Mar;292(3):C987-95 [16943240] J Exp Med. 2007 Apr 16;204(4):793-804 [17389238] Curr Med Chem. 2008;15(11):1044-71 [18473802] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu039 ER - TY - JOUR T1 - Tumor suppressor PDCD4 inhibits NF-κB-dependent transcription in human glioblastoma cells by direct interaction with p65. AN - 1542650118; 24413684 AB - PDCD4 is a tumor suppressor induced by apoptotic stimuli that regulates both translation and transcription. Previously, we showed that overexpression of PDCD4 leads to decreased anchorage-independent growth in glioblastoma (GBM)-derived cell lines and decreased tumor growth in a GBM xenograft model. In inflammatory cells, PDCD4 stimulates tumor necrosis factor-induced activation of the transcription factor NF-κB, an oncogenic driver in many cancer sites. However, the effect of PDCD4 on NF-κB transcriptional activity in most cancers including GBM is still unknown. We studied the effect of PDCD4 on NF-κB-dependent transcriptional activity in GBM by stably overexpressing PDCD4 in U251 and LN229 cells. Stable PDCD4 expression inhibits NF-κB transcriptional activation measured by a luciferase reporter. The molecular mechanism by which PDCD4 inhibits NF-κB transcriptional activation does not involve inhibited expression of NF-κB p65 or p50 proteins. PDCD4 does not inhibit pathways upstream of NF-κB including the activation of IKKα and IKKβ kinases or degradation of IκBα, events needed for nuclear transport of p65 and p50. PDCD4 overexpression does inhibit localization of p65 but not p50 in the nucleus. PDCD4 protein interacts preferentially with p65 protein as shown by co-immunoprecipitation and confocal imaging. PDCD4 overexpression inhibits the mRNA expression of two NF-κB target genes in a p65-dependent manner. These results suggest that PDCD4 can significantly inhibit NF-κB activity in GBM cells by a mechanism that involves direct or indirect protein-protein interaction independent of the expected mRNA-selective translational inhibition. These findings offer novel opportunities for NF-κB-targeted interventions to prevent or treat cancer. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Hwang, Soon-Kyung AU - Baker, Alyson R AU - Young, Matthew R AU - Colburn, Nancy H AD - Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick National Laboratory, 1050 Boyles Street, Bldg 576, Rm 101, Frederick, MD 21702, USA police042@naver.com. ; Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute, Frederick National Laboratory, 1050 Boyles Street, Bldg 576, Rm 101, Frederick, MD 21702, USA. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 1469 EP - 1480 VL - 35 IS - 7 KW - Apoptosis Regulatory Proteins KW - 0 KW - NF-kappa B p50 Subunit KW - PDCD4 protein, human KW - RNA, Messenger KW - RNA-Binding Proteins KW - Transcription Factor RelA KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Cell Movement KW - Blotting, Western KW - Apoptosis KW - Tumor Cells, Cultured KW - Humans KW - Immunoprecipitation KW - Chromatin Immunoprecipitation KW - Transcription, Genetic KW - Reverse Transcriptase Polymerase Chain Reaction KW - RNA, Messenger -- genetics KW - Cell Proliferation KW - Gene Expression Regulation, Neoplastic KW - Glioblastoma -- genetics KW - Apoptosis Regulatory Proteins -- genetics KW - RNA-Binding Proteins -- metabolism KW - RNA-Binding Proteins -- genetics KW - Transcription Factor RelA -- metabolism KW - Transcription Factor RelA -- genetics KW - NF-kappa B p50 Subunit -- genetics KW - Glioblastoma -- pathology KW - Glioblastoma -- metabolism KW - Apoptosis Regulatory Proteins -- metabolism KW - NF-kappa B p50 Subunit -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542650118?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tumor+suppressor+PDCD4+inhibits+NF-%CE%BAB-dependent+transcription+in+human+glioblastoma+cells+by+direct+interaction+with+p65.&rft.au=Hwang%2C+Soon-Kyung%3BBaker%2C+Alyson+R%3BYoung%2C+Matthew+R%3BColburn%2C+Nancy+H&rft.aulast=Hwang&rft.aufirst=Soon-Kyung&rft.date=2014-07-01&rft.volume=35&rft.issue=7&rft.spage=1469&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-25 N1 - Date created - 2014-07-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1999 Nov 23;96(24):14037-42 [10570194] J Biol Chem. 2012 Dec 28;287(53):44164-72 [23135283] Cell. 2002 Apr;109 Suppl:S81-96 [11983155] J Dent Res. 2002 Dec;81(12):831-5 [12454097] Mol Cell Biol. 2003 Jan;23(1):26-37 [12482958] J Pathol. 2003 Aug;200(5):640-6 [12898601] Mol Cell Endocrinol. 2004 Feb 12;214(1-2):149-53 [15062553] Mol Cell Biol. 2004 May;24(9):3894-906 [15082783] Genes Dev. 2004 Sep 15;18(18):2195-224 [15371334] Oncogene. 2004 Sep 30;23(45):7484-93 [15334056] Oncogene. 2004 Oct 21;23(49):8135-45 [15361828] Mol Cell Biol. 1993 Dec;13(12):7358-63 [8246956] Gene. 1995 Dec 12;166(2):297-301 [8543179] Curr Opin Cell Biol. 1998 Apr;10(2):268-75 [9561852] Cancer Res. 2005 Jul 15;65(14):6034-41 [16024603] Mol Cell Biol. 2006 Feb;26(4):1297-306 [16449643] Cancer Cell. 2006 Mar;9(3):209-23 [16530705] Mol Cancer Ther. 2006 Apr;5(4):1041-9 [16648576] Oncogene. 2006 Oct 5;25(45):6101-12 [16682950] J Immunol. 2006 Dec 1;177(11):8095-102 [17114484] Oncol Rep. 2007 Jan;17(1):123-8 [17143488] Mol Cell Biol. 2007 Jan;27(1):147-56 [17060447] Oncogene. 2007 Jul 5;26(31):4550-62 [17297470] Cancer. 2007 Oct 15;110(8):1697-707 [17849461] Cancer Res. 2008 Mar 1;68(5):1254-60 [18296647] Oncogene. 2008 Aug 14;27(35):4820-9 [18427550] EMBO J. 2009 Feb 4;28(3):274-85 [19153607] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3148-53 [19204291] Clin Cancer Res. 2009 Mar 15;15(6):1915-22 [19276261] Cancer Res. 2009 Apr 1;69(7):3148-56 [19318582] Nat Immunol. 2010 Feb;11(2):141-7 [19946272] PLoS One. 2010;5(2):e9428 [20195534] Cold Spring Harb Perspect Biol. 2010 Jun;2(6):a000109 [20516126] Oncogene. 2010 Jul 8;29(27):3921-32 [20498644] Biochem Pharmacol. 2011 Feb 1;81(3):412-24 [21040711] J Biol Chem. 2011 Mar 4;286(9):7052-9 [21189258] Neuro Oncol. 2011 Jun;13(6):580-90 [21636706] PLoS One. 2011;6(8):e23837 [21887328] J Biol Chem. 2011 Dec 16;286(50):42855-62 [22033922] Oncogene. 2011 Dec 8;30(49):4864-73 [21643008] Mol Cell Biol. 2012 May;32(10):1818-29 [22431522] Nat Commun. 2012;3:976 [22864569] Oncogene. 2001 Feb 8;20(6):669-76 [11314000] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu008 ER - TY - JOUR T1 - Modulation of aryl hydrocarbon receptor (AHR)-dependent signaling by peroxisome proliferator-activated receptor β/δ (PPARβ/δ) in keratinocytes. AN - 1542649766; 24639079 AB - Whether peroxisome proliferator-activated receptor β/δ (PPARβ/δ) reduces skin tumorigenesis by altering aryl hydrocarbon receptor (AHR)-dependent activities was examined. Polycyclic aromatic hydrocarbons (PAH) increased expression of cytochrome P4501A1 (CYP1A1), CYP1B1 and phase II xenobiotic metabolizing enzymes in wild-type skin and keratinocytes. Surprisingly, this effect was not found in Pparβ/δ-null skin and keratinocytes. Pparβ/δ-null keratinocytes exhibited decreased AHR occupancy and histone acetylation on the Cyp1a1 promoter in response to a PAH compared with wild-type keratinocytes. Bisulfite sequencing of the Cyp1a1 promoter and studies using a DNA methylation inhibitor suggest that PPARβ/δ promotes demethylation of the Cyp1a1 promoter. Experiments with human HaCaT keratinocytes stably expressing shRNA against PPARβ/δ also support this conclusion. Consistent with the lower AHR-dependent activities in Pparβ/δ-null mice compared with wild-type mice, 7,12-dimethylbenz[a]anthracene (DMBA)-induced skin tumorigenesis was inhibited in Pparβ/δ-null mice compared with wild-type. Results from these studies demonstrate that PPARβ/δ is required to mediate complete carcinogenesis by DMBA. The mechanisms underlying this PPARβ/δ-dependent reduction of AHR signaling by PAH are not due to alterations in the expression of AHR auxiliary proteins, ligand binding or AHR nuclear translocation between genotypes, but are likely influenced by PPARβ/δ-dependent demethylation of AHR target gene promoters including Cyp1a1 that reduces AHR accessibility as shown by reduced promoter occupancy. This PPARβ/δ/AHR crosstalk is unique to keratinocytes and conserved between mice and humans. Published by Oxford University Press 2014. JF - Carcinogenesis AU - Borland, Michael G AU - Krishnan, Prasad AU - Lee, Christina AU - Albrecht, Prajakta P AU - Shan, Weiwei AU - Bility, Moses T AU - Marcus, Craig B AU - Lin, Jyh M AU - Amin, Shantu AU - Gonzalez, Frank J AU - Perdew, Gary H AU - Peters, Jeffrey M AD - Department of Veterinary and Biomedical Sciences and the Center of Molecular Toxicology and Carcinogenesis and The Graduate Program in Biochemistry, Microbiology, and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA. ; Department of Veterinary and Biomedical Sciences and the Center of Molecular Toxicology and Carcinogenesis and. ; Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, USA. ; Department of Pharmacology, Penn State Cancer Institute, The Pennsylvania State University, Milton S. Hershey Medical Center, Hershey, PA 17033, USA and. ; Laboratory of Metabolism, National Cancer Institute, Bethesda, MD 20892, USA. ; Department of Veterinary and Biomedical Sciences and the Center of Molecular Toxicology and Carcinogenesis and The Graduate Program in Biochemistry, Microbiology, and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA, jmp21@psu.edu. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 1602 EP - 1612 VL - 35 IS - 7 KW - Ahr protein, mouse KW - 0 KW - Basic Helix-Loop-Helix Transcription Factors KW - Carcinogens KW - PPAR delta KW - PPAR-beta KW - RNA, Messenger KW - Receptors, Aryl Hydrocarbon KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Animals KW - Cell Transformation, Neoplastic -- pathology KW - Dermis -- cytology KW - Humans KW - Cell Transformation, Neoplastic -- metabolism KW - Carcinogens -- toxicity KW - Skin Neoplasms -- pathology KW - Mice KW - Fibroblasts -- cytology KW - Reverse Transcriptase Polymerase Chain Reaction KW - RNA, Messenger -- genetics KW - Skin Neoplasms -- metabolism KW - Fibroblasts -- metabolism KW - Dermis -- metabolism KW - Mice, Knockout KW - Blotting, Western KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity KW - Cells, Cultured KW - Skin Neoplasms -- chemically induced KW - Cell Transformation, Neoplastic -- chemically induced KW - Chromatin Immunoprecipitation KW - Signal Transduction KW - Immunoenzyme Techniques KW - Female KW - PPAR delta -- physiology KW - Receptors, Aryl Hydrocarbon -- physiology KW - Basic Helix-Loop-Helix Transcription Factors -- physiology KW - Keratinocytes -- cytology KW - Keratinocytes -- metabolism KW - PPAR-beta -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542649766?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Modulation+of+aryl+hydrocarbon+receptor+%28AHR%29-dependent+signaling+by+peroxisome+proliferator-activated+receptor+%CE%B2%2F%CE%B4+%28PPAR%CE%B2%2F%CE%B4%29+in+keratinocytes.&rft.au=Borland%2C+Michael+G%3BKrishnan%2C+Prasad%3BLee%2C+Christina%3BAlbrecht%2C+Prajakta+P%3BShan%2C+Weiwei%3BBility%2C+Moses+T%3BMarcus%2C+Craig+B%3BLin%2C+Jyh+M%3BAmin%2C+Shantu%3BGonzalez%2C+Frank+J%3BPerdew%2C+Gary+H%3BPeters%2C+Jeffrey+M&rft.aulast=Borland&rft.aufirst=Michael&rft.date=2014-07-01&rft.volume=35&rft.issue=7&rft.spage=1602&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu067 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-25 N1 - Date created - 2014-07-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Cell Physiol. 2007 Nov;213(2):384-90 [17708532] Biochem Biophys Res Commun. 2007 Dec 28;364(4):896-901 [17963696] J Invest Dermatol. 2008 Feb;128(2):370-7 [17713572] Crit Rev Eukaryot Gene Expr. 2008;18(3):207-50 [18540824] Annu Rev Pharmacol Toxicol. 2013;53:401-26 [23294312] Biochem Pharmacol. 2000 Jan 1;59(1):65-85 [10605936] Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):779-82 [10639156] Science. 2000 Feb 18;287(5456):1262-5 [10678832] Mol Carcinog. 2000 Apr;27(4):298-307 [10747294] Mutat Res. 2008 Jul-Aug;659(1-2):40-8 [18407786] Mol Pharmacol. 2008 Nov;74(5):1429-42 [18687807] Carcinogenesis. 2008 Dec;29(12):2406-14 [18799709] Int J Oncol. 2009 Apr;34(4):1085-91 [19287966] Stress. 2009 May;12(3):193-205 [19051126] Biochemistry (Mosc). 2009 Jun;74(6):613-9 [19645665] Toxicol Sci. 2009 Oct;111(2):238-46 [19474220] Biochim Biophys Acta. 2009 Dec;1796(2):230-41 [19505534] Toxicol Sci. 2010 Jan;113(1):27-36 [19748995] Trends Endocrinol Metab. 2010 Jan;21(1):3-9 [19800253] Toxicol Lett. 2010 Apr 15;194(1-2):26-33 [20116417] Life Sci. 2010 Mar 27;86(13-14):493-8 [20153754] Mol Pharmacol. 2010 Sep;78(3):419-30 [20516370] Mol Pharmacol. 2010 Oct;78(4):608-16 [20631054] Mol Cancer Ther. 2010 Dec;9(12):3267-77 [21159610] PLoS One. 2011;6(1):e14629 [21304969] J Dermatol Sci. 2011 Apr;62(1):42-9 [21316925] Cancer Prev Res (Phila). 2011 Jun;4(6):860-70 [21367956] Cell Signal. 2011 Dec;23(12):2039-50 [21843636] Nat Rev Cancer. 2012 Mar;12(3):181-95 [22318237] Mol Cell Biol. 2012 Jun;32(11):2065-82 [22473992] Biochim Biophys Acta. 2012 Jul;1819(7):631 [22677544] Mol Cell Biol. 2000 Jul;20(14):5119-28 [10866668] Carcinogenesis. 2001 Jan;22(1):5-10 [11159734] J Cell Biol. 2001 Aug 20;154(4):799-814 [11514592] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):2613-8 [11867749] Arch Biochem Biophys. 2003 Jan 1;409(1):153-8 [12464254] Carcinogenesis. 2003 Feb;24(2):225-34 [12584171] Toxicol Lett. 2003 Sep 30;144(2):247-56 [12927368] J Invest Dermatol. 2004 Apr;122(4):971-83 [15102088] J Biol Chem. 2004 May 28;279(22):23719-27 [15033975] Cancer Lett. 2004 Oct 8;214(1):35-41 [15331171] Int J Cancer. 2004 Nov 1;112(2):179-83 [15352028] Cancer Res. 1982 Sep;42(9):3519-25 [6286109] Environ Health Perspect. 1983 Jan;47:255-68 [6825618] J Biol Chem. 1983 Apr 10;258(7):4590-8 [6403529] Cancer Invest. 1983;1(5):425-36 [6365275] Carcinogenesis. 1984 Mar;5(3):301-7 [6323045] Cancer Res. 1985 Nov;45(11 Pt 2):5656-62 [4053037] Carcinogenesis. 1986 Sep;7(9):1543-51 [3017601] Food Chem Toxicol. 1986 Jun-Jul;24(6-7):781-7 [3023216] Mol Pharmacol. 1988 Aug;34(2):229-37 [2842655] Carcinogenesis. 1989 Oct;10(10):1971-4 [2676227] Arch Biochem Biophys. 1991 Dec;291(2):284-90 [1659322] Arch Biochem Biophys. 1993 Aug 15;305(1):170-5 [8393644] Science. 1995 May 5;268(5211):722-6 [7732381] Methods Enzymol. 1995;254:3-20 [8531694] Drug Metab Dispos. 1998 Dec;26(12):1194-8 [9860927] Trends Genet. 1999 Jan;15(1):34-7 [10087932] Cancer Lett. 1999 Sep 1;143(2):199-204 [10503904] J Vet Med Sci. 2004 Nov;66(11):1377-86 [15585952] Chem Res Toxicol. 2004 Dec;17(12):1667-74 [15606143] J Biol Chem. 2005 Mar 11;280(10):9519-27 [15632134] Arch Pharm Res. 2005 Mar;28(3):249-68 [15832810] Arch Biochem Biophys. 2005 Jul 1;439(1):53-60 [15953582] Cell Death Differ. 2006 Jan;13(1):53-60 [16021179] Carcinogenesis. 2006 May;27(5):1105-12 [16418176] Cancer Res. 2006 Aug 1;66(15):7420-8 [16885337] Cell Signal. 2007 Jun;19(6):1163-71 [17254750] Proc Natl Acad Sci U S A. 2007 May 22;104(21):8851-6 [17502624] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu067 ER - TY - JOUR T1 - CRBP-1 expression in ovarian cancer: a potential therapeutic target. AN - 1542299828; 24982334 AB - Cellular retinol binding protein-1 regulates retinol bioavailability and contributes to cell differentiation maintenance, but its role in ovarian carcinogenesis remains uncertain. We investigated CRBP-1 expression in ovarian tumors and CRBP-1 signaling-regulated pathways. We performed immunohistochemistry, methylation-specific PCR, gene copy number analysis in ovarian tumors and proliferation/apoptosis evaluation, gene array, blot and real-time PCR in CRBP-1-transfected A2780 ovarian cancer cells. CRBP-1 expression was reduced or absent in G2 and G3 ovarian carcinomas. CRBP-1 silencing in 60% of G2 and 66.7% of G3 carcinomas was due to CRBP-1 promoter methylation. A2780 CRBP-1-transfected cells showed increased retinol-induced apoptosis, retinoid-induced reduced clonogenicity and down-regulation of proliferation and transcription genes, including AKT1, AKT3, EGFR, FOS, JUN, STAT1 and STAT5A. CRBP-1 loss in G2/G3 ovarian carcinomas and increased apoptotic susceptibility to retinoids in CRBP-1-transfected-A2780 cells suggest CRBP-1 screening as a target to ensure efficacy of an adjuvant retinoid therapy. Copyright© 2014 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved. JF - Anticancer research AU - Doldo, Elena AU - Costanza, Gaetana AU - Ferlosio, Amedeo AU - Passeri, Daniela AU - Bernardini, Sergio AU - Scioli, Maria Giovanna AU - Mazzaglia, Donatella AU - Agostinelli, Sara AU - Del Bufalo, Donatella AU - Czernobilsky, Bernard AU - Orlandi, Augusto AD - Anatomic Pathology, Department of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy. ; Department of Laboratory Medicine, Tor Vergata University of Rome, Rome, Italy. ; Experimental Chemotherapy Laboratory, Regina Elena National Cancer Institute, Rome, Italy. ; Patho-Lab Diagnostics, Ness-Zione, Israel. ; Anatomic Pathology, Department of Biomedicine and Prevention, Tor Vergata University of Rome, Rome, Italy orlandi@uniroma2.it. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 3303 EP - 3312 VL - 34 IS - 7 KW - Retinol-Binding Proteins, Cellular KW - 0 KW - Vitamin A KW - 11103-57-4 KW - Proteasome Endopeptidase Complex KW - EC 3.4.25.1 KW - Index Medicus KW - Retinol KW - apoptosis KW - ovarian tumor KW - gynecological cancer KW - retinol binding protein KW - Humans KW - Vitamin A -- pharmacology KW - Aged KW - Cell Line, Tumor KW - Cell Growth Processes -- genetics KW - Gene Expression Regulation, Neoplastic KW - Promoter Regions, Genetic KW - Tissue Array Analysis KW - Proteasome Endopeptidase Complex -- metabolism KW - DNA Methylation KW - Aged, 80 and over KW - Adult KW - MCF-7 Cells KW - Middle Aged KW - Gene Dosage KW - Immunohistochemistry KW - Signal Transduction KW - Female KW - Ovarian Neoplasms -- metabolism KW - Retinol-Binding Proteins, Cellular -- genetics KW - Ovarian Neoplasms -- genetics KW - Retinol-Binding Proteins, Cellular -- biosynthesis KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542299828?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anticancer+research&rft.atitle=CRBP-1+expression+in+ovarian+cancer%3A+a+potential+therapeutic+target.&rft.au=Doldo%2C+Elena%3BCostanza%2C+Gaetana%3BFerlosio%2C+Amedeo%3BPasseri%2C+Daniela%3BBernardini%2C+Sergio%3BScioli%2C+Maria+Giovanna%3BMazzaglia%2C+Donatella%3BAgostinelli%2C+Sara%3BDel+Bufalo%2C+Donatella%3BCzernobilsky%2C+Bernard%3BOrlandi%2C+Augusto&rft.aulast=Doldo&rft.aufirst=Elena&rft.date=2014-07-01&rft.volume=34&rft.issue=7&rft.spage=3303&rft.isbn=&rft.btitle=&rft.title=Anticancer+research&rft.issn=1791-7530&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-21 N1 - Date created - 2014-07-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Stable enhanced green fluorescent protein expression after differentiation and transplantation of reporter human induced pluripotent stem cells generated by AAVS1 transcription activator-like effector nucleases. AN - 1542009553; 24833591 AB - Human induced pluripotent stem (hiPS) cell lines with tissue-specific or ubiquitous reporter genes are extremely useful for optimizing in vitro differentiation conditions as well as for monitoring transplanted cells in vivo. The adeno-associated virus integration site 1 (AAVS1) locus has been used as a "safe harbor" locus for inserting transgenes because of its open chromatin structure, which permits transgene expression without insertional mutagenesis. However, it is not clear whether targeted transgene expression at the AAVS1 locus is always protected from silencing when driven by various promoters, especially after differentiation and transplantation from hiPS cells. In this paper, we describe a pair of transcription activator-like effector nucleases (TALENs) that enable more efficient genome editing than the commercially available zinc finger nuclease at the AAVS1 site. Using these TALENs for targeted gene addition, we find that the cytomegalovirus-immediate early enhancer/chicken β-actin/rabbit β-globin (CAG) promoter is better than cytomegalovirus 7 and elongation factor 1α short promoters in driving strong expression of the transgene. The two independent AAVS1, CAG, and enhanced green fluorescent protein (EGFP) hiPS cell reporter lines that we have developed do not show silencing of EGFP either in undifferentiated hiPS cells or in randomly and lineage-specifically differentiated cells or in teratomas. Transplanting cardiomyocytes from an engineered AAVS1-CAG-EGFP hiPS cell line in a myocardial infarcted mouse model showed persistent expression of the transgene for at least 7 weeks in vivo. Our results show that high-efficiency targeting can be obtained with open-source TALENs and that careful optimization of the reporter and transgene constructs results in stable and persistent expression in vitro and in vivo. ©AlphaMed Press. JF - Stem cells translational medicine AU - Luo, Yongquan AU - Liu, Chengyu AU - Cerbini, Trevor AU - San, Hong AU - Lin, Yongshun AU - Chen, Guokai AU - Rao, Mahendra S AU - Zou, Jizhong AD - NIH Center for Regenerative Medicine, Laboratory of Stem Cell Biology, National Institute of Arthritis, Musculoskeletal and Skin Diseases, Bethesda, Maryland, USA; Center for Molecular Medicine, Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA. ; NIH Center for Regenerative Medicine, Laboratory of Stem Cell Biology, National Institute of Arthritis, Musculoskeletal and Skin Diseases, Bethesda, Maryland, USA; Center for Molecular Medicine, Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA zouj2@mail.nih.gov. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 821 EP - 835 VL - 3 IS - 7 SN - 2157-6564, 2157-6564 KW - Actins KW - 0 KW - Peptide Elongation Factor 1 KW - enhanced green fluorescent protein KW - Green Fluorescent Proteins KW - 147336-22-9 KW - NADH Dehydrogenase KW - EC 1.6.99.3 KW - Deoxyribonucleases KW - EC 3.1.- KW - Index Medicus KW - Differentiation KW - Transplantation KW - Human induced pluripotent stem cells KW - Transcription activator-like effector nuclease (TALEN) KW - Genome editing KW - AAVS1 KW - Myocardial Infarction -- pathology KW - Animals KW - Myocardial Infarction -- surgery KW - Cell Lineage KW - Myocardium -- pathology KW - Cell Tracking KW - Gene Silencing KW - Humans KW - Myocardial Infarction -- genetics KW - Disease Models, Animal KW - Mice KW - Myocytes, Cardiac -- pathology KW - Myocardium -- metabolism KW - Myocytes, Cardiac -- transplantation KW - NADH Dehydrogenase -- genetics KW - Myocardial Infarction -- metabolism KW - Promoter Regions, Genetic KW - Actins -- genetics KW - Cells, Cultured KW - Cytomegalovirus -- genetics KW - NADH Dehydrogenase -- biosynthesis KW - Gene Expression Regulation KW - Time Factors KW - Peptide Elongation Factor 1 -- genetics KW - Myocytes, Cardiac -- metabolism KW - Induced Pluripotent Stem Cells -- metabolism KW - Transfection -- methods KW - Green Fluorescent Proteins -- biosynthesis KW - Transduction, Genetic KW - Induced Pluripotent Stem Cells -- transplantation KW - Genes, Reporter KW - Dependovirus -- genetics KW - Cell Differentiation KW - Deoxyribonucleases -- metabolism KW - Green Fluorescent Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542009553?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+translational+medicine&rft.atitle=Stable+enhanced+green+fluorescent+protein+expression+after+differentiation+and+transplantation+of+reporter+human+induced+pluripotent+stem+cells+generated+by+AAVS1+transcription+activator-like+effector+nucleases.&rft.au=Luo%2C+Yongquan%3BLiu%2C+Chengyu%3BCerbini%2C+Trevor%3BSan%2C+Hong%3BLin%2C+Yongshun%3BChen%2C+Guokai%3BRao%2C+Mahendra+S%3BZou%2C+Jizhong&rft.aulast=Luo&rft.aufirst=Yongquan&rft.date=2014-07-01&rft.volume=3&rft.issue=7&rft.spage=821&rft.isbn=&rft.btitle=&rft.title=Stem+cells+translational+medicine&rft.issn=21576564&rft_id=info:doi/10.5966%2Fsctm.2013-0212 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-07 N1 - Date created - 2014-06-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Virol. 2000 Aug;74(16):7671-7 [10906224] J Cell Biochem. 2012 Oct;113(10):3061-8 [22573568] Physiol Genomics. 2004 Feb 13;16(3):349-60 [14679301] Arch Virol. 1990;112(1-2):67-80 [2142416] Proc Natl Acad Sci U S A. 1996 Aug 20;93(17):9067-72 [8799155] Neuron. 1997 Oct;19(4):773-85 [9354325] Exp Neurol. 1998 Jan;149(1):28-41 [9454612] Trends Biotechnol. 2007 Jan;25(1):24-32 [17084475] Stem Cells Dev. 2007 Feb;16(1):167-76 [17348812] Nat Biotechnol. 2007 Dec;25(12):1477-82 [18037879] Stem Cells. 2008 Feb;26(2):496-504 [18024421] Stem Cell Res. 2007 Oct;1(1):9-24 [19383383] Cell Stem Cell. 2009 Jul 2;5(1):97-110 [19540188] Nat Biotechnol. 2009 Sep;27(9):851-7 [19680244] Genome Res. 2010 Aug;20(8):1133-42 [20508142] Annu Rev Phytopathol. 2010;48:419-36 [19400638] Am J Physiol Cell Physiol. 2010 Dec;299(6):C1234-49 [20844252] Nat Biotechnol. 2011 Feb;29(2):143-8 [21179091] Cell Res. 2011 Mar;21(3):518-29 [21243013] Nat Methods. 2011 May;8(5):424-9 [21478862] Blood. 2011 May 26;117(21):5561-72 [21411759] Nucleic Acids Res. 2011 Jul;39(12):e82 [21493687] Nat Biotechnol. 2011 Aug;29(8):731-4 [21738127] PLoS One. 2011;6(8):e23376 [21853122] Nat Protoc. 2012 Jan;7(1):171-92 [22222791] Stem Cells Dev. 2012 Jan 20;21(2):191-205 [21699412] Stem Cell Rev. 2012 Mar;8(1):100-15 [21671061] Proc Natl Acad Sci U S A. 2012 Jul 3;109(27):E1848-57 [22645348] J Virol. 2003 Aug;77(16):9000-7 [12885916] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.5966/sctm.2013-0212 ER - TY - JOUR T1 - Efficient generation of integration-free human induced pluripotent stem cells from keratinocytes by simple transfection of episomal vectors. AN - 1542009230; 24904173 AB - Keratinocytes represent an easily accessible cell source for derivation of human induced pluripotent stem (hiPS) cells, reportedly achieving higher reprogramming efficiency than fibroblasts. However, most studies utilized a retroviral or lentiviral method for reprogramming of keratinocytes, which introduces undesirable transgene integrations into the host genome. Moreover, current protocols of generating integration-free hiPS cells from keratinocytes are mostly inefficient. In this paper, we describe a more efficient, simple-to-use, and cost-effective method for generating integration-free hiPS cells from keratinocytes. Our improved method using lipid-mediated transfection achieved a reprogramming efficiency of ∼0.14% on average. Keratinocyte-derived hiPS cells showed no integration of episomal vectors, expressed stem cell-specific markers and possessed potentials to differentiate into all three germ layers by in vitro embryoid body formation as well as in vivo teratoma formation. To our knowledge, this represents the most efficient method to generate integration-free hiPS cells from keratinocytes. ©AlphaMed Press. JF - Stem cells translational medicine AU - Piao, Yulan AU - Hung, Sandy Shen-Chi AU - Lim, Shiang Y AU - Wong, Raymond Ching-Bong AU - Ko, Minoru S H AD - Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA; ; Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA; Centre for Eye Research Australia, Department of Ophthalmology, University of Melbourne, Australia; ; O'Brien Institute and University of Melbourne, Department of Surgery, St. Vincent's Hospital, Australia; ; Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA; Department of Systems Medicine, Sakaguchi Laboratory, Keio University School of Medicine, Shinjuku, Tokyo, Japan KoM@z7.keio.jp. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 787 EP - 791 VL - 3 IS - 7 SN - 2157-6564, 2157-6564 KW - Transcription Factors KW - 0 KW - Index Medicus KW - Lipid mediated transfection KW - Episomal vectors KW - Integration-free KW - Keratinocytes KW - Derivation of human induced pluripotent stem cells KW - Embryoid Bodies -- metabolism KW - Teratoma -- metabolism KW - Teratoma -- genetics KW - Coculture Techniques KW - Animals KW - Cellular Reprogramming KW - Humans KW - Cell Differentiation KW - Mice KW - Fibroblasts -- metabolism KW - Feeder Cells KW - Gene Expression Regulation, Developmental KW - Induced Pluripotent Stem Cells -- metabolism KW - Transfection -- methods KW - Transcription Factors -- metabolism KW - Plasmids -- genetics KW - Genetic Vectors KW - Keratinocytes -- metabolism KW - Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542009230?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+translational+medicine&rft.atitle=Efficient+generation+of+integration-free+human+induced+pluripotent+stem+cells+from+keratinocytes+by+simple+transfection+of+episomal+vectors.&rft.au=Piao%2C+Yulan%3BHung%2C+Sandy+Shen-Chi%3BLim%2C+Shiang+Y%3BWong%2C+Raymond+Ching-Bong%3BKo%2C+Minoru+S+H&rft.aulast=Piao&rft.aufirst=Yulan&rft.date=2014-07-01&rft.volume=3&rft.issue=7&rft.spage=787&rft.isbn=&rft.btitle=&rft.title=Stem+cells+translational+medicine&rft.issn=21576564&rft_id=info:doi/10.5966%2Fsctm.2013-0036 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-07 N1 - Date created - 2014-06-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2012 Jan 19;481(7381):295-305 [22258608] Stem Cells. 2011 Oct;29(10):1517-27 [21898682] Fertil Steril. 2012 Jun;97(6):1250-9 [22656305] Stem Cells Transl Med. 2013 Sep;2(9):715-25 [23884641] Gene. 1991 Dec 15;108(2):193-9 [1660837] Cell. 2007 Nov 30;131(5):861-72 [18035408] Science. 2007 Dec 21;318(5858):1917-20 [18029452] Nat Biotechnol. 2008 Nov;26(11):1276-84 [18931654] Science. 2009 May 8;324(5928):797-801 [19325077] PLoS One. 2009;4(9):e7076 [19763270] Nat Biotechnol. 2009 Nov;27(11):1033-7 [19826408] Cell Res. 2011 Mar;21(3):518-29 [21243013] PLoS One. 2011;6(4):e18293 [21494607] Nat Methods. 2011 May;8(5):409-12 [21460823] Nat Methods. 2011 May;8(5):424-9 [21478862] Nature. 2011 Jun 9;474(7350):225-9 [21654807] Biochem Biophys Res Commun. 2012 May 25;422(1):75-9 [22560904] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.5966/sctm.2013-0036 ER - TY - JOUR T1 - Mechanism and Significance of Cell Type-Dependent Neutralization of Flaviviruses AN - 1540231965; 20124367 AB - The production of neutralizing antibodies (NAbs) is a correlate of protection for many human vaccines, including currently licensed vaccines against flaviviruses. NAbs are typically measured using a plaque reduction neutralization test (PRNT). Despite its extensive use, parameters that impact the performance of the PRNT have not been investigated from a mechanistic perspective. The results of a recent phase IIb clinical trial of a tetravalent dengue virus (DENV) vaccine suggest that NAbs, as measured using a PRNT performed with Vero cells, do not correlate with protection. This surprising finding highlights the importance of understanding how well the PRNT captures the complexity of the NAb response to DENV. In this study, we demonstrated that the structural heterogeneity of flaviviruses arising from inefficient virion maturation impacts the results of neutralization assays in a cell type-dependent manner. Neutralization titers of several monoclonal antibodies were significantly reduced when assayed on Vero cells compared to Raji cells expressing DC-SIGNR. This pattern can be explained by differences in the efficiency with which partially mature flaviviruses attach to each cell type, rather than a differential capacity of antibody to block infection. Vero cells are poorly permissive to the fraction of virions that are most sensitive to neutralization. Analysis of sera from recipients of live-attenuated monovalent DENV vaccine candidates revealed a strong correlation between the sensitivity of serum antibodies to the maturation state of DENV and cell type-dependent patterns of neutralization. Cross-reactive patterns of neutralization may be underrepresented by the "gold-standard" PRNT that employs Vero cells. IMPORTANCE Cell type-dependent patterns of neutralization describe a differential capacity of antibodies to inhibit virus infection when assayed on multiple cellular substrates. In this study, we established a link between antibodies that neutralize infection in a cell type-dependent fashion and those sensitive to the maturation state of the flavivirus virion. We demonstrated that cell type-dependent neutralization reflects a differential capacity to measure neutralization of viruses that are incompletely mature. Partially mature virions that most efficiently bind maturation state-sensitive antibodies are poorly represented by assays typically used in support of flavivirus vaccine development. The selection of cellular substrate for neutralization assays may significantly impact evaluation of the neutralization potency of the polyclonal response. These data suggest that current assays do not adequately capture the full complexity of the neutralizing antibody response and may hinder the identification of correlates of protection following flavivirus vaccination. JF - Journal of Virology AU - Mukherjee, Swati AU - Dowd, Kimberly A AU - Manhart, Carolyn J AU - Ledgerwood, Julie E AU - Durbin, Anna P AU - Whitehead, Stephen S AU - Pierson, Theodore C AD - Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institutes of Health, Bethesda, Maryland, USA, piersontc@mail.nih.gov. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 7210 EP - 7220 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 88 IS - 13 SN - 0022-538X, 0022-538X KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Virology & AIDS Abstracts KW - Dengue virus KW - Virions KW - Virology KW - Data processing KW - Vero cells KW - Monoclonal antibodies KW - Viruses KW - Disease control KW - Antibody response KW - Infection KW - Clinical trials KW - Vaccination KW - Flavivirus KW - Antibodies KW - Viral diseases KW - Substrate preferences KW - Sexual maturity KW - Plaques KW - Vaccines KW - Q1 08484:Species interactions: parasites and diseases KW - V 22320:Replication KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1540231965?accountid=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=Mechanism+and+Significance+of+Cell+Type-Dependent+Neutralization+of+Flaviviruses&rft.au=Mukherjee%2C+Swati%3BDowd%2C+Kimberly+A%3BManhart%2C+Carolyn+J%3BLedgerwood%2C+Julie+E%3BDurbin%2C+Anna+P%3BWhitehead%2C+Stephen+S%3BPierson%2C+Theodore+C&rft.aulast=Mukherjee&rft.aufirst=Swati&rft.date=2014-07-01&rft.volume=88&rft.issue=13&rft.spage=7210&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.03690-13 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Number of references - 63 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Virology; Antibodies; Substrate preferences; Viral diseases; Monoclonal antibodies; Sexual maturity; Viruses; Disease control; Vaccines; Virions; Data processing; Vero cells; Plaques; Antibody response; Infection; Vaccination; Clinical trials; Dengue virus; Flavivirus DO - http://dx.doi.org/10.1128/JVI.03690-13 ER - TY - JOUR T1 - PET imaging of neuroinflammation in a rat traumatic brain injury model with radiolabeled TSPO ligand DPA-714 AN - 1540229425; 20130323 AB - Purpose: The inflammatory response in injured brain parenchyma after traumatic brain injury (TBI) is crucial in the pathological process. In order to follow microglia activation and neuroinflammation after TBI, we performed PET imaging in a rat model of TBI using super(18)F-labeled DPA-714, a ligand of the 18-kDa translocator protein (TSPO). Methods: TBI was induced in male SD rats by a controlled cortical impact. The success of the TBI model was confirmed by MRI. [ super(18)F]DPA-714 was synthesized using a slightly modified TRACERLab FX-FN module and an automated procedure. In vivo PET imaging was performed at different time points after surgery using an Inveon small-animal PET scanner. The specificity of [ super(18)F]DPA-714 was confirmed by a displacement study with an unlabeled competitive TSPO ligand, PK11195. Ex vivo autoradiography as well as immunofluorescence staining was carried out to confirm the in vivo PET results. Results: Both in vivo T sub(2)-weighted MR images and ex vivo TTC staining results revealed successful establishment of the TBI model. Compared with the sham-treated group, [ super(18)F]DPA-714 uptake was significantly higher in the injured brain area on PET images. Increased lesion-to-normal ratios of [ super(18)F]DPA-714 were observed in the brain of TBI rats on day 2 after surgery. Ratios peaked around day 6 (2.65 plus or minus 0.36) and then decreased gradually to nearly normal levels on day 28. The displacement study using PK11195 confirmed the specific binding of [ super(18)F]DPA-714 to TSPO. The results of ex vivo autoradiography were consistent with in vivo PET results. Immunofluorescence staining showed the time course of TSPO expression after TBI and the temporal and the spatial distribution of microglia in the damaged brain area. Conclusion: TSPO-targeted PET using [ super(18)F]DPA-714 as the imaging probe can be used to dynamically monitor the inflammatory response after TBI in a noninvasive manner. This method will not only facilitate a better understanding of the inflammatory process after TBI, but also provide a useful in vivo monitoring strategy for antiinflammation therapy of TBI. JF - European Journal of Nuclear Medicine and Molecular Imaging AU - Wang, Yu AU - Yue, Xuyi AU - Kiesewetter, Dale O AU - Niu, Gang AU - Teng, Gaojun AU - Chen, Xiaoyuan AD - Jiangsu Key Laboratory of Molecular Imaging and Functional Imaging, Department of Radiology, Zhongda Hospital, Medical School of Southeast University, Nanjing, 210009, China, niug@mail.nih.gov Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 1440 EP - 1449 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 41 IS - 7 SN - 1619-7070, 1619-7070 KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - Parenchyma KW - Neuroimaging KW - Spatial distribution KW - Magnetic resonance imaging KW - Brain KW - Animal models KW - Probes KW - Immunofluorescence KW - Autoradiography KW - Microglia KW - Inflammation KW - Surgery KW - Positron emission tomography KW - Nuclear medicine KW - Traumatic brain injury KW - W 30910:Imaging KW - N3 11145:Methodology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1540229425?accountid=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+neuroinflammation+in+a+rat+traumatic+brain+injury+model+with+radiolabeled+TSPO+ligand+DPA-714&rft.au=Wang%2C+Yu%3BYue%2C+Xuyi%3BKiesewetter%2C+Dale+O%3BNiu%2C+Gang%3BTeng%2C+Gaojun%3BChen%2C+Xiaoyuan&rft.aulast=Wang&rft.aufirst=Yu&rft.date=2014-07-01&rft.volume=41&rft.issue=7&rft.spage=1440&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-014-2727-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Number of references - 34 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Parenchyma; Neuroimaging; Spatial distribution; Magnetic resonance imaging; Probes; Animal models; Brain; Immunofluorescence; Microglia; Autoradiography; Inflammation; Surgery; Positron emission tomography; Nuclear medicine; Traumatic brain injury DO - http://dx.doi.org/10.1007/s00259-014-2727-5 ER - TY - JOUR T1 - Idiosyncratic drug-induced liver injury is associated with substantial morbidity and mortality within 6 months from onset. AN - 1539711230; 24681128 AB - Little is known about the incidence of drug-induced liver injury (DILI) and risk factors for adverse outcomes. We evaluated short-term outcomes of a large cohort of patients with DILI enrolled in an ongoing multicenter prospective study. Data were collected from 660 adults with definite, highly likely, or probable DILI. Regression methods were used to identify risk factors for early liver-related death or liver transplantation and chronic liver injury. Patients' median age was 51.4 years; 59.5% were female and 59.1% required hospitalization. Within 6 months of DILI onset, 30 patients received liver transplants (4.5%; 95% confidence interval [CI], 3.0%-6.1%) and 32 died (5%; 95% CI, 3.2%-6.5%); 53% of the deaths were liver related. Asian race, absence of itching, lung disease, low serum albumin levels, low platelet counts, and high serum levels of alanine aminotransferase and total bilirubin at presentation were independent risk factors for reduced times to liver-related death or liver transplantation (C-statistic = 0.87). At 6 months after DILI onset, 18.9% of the 598 evaluable subjects had persistent liver damage. African-American race, higher serum levels of alkaline phosphatase, and prior heart disease or malignancy requiring treatment were independent risk factors for chronic DILI (C-statistic = 0.71). Nearly 1 in 10 patients die or undergo liver transplantation within 6 months of DILI onset and nearly 1 in 5 of the remaining patients have evidence of persistent liver injury at 6 months. The profile of liver injury at presentation, initial severity, patient's race, and medical comorbidities are important determinants of the likelihood of death/transplantation or persistent liver injury within 6 months. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved. JF - Gastroenterology AU - Fontana, Robert J AU - Hayashi, Paul H AU - Gu, Jiezhun AU - Reddy, K Rajender AU - Barnhart, Huiman AU - Watkins, Paul B AU - Serrano, Jose AU - Lee, William M AU - Chalasani, Naga AU - Stolz, Andrew AU - Davern, Timothy AU - Talwakar, Jayant A AU - DILIN Network AD - Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan. Electronic address: rfontana@med.umich.edu. ; University of North Carolina, Chapel Hill, North Carolina. ; Duke Clinical Research Institute, Durham, North Carolina. ; Division of Gastroenterology and Hepatology, University of Pennsylvania, Philadelphia, Pennsylvania. ; Liver Disease Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. ; Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, Texas. ; Department of Medicine, Indiana University, Indianapolis, Indiana. ; University of Southern California, Los Angeles, California. ; California Pacific Medical Center, San Francisco, California. ; Mayo Clinic, Rochester, Minnesota. ; DILIN Network Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 96 EP - 108.e4 VL - 147 IS - 1 KW - Abridged Index Medicus KW - Index Medicus KW - Causality KW - Transplantation KW - Acute Liver Failure KW - Hepatotoxicity KW - United States KW - Prospective Studies KW - Survival Rate KW - Humans KW - Cohort Studies KW - Adult KW - Aged KW - Middle Aged KW - Time Factors KW - Male KW - Liver Transplantation KW - Female KW - Comorbidity KW - Chemical and Drug Induced Liver Injury -- mortality KW - Chemical and Drug Induced Liver Injury -- epidemiology KW - Chemical and Drug Induced Liver Injury -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1539711230?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=Idiosyncratic+drug-induced+liver+injury+is+associated+with+substantial+morbidity+and+mortality+within+6+months+from+onset.&rft.au=Fontana%2C+Robert+J%3BHayashi%2C+Paul+H%3BGu%2C+Jiezhun%3BReddy%2C+K+Rajender%3BBarnhart%2C+Huiman%3BWatkins%2C+Paul+B%3BSerrano%2C+Jose%3BLee%2C+William+M%3BChalasani%2C+Naga%3BStolz%2C+Andrew%3BDavern%2C+Timothy%3BTalwakar%2C+Jayant+A%3BDILIN+Network&rft.aulast=Fontana&rft.aufirst=Robert&rft.date=2014-07-01&rft.volume=147&rft.issue=1&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2014.03.045 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-30 N1 - Date created - 2014-06-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hepatology. 2001 Jan;33(1):123-30 [11124828] Hepatology. 2002 Aug;36(2):451-5 [12143055] Ann Intern Med. 2002 Dec 17;137(12):947-54 [12484709] Clin Gastroenterol Hepatol. 2004 Mar;2(3):262-5 [15017611] Liver Transpl. 2004 Aug;10(8):1018-23 [15390328] Cleve Clin J Med. 1999 Apr;66(4):239-45 [10199060] Gut. 1999 May;44(5):731-5 [10205214] J Clin Gastroenterol. 2005 Jan;39(1):64-7 [15599214] Hepatology. 2005 Aug;42(2):481-9 [16025496] Gastroenterology. 2005 Aug;129(2):512-21 [16083708] Hepatology. 2006 Dec;44(6):1581-8 [17133470] Am J Gastroenterol. 2007 Mar;102(3):558-62; quiz 693 [17156142] Aliment Pharmacol Ther. 2007 Jul 1;26(1):79-85 [17555424] Gastroenterology. 2008 Dec;135(6):1924-34, 1934.e1-4 [18955056] Drug Saf. 2009;32(1):55-68 [19132805] J Hepatol. 2009 Mar;50(3):511-7 [19155082] Clin Gastroenterol Hepatol. 2010 May;8(5):463-70 [20170750] Hepatology. 2010 Jun;51(6):2117-26 [20512999] Hepatology. 2010 Aug;52(2):730-42 [20564754] Hepatology. 2010 Dec;52(6):2065-76 [20949552] Gastroenterology. 2011 Nov;141(5):1665-72.e1-9 [21855518] Dig Dis Sci. 2013 Sep;58(9):2682-90 [23625293] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1053/j.gastro.2014.03.045 ER - TY - JOUR T1 - Tofacitinib suppresses antibody responses to protein therapeutics in murine hosts. AN - 1539475996; 24890727 AB - Immunogenicity remains the "Achilles' heel" of protein-based therapeutics. Anti-drug Abs produced in response to protein therapeutics can severely limit both the safety and efficacy of this expanding class of agent. In this article, we report that monotherapy of mice with tofacitinib (the JAK inhibitor) quells Ab responses to an immunotoxin derived from the bacterial protein Pseudomonas exotoxin A, as well as to the model Ag keyhole limpet hemocyanin. Thousand-fold reductions in IgG1 titers to both Ags were observed 21 d post immunization. In fact, suppression was evident for all IgG isotypes and IgM. A reduction in IgG3 production was also noted with a thymus-independent type II Ag. Mechanistic investigations revealed that tofacitinib treatment led to reduced numbers of CD127+ pro-B cells. Furthermore, we observed fewer germinal center B cells and the impaired formation of germinal centers of mice treated with tofacitinib. Because normal Ig levels were still present during tofacitinib treatment, this agent specifically reduced anti-drug Abs, thus preserving the potential efficacy of biological therapeutics, including those used as cancer therapeutics. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Onda, Masanori AU - Ghoreschi, Kamran AU - Steward-Tharp, Scott AU - Thomas, Craig AU - O'Shea, John J AU - Pastan, Ira H AU - FitzGerald, David J AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; ondam@mail.nih.gov fitzgerd@helix.nih.gov. ; Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892; and. ; Division of Pre-Clinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD 20892. ; Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; Y1 - 2014/07/01/ PY - 2014 DA - 2014 Jul 01 SP - 48 EP - 55 VL - 193 IS - 1 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunoglobulin G KW - Immunoglobulin M KW - Immunotoxins KW - Piperidines KW - Protein Kinase Inhibitors KW - Pyrimidines KW - Pyrroles KW - Virulence Factors KW - tofacitinib KW - 87LA6FU830 KW - Hemocyanin KW - 9013-72-3 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Janus Kinases KW - EC 2.7.10.2 KW - keyhole-limpet hemocyanin KW - FV4Y0JO2CX KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Janus Kinases -- antagonists & inhibitors KW - Janus Kinases -- immunology KW - Immunoglobulin M -- immunology KW - Mice KW - B-Lymphocytes -- immunology KW - Germinal Center -- immunology KW - Mice, Inbred BALB C KW - Immunoglobulin G -- immunology KW - Female KW - Virulence Factors -- pharmacology KW - Piperidines -- pharmacology KW - Exotoxins -- pharmacology KW - Protein Kinase Inhibitors -- pharmacology KW - Hemocyanin -- pharmacology KW - Pyrimidines -- pharmacology KW - Bacterial Toxins -- pharmacology KW - Pyrroles -- pharmacology KW - Immunotoxins -- pharmacology KW - ADP Ribose Transferases -- pharmacology KW - Antibody Formation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1539475996?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tofacitinib+suppresses+antibody+responses+to+protein+therapeutics+in+murine+hosts.&rft.au=Onda%2C+Masanori%3BGhoreschi%2C+Kamran%3BSteward-Tharp%2C+Scott%3BThomas%2C+Craig%3BO%27Shea%2C+John+J%3BPastan%2C+Ira+H%3BFitzGerald%2C+David+J&rft.aulast=Onda&rft.aufirst=Masanori&rft.date=2014-07-01&rft.volume=193&rft.issue=1&rft.spage=48&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.1400063 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-18 N1 - Date created - 2014-06-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Blood. 1999 Dec 1;94(11):3781-90 [10572092] Clin Cancer Res. 2005 Aug 15;11(16):5840-6 [16115924] Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8548-53 [10890891] Cancer Res. 2001 Jul 1;61(13):5070-7 [11431343] N Engl J Med. 2001 Jul 26;345(4):241-7 [11474661] Nat Rev Mol Cell Biol. 2002 Sep;3(9):651-62 [12209125] Nat Rev Immunol. 2006 Feb;6(2):107-16 [16491135] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638] Clin Cancer Res. 2006 Aug 1;12(15):4695-701 [16899620] Nat Rev Immunol. 2007 Feb;7(2):144-54 [17259970] Science. 2003 Oct 31;302(5646):875-8 [14593182] Nat Rev Immunol. 2003 Nov;3(11):900-11 [14668806] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569] Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):17099-104 [17940013] Immunol Rev. 2008 Jun;223:132-42 [18613833] Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11311-6 [18678888] J Med Chem. 2008 Dec 25;51(24):8012-8 [19053756] Immunol Rev. 2009 Mar;228(1):273-87 [19290934] Nat Immunol. 2009 Apr;10(4):356-60 [19295632] J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673] Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873] Clin Cancer Res. 2010 Mar 15;16(6):1894-903 [20215554] J Immunol. 2011 Apr 1;186(7):4234-43 [21383241] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054] Clin Cancer Res. 2011 Jun 1;17(11):3697-705 [21521777] Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11782-7 [22753489] N Engl J Med. 2012 Aug 9;367(6):508-19 [22873531] Br J Dermatol. 2012 Sep;167(3):668-77 [22924949] Mol Cancer Ther. 2013 Jan;12(1):48-57 [23136186] Drugs. 2013 Jun;73(8):857-74 [23716132] Ann Rheum Dis. 2013 Dec;72(12):1947-55 [23223420] Am J Transplant. 2004 Jan;4(1):51-7 [14678034] J Exp Med. 1980 Apr 1;151(4):853-62 [6966310] Nature. 1989 Jun 1;339(6223):394-7 [2498664] J Exp Med. 1994 Nov 1;180(5):1955-60 [7964471] Science. 1995 Nov 3;270(5237):794-7 [7481767] Science. 1995 Nov 3;270(5237):800-2 [7481769] Immunol Rev. 1995 Dec;148:97-114 [8825284] Int Arch Allergy Immunol. 1999 Jan;118(1):23-9 [9925959] Trends Mol Med. 2004 Nov;10(11):532-41 [15519279] Eur J Immunol. 2004 Dec;34(12):3595-603 [15495160] J Exp Med. 2005 Apr 18;201(8):1197-203 [15837809] J Clin Oncol. 2000 Apr;18(8):1622-36 [10764422] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4049/jimmunol.1400063 ER - TY - JOUR T1 - Exceptionally potent neutralization of Middle East respiratory syndrome coronavirus by human monoclonal antibodies. AN - 1539475796; 24789777 AB - The recently discovered Middle East respiratory syndrome coronavirus (MERS-CoV) continues to infect humans, with high mortality. Specific, highly effective therapeutics and vaccines against the MERS-CoV are urgently needed to save human lives and address the pandemic concerns. We identified three human monoclonal antibodies (MAbs), m336, m337, and m338, targeting the receptor (CD26/DPP4) binding domain (RBD) of the MERS-CoV spike glycoprotein from a very large naïve-antibody library (containing ∼10(11) antibodies). They bound with high affinity: equilibrium dissociation constants for the three MAbs were equal to 4.2, 9.3, and 15 nM, respectively, as measured by Biacore for Fabs binding to RBD. The avidity for IgG1 m336, m337, and m338 was even higher: 99, 820, and 560 pM, respectively. The antibodies bound to overlapping epitopes that overlap the receptor binding site on the RBD as suggested by competition experiments and further supported by site-directed mutagenesis of the RBD and a docking model of the m336-RBD complex. The highest-affinity MAb, m336, neutralized both pseudotyped and live MERS-CoV with exceptional potency, 50% neutralization at 0.005 and 0.07 μg/ml, respectively, likely by competing with DPP4 for binding to the S glycoprotein. The exceptionally high neutralization activity of these antibodies and especially m336 suggests that they have great potential for prophylaxis and therapy of MERS-CoV infection in humans and as a tool for development of vaccine immunogens. The rapid identification (within several weeks) of potent MAbs suggests a possibility to use the new large antibody library and related methodology for a quick response to the public threat resulting from emerging coronaviruses. Importance: A novel human coronavirus, the Middle East respiratory syndrome coronavirus (MERS-CoV), was found to infect humans with a high mortality rate in 2012, just 1 decade after the appearance of the first highly pathogenic coronavirus, severe acute respiratory syndrome coronavirus (SARS-CoV). There are no effective therapeutics available. It is highly desirable to find an approach for rapidly developing potent therapeutics against MERS-CoV, which not only can be implemented for MERS treatment but also can help to develop a platform strategy to combat future emerging coronaviruses. We report here the identification of human monoclonal antibodies (MAbs) from a large nonimmune antibody library that target MERS-CoV. One of the antibodies, m336, neutralized the virus with exceptional potency. It therefore may have great potential as a candidate therapeutic and as a reagent to facilitate the development of vaccines against MERS-CoV. Copyright © 2014, American Society for Microbiology. All Rights Reserved. JF - Journal of virology AU - Ying, Tianlei AU - Du, Lanying AU - Ju, Tina W AU - Prabakaran, Ponraj AU - Lau, Candy C Y AU - Lu, Lu AU - Liu, Qi AU - Wang, Lili AU - Feng, Yang AU - Wang, Yanping AU - Zheng, Bo-Jian AU - Yuen, Kwok-Yung AU - Jiang, Shibo AU - Dimitrov, Dimiter S AD - Protein Interactions Group, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA yingt@mail.nih.gov dimiter.dimitrov@nih.gov. ; Lindsley F. Kimball Research Institute, New York Blood Center, New York, New York, USA. ; Protein Interactions Group, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA. ; Protein Interactions Group, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA Basic Science Program, Leidos Biomedical Research, Inc., Frederick National Laboratory, Frederick, Maryland, USA. ; Department of Microbiology, University of Hong Kong, Pokfulam, Hong Kong. ; Key Laboratory of Medical Molecular Virology of Ministries of Education and Health, Shanghai Medical College and Institute of Medical Microbiology, Fudan University, Shanghai, China. ; Basic Science Program, Leidos Biomedical Research, Inc., Frederick National Laboratory, Frederick, Maryland, USA. ; Lindsley F. Kimball Research Institute, New York Blood Center, New York, New York, USA Key Laboratory of Medical Molecular Virology of Ministries of Education and Health, Shanghai Medical College and Institute of Medical Microbiology, Fudan University, Shanghai, China. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 7796 EP - 7805 VL - 88 IS - 14 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Neutralizing KW - Antibodies, Viral KW - Immunoglobulin G KW - Peptide Library KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Molecular Docking Simulation KW - Kinetics KW - Immunoglobulin G -- isolation & purification KW - Humans KW - Neutralization Tests KW - Antibody Affinity KW - Immunoglobulin G -- immunology KW - Protein Binding KW - Epitope Mapping KW - Binding Sites KW - Antibodies, Viral -- isolation & purification KW - Antibodies, Monoclonal -- isolation & purification KW - Coronavirus -- immunology KW - Antibodies, Neutralizing -- immunology KW - Antibodies, Viral -- immunology KW - Antibodies, Neutralizing -- isolation & purification KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1539475796?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Exceptionally+potent+neutralization+of+Middle+East+respiratory+syndrome+coronavirus+by+human+monoclonal+antibodies.&rft.au=Ying%2C+Tianlei%3BDu%2C+Lanying%3BJu%2C+Tina+W%3BPrabakaran%2C+Ponraj%3BLau%2C+Candy+C+Y%3BLu%2C+Lu%3BLiu%2C+Qi%3BWang%2C+Lili%3BFeng%2C+Yang%3BWang%2C+Yanping%3BZheng%2C+Bo-Jian%3BYuen%2C+Kwok-Yung%3BJiang%2C+Shibo%3BDimitrov%2C+Dimiter+S&rft.aulast=Ying&rft.aufirst=Tianlei&rft.date=2014-07-01&rft.volume=88&rft.issue=14&rft.spage=7796&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.00912-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-22 N1 - Date created - 2014-06-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Blood. 2001 Feb 15;97(4):1023-6 [11159532] Lancet Infect Dis. 2014 Feb;14(2):140-5 [24355866] Nat Rev Microbiol. 2004 Sep;2(9):695-703 [15372080] Drugs. 1999 Aug;58(2):305-11; discussion 312-3 [10473022] J Virol. 2006 Jan;80(2):891-9 [16378991] Nat Rev Drug Discov. 2006 Feb;5(2):147-59 [16424916] Nat Rev Immunol. 2006 May;6(5):343-57 [16622479] Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12123-8 [17620608] Nat Biotechnol. 2007 Dec;25(12):1421-34 [18066039] Virology. 2008 Mar 15;372(2):357-71 [18054977] Bioinformatics. 2008 Sep 1;24(17):1953-4 [18641403] Expert Opin Biol Ther. 2009 Mar;9(3):355-68 [19216624] PLoS Pathog. 2009 Oct;5(10):e1000642 [19888339] J Virol. 2011 Nov;85(21):11048-57 [21865387] Sci Transl Med. 2011 Oct 19;3(105):105ra103 [22013123] Methods Mol Biol. 2012;899:1-26 [22735943] Immunity. 2012 Sep 21;37(3):412-25 [22999947] N Engl J Med. 2012 Nov 8;367(19):1814-20 [23075143] Virol Sin. 2013 Apr;28(2):71-80 [23575729] N Engl J Med. 2013 Jun 27;368(26):2487-94 [23718156] Cell Res. 2013 Aug;23(8):986-93 [23835475] N Engl J Med. 2013 Aug 1;369(5):407-16 [23782161] Nat Med. 2013 Aug;19(8):952 [23921729] Nature. 2013 Aug 8;500(7461):227-31 [23831647] J Virol. 2013 Sep;87(17):9939-42 [23824801] Emerg Infect Dis. 2013 Oct;19(10):1697-9 [24050621] Nat Med. 2013 Oct;19(10):1313-7 [24013700] Nat Rev Microbiol. 2013 Dec;11(12):836-48 [24217413] PLoS One. 2013;8(12):e81587 [24324708] Lancet. 2013 Dec 14;382(9909):1993-2002 [24055451] Proteins. 2003 Jul 1;52(1):80-7 [12784371] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/JVI.00912-14 ER - TY - JOUR T1 - Heme-related gene expression signatures of meat intakes in lung cancer tissues. AN - 1537592543; 23681825 AB - Lung cancer causes more deaths worldwide than any other cancer. In addition to cigarette smoking, dietary factors may contribute to lung carcinogenesis. Epidemiologic studies, including the environment and genetics in lung cancer etiology (EAGLE), have reported increased consumption of red/processed meats to be associated with higher risk of lung cancer. Heme-iron toxicity may link meat intake with cancer. We investigated this hypothesis in meat-related lung carcinogenesis using whole genome expression. We measured genome-wide expression (HG-U133A) in 49 tumor and 42 non-involved fresh frozen lung tissues of 64 adenocarcinoma EAGLE patients. We studied gene expression profiles by high-versus-low meat consumption, with and without adjustment by sex, age, and smoking. Threshold for significance was a false discovery rate (FDR) ≤ 0.15. We studied whether the identified genes played a role in heme-iron related processes by means of manually curated literature search and gene ontology-based pathway analysis. We found that gene expression of 232 annotated genes in tumor tissue significantly distinguished lung adenocarcinoma cases who consumed above/below the median intake of fresh red meats (FDR = 0.12). Sixty-three (∼ 28%) of the 232 identified genes (12 expected by chance, P-value < 0.001) were involved in heme binding, absorption, transport, and Wnt signaling pathway (e.g., CYPs, TPO, HPX, HFE, SLCs, and WNTs). We also identified several genes involved in lipid metabolism (e.g., NCR1, TNF, and UCP3) and oxidative stress (e.g., TPO, SGK2, and MTHFR) that may be indirectly related to heme-toxicity. The study's results provide preliminary evidence that heme-iron toxicity might be one underlying mechanism linking fresh red meat intake and lung cancer. © 2013 Wiley Periodicals, Inc. JF - Molecular carcinogenesis AU - Lam, Tram Kim AU - Rotunno, Melissa AU - Ryan, Brid M AU - Pesatori, Angela C AU - Bertazzi, Pier Alberto AU - Spitz, Margaret AU - Caporaso, Neil E AU - Landi, Maria Teresa AD - Cancer Prevention Fellowship Program, Office of Preventive Oncology, Genetic Epidemiology Branch, National Cancer Institute, National Institutes of Health (NIH), DHHS, Bethesda, Maryland; Division of Cancer Epidemiology and Genetics, Genetic Epidemiology Branch, National Cancer Institute, National Institutes of Health (NIH), DHHS, Bethesda, Maryland. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 548 EP - 556 VL - 53 IS - 7 KW - Iron, Dietary KW - 0 KW - Heme KW - 42VZT0U6YR KW - Index Medicus KW - heme-iron KW - lung cancer KW - gene expression KW - Humans KW - Aged KW - Lipid Metabolism -- genetics KW - Oxidative Stress -- genetics KW - Feeding Behavior KW - Risk KW - Gene Expression Profiling KW - Protein Transport -- genetics KW - Risk Factors KW - Case-Control Studies KW - Middle Aged KW - Protein Binding -- genetics KW - Wnt Signaling Pathway -- genetics KW - Diet KW - Female KW - Male KW - Eating KW - Carcinogenesis -- genetics KW - Meat -- adverse effects KW - Lung Neoplasms -- genetics KW - Iron, Dietary -- adverse effects KW - Adenocarcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1537592543?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Heme-related+gene+expression+signatures+of+meat+intakes+in+lung+cancer+tissues.&rft.au=Lam%2C+Tram+Kim%3BRotunno%2C+Melissa%3BRyan%2C+Brid+M%3BPesatori%2C+Angela+C%3BBertazzi%2C+Pier+Alberto%3BSpitz%2C+Margaret%3BCaporaso%2C+Neil+E%3BLandi%2C+Maria+Teresa&rft.aulast=Lam&rft.aufirst=Tram&rft.date=2014-07-01&rft.volume=53&rft.issue=7&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=1098-2744&rft_id=info:doi/10.1002%2Fmc.22006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-19 N1 - Date created - 2014-06-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Drug Metab Rev. 1993;25(1-2):49-152 [8449148] Free Radic Biol Med. 1987;3(1):9-14 [3040539] Carcinogenesis. 2005 Jan;26(1):73-9 [15539406] Cancer Lett. 2005 May 10;222(1):1-10 [15837535] Toxicol Appl Pharmacol. 2006 Jan 1;210(1-2):17-23 [15993455] Bioinformatics. 2006 Apr 15;22(8):943-9 [16473874] Oncogene. 2006 Dec 4;25(57):7531-7 [17143297] Med Hypotheses. 2007;68(3):562-4 [17045417] PLoS Med. 2007 Dec;4(12):e325 [18076279] Oncogene. 2008 Feb 7;27(7):966-75 [17700530] PLoS One. 2008;3(2):e1651 [18297132] Nutr Cancer. 2008;60(2):131-44 [18444144] BMC Public Health. 2008;8:203 [18538025] Drug Metab Rev. 2008;40(3):405-26 [18642140] J Am Soc Nephrol. 2008 Aug;19(8):1500-8 [18448584] Cancer Res. 2009 Feb 1;69(3):932-9 [19141639] Cell Metab. 2009 Mar;9(3):217-27 [19254567] Am J Clin Nutr. 2009 May;89(5):1402-9 [19261724] Am J Clin Nutr. 2009 Jun;89(6):1884-94 [19369370] Cancer Causes Control. 2009 Nov;20(9):1635-43 [19685149] Antioxid Redox Signal. 2010 Feb;12(2):305-20 [19650691] Cancer Res. 2010 Mar 15;70(6):2406-14 [20215514] Carcinogenesis. 2010 Apr;31(4):625-33 [20106900] Nutr Cancer. 2010;62(5):567-73 [20574917] Cancer Prev Res (Phila). 2010 Jul;3(7):852-64 [20530708] Genes Chromosomes Cancer. 2011 Jan;50(1):1-12 [20842733] Int J Cancer. 2011 Jan 15;128(2):402-11 [20232386] Carcinogenesis. 2010 Dec;31(12):2091-6 [20935060] Cancer Prev Res (Phila). 2011 Feb;4(2):177-84 [21209396] Biochem J. 2011 Mar 15;434(3):365-81 [21348856] Int J Cancer. 2010 Dec 15;127(12):2893-917 [21351269] Acta Physiol (Oxf). 2011 Jul;202(3):563-81 [20958924] Cancer Prev Res (Phila). 2011 Sep;4(9):1465-75 [21685236] Lung Cancer. 2011 Dec;74(3):411-8 [21640426] Food Chem Toxicol. 2012 Feb;50(2):95-103 [22019696] Curr Atheroscler Rep. 2012 Dec;14(6):515-24 [23001745] Nat Genet. 2000 May;25(1):25-9 [10802651] Cancer Epidemiol Biomarkers Prev. 2001 Apr;10(4):397-401 [11319182] DNA Cell Biol. 2002 Apr;21(4):297-306 [12042069] Public Health Nutr. 2002 Dec;5(6B):1243-58 [12639230] Genome Biol. 2003;4(4):R28 [12702209] Cancer Res. 2003 May 15;63(10):2358-60 [12750250] Prostaglandins Leukot Med. 1985 Aug;19(2):177-86 [2864701] Cancer Causes Control. 1998 Dec;9(6):621-30 [10189048] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/mc.22006 ER - TY - JOUR T1 - Impact of subdomain D1 of the short form S1b of the human prolactin receptor on its inhibitory action on the function of the long form of the receptor induced by prolactin. AN - 1536685111; 24735798 AB - Long-form (LF) homodimers of the human prolactin receptor (PRLR) mediate prolactin's diverse actions. Short form S1b inhibits the LF function through heterodimerization. Reduced S1b/LF-ratio in breast cancer could contribute to tumor development/progression. Current work defines the structural and functional relevance of the D1 domain of S1b on its inhibitory function on prolactin-induced LF function. Studies were conducted using mutagenesis, promoter/signaling analyses, bioluminescence resonance energy transfer (BRET) and molecular modeling approaches. Mutation of E69 in D1 S1b or adjacent residues at the receptor surface near to the binding pocket (S) causes loss of its inhibitory effect while mutations away from this region (A) or in the D2 domain display inhibitory action as the wild-type. All S1b mutants preserved prolactin-induced Jak2 activation. BRET reveals an increased affinity in D1 mutated S1b (S) homodimers in transfected cells stably expressing LF. In contrast, affinity in S1b homodimers with either D1 (A) or D2 mutations remained unchanged. This favors LF mediated signaling induced by prolactin. Molecular dynamics simulations show that mutations (S) elicit major conformational changes that propagate downward to the D1/D2 interface and change their relative orientation in the dimers. These findings demonstrate the essential role of D1 on the S1b structure and its inhibitory action on prolactin-induced LF-mediated function. Major changes in receptor conformation and dimerization affinity are triggered by single mutations in critical regions of D1. Our structure-function/simulation studies provide a basis for modeling and design of small molecules to enhance inhibition of LF activation for potential use in breast cancer treatment. Published by Elsevier B.V. JF - Biochimica et biophysica acta AU - Kang, J-H AU - Hassan, S A AU - Zhao, P AU - Tsai-Morris, C H AU - Dufau, M L AD - Section on Molecular Endocrinology, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institutes of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-4510, USA. ; Center for Molecular Modeling, Division of Computational Bioscience, Center for Information Technology, National Institutes of Health, Bethesda, MD 20892-4510, USA. ; Section on Molecular Endocrinology, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institutes of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-4510, USA. Electronic address: dufaum@mail.nih.gov. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 2272 EP - 2280 VL - 1840 IS - 7 SN - 0006-3002, 0006-3002 KW - Protein Isoforms KW - 0 KW - Receptors, Prolactin KW - Prolactin KW - 9002-62-4 KW - JAK2 protein, human KW - EC 2.7.10.2 KW - Janus Kinase 2 KW - Index Medicus KW - Structure/function KW - Subdomain D1 KW - Human prolactin receptor KW - Short and long form KW - HEK293 Cells KW - Humans KW - Janus Kinase 2 -- chemistry KW - Protein Binding KW - Structure-Activity Relationship KW - Promoter Regions, Genetic KW - Signal Transduction -- genetics KW - Janus Kinase 2 -- metabolism KW - Protein Structure, Tertiary KW - Mutation KW - Cell Line KW - Female KW - Protein Conformation KW - Breast Neoplasms -- genetics KW - Receptors, Prolactin -- metabolism KW - Prolactin -- chemistry KW - Breast Neoplasms -- pathology KW - Receptors, Prolactin -- chemistry KW - Dimerization KW - Breast Neoplasms -- therapy KW - Prolactin -- genetics KW - Receptors, Prolactin -- genetics KW - Prolactin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1536685111?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Impact+of+subdomain+D1+of+the+short+form+S1b+of+the+human+prolactin+receptor+on+its+inhibitory+action+on+the+function+of+the+long+form+of+the+receptor+induced+by+prolactin.&rft.au=Kang%2C+J-H%3BHassan%2C+S+A%3BZhao%2C+P%3BTsai-Morris%2C+C+H%3BDufau%2C+M+L&rft.aulast=Kang&rft.aufirst=J-H&rft.date=2014-07-01&rft.volume=1840&rft.issue=7&rft.spage=2272&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbagen.2014.04.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-18 N1 - Date created - 2014-06-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Endocrinology. 2002 Jun;143(6):2139-42 [12021177] J Biol Chem. 2001 Nov 2;276(44):41086-94 [11518703] J Biol Chem. 1996 Mar 1;271(9):4699-708 [8617735] Mol Endocrinol. 1997 Sep;11(10):1449-57 [9280060] Endocr Rev. 1998 Jun;19(3):225-68 [9626554] J Clin Endocrinol Metab. 1999 Mar;84(3):1153-6 [10084611] Proteins. 2005 Aug 15;60(3):464-84 [15959866] Clin Cancer Res. 2005 Aug 15;11(16):5863-8 [16115927] Mol Endocrinol. 2006 Aug;20(8):1912-23 [16556730] J Mammary Gland Biol Neoplasia. 2008 Mar;13(1):29-40 [18219562] Mol Cell Biol. 2009 May;29(10):2546-55 [19273600] Mol Cell Biol. 2011 Aug;31(16):3208-22 [21670145] Cancer Lett. 2011 Nov 1;310(1):101-8 [21775057] Cell Signal. 2011 Nov;23(11):1794-805 [21726627] J Phys Chem B. 2011 Dec 15;115(49):14668-82 [22007697] Structure. 2012 Feb 8;20(2):270-82 [22325776] J R Soc Interface. 2013 Feb;10(79):20120835 [23235262] Proc Natl Acad Sci U S A. 2013 Mar 26;110(13):5211-6 [23479653] Semin Cancer Biol. 2013 Aug;23(4):219-26 [23680723] Cancer Res. 2013 Aug 1;73(15):4810-9 [23783576] J Phys Chem B. 2013 Oct 17;117(41):12360-74 [24044772] Cancer Res. 2004 Aug 15;64(16):5677-82 [15313907] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbagen.2014.04.006 ER - TY - JOUR T1 - Persistent organochlorines and hypertensive disorders of pregnancy. AN - 1536683829; 24742720 AB - Although there is indirect evidence to suggest that persistent organochlorines might increase risk of hypertensive disorders of pregnancy, there are no epidemiologic studies directly addressing this question. In this cohort study, sampled from the Collaborative Perinatal Project, 1933 women had complete data on organochlorine measurements, covariates, and pregnancy outcomes. Exposures to organochlorines were divided into quintiles, and levels were much higher in these patients recruited from 1959 to 1965 compared to levels in the general population at present. Among included women, 364 developed gestational hypertension (hypertension without proteinuria) and 131 developed preeclampsia (hypertension with proteinuria). We found essentially no association between serum DDE and total PCBs and risk of either gestational hypertension or preeclampsia. Results for other organochlorines showed varying patterns of results: DDT was inversely associated with risk of gestational hypertension (p for trend <0.001), B-Hexachlorocyclohexane and heptachlor epoxide were inversely related to gestational hypertension (p trend <0.01 and 0.10, respectively), dieldrin had a modestly positive association with gestational hypertension (p for trend=0.12), and hexachlorobenzene, trans-nonachlor, and oxychlordane yielded results close to the null. Hexachlorobenzene showed an inverse association with preeclampsia (p for trend <0.001). The study suggests that persistent organochlorines present at historically high level are not likely to increase the risk of hypertensive disorders of pregnancy, suggesting that other toxicants that have similar biologic effects are also unlikely to do so. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Environmental research AU - Savitz, David A AU - Klebanoff, Mark A AU - Wellenius, Gregory A AU - Jensen, Elizabeth T AU - Longnecker, Matthew P AD - Department of Epidemiology, Brown University School of Public Health, Providence, Rhode Island, 47 George Street, Room 302, Providence, RI 02912, USA. Electronic address: david_savitz@brown.edu. ; Nationwide Children׳s Hospital, Departments of Pediatrics and Obstetrics and Gynecology, The Ohio State University College of Medicine, Columbus, Ohio, USA. Electronic address: Mark.Klebanoff@nationwidechildrens.org. ; Department of Epidemiology, Brown University School of Public Health, Providence, Rhode Island, 47 George Street, Room 302, Providence, RI 02912, USA. Electronic address: Gregory_wellenius@brown.edu. ; Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. Electronic address: elizabeth.jensen@nih.gov. ; Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. Electronic address: Longnec1@niehs.nih.gov. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 1 EP - 5 VL - 132 KW - Hydrocarbons, Chlorinated KW - 0 KW - Index Medicus KW - Organochlorines KW - DDT KW - PCBs KW - Gestational hypertension KW - Preeclampsia KW - Young Adult KW - Humans KW - Cohort Studies KW - Adolescent KW - United States -- epidemiology KW - Female KW - Pregnancy KW - Hydrocarbons, Chlorinated -- blood KW - Hypertension, Pregnancy-Induced -- epidemiology KW - Hypertension, Pregnancy-Induced -- etiology KW - Hydrocarbons, Chlorinated -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1536683829?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+research&rft.atitle=Persistent+organochlorines+and+hypertensive+disorders+of+pregnancy.&rft.au=Savitz%2C+David+A%3BKlebanoff%2C+Mark+A%3BWellenius%2C+Gregory+A%3BJensen%2C+Elizabeth+T%3BLongnecker%2C+Matthew+P&rft.aulast=Savitz&rft.aufirst=David&rft.date=2014-07-01&rft.volume=132&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Environmental+research&rft.issn=1096-0953&rft_id=info:doi/10.1016%2Fj.envres.2014.03.020 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-12 N1 - Date created - 2014-06-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: N Engl J Med. 2010 Apr 8;362(14):1282-91 [20375405] Best Pract Res Clin Obstet Gynaecol. 2011 Jun;25(3):329-42 [21349772] Best Pract Res Clin Obstet Gynaecol. 2011 Aug;25(4):391-403 [21333604] Epidemiology. 2012 May;23(3):386-92 [22370857] J Obstet Gynaecol. 2012 Aug;32(6):512-7 [22779950] Environ Health Perspect. 2012 Aug;120(8):1201-7 [22450153] Matern Child Health J. 2013 Apr;17(3):545-55 [22544506] Environ Int. 2013 May;55:1-8 [23454278] Am J Obstet Gynecol. 2013 Oct;209(4):327.e1-17 [23711667] Matern Child Health J. 2014 May;18(4):829-38 [23793484] Lancet. 2001 Jul 14;358(9276):110-4 [11463412] Epidemiology. 1995 Jul;6(4):450-4 [7548361] J Anal Toxicol. 1996 Nov-Dec;20(7):528-36 [8934301] BMJ. 2005 Mar 12;330(7491):565 [15743856] Epidemiology. 2005 Sep;16(5):641-7 [16135940] Epidemiology. 2007 Jul;18(4):461-8 [17568219] Environ Health Perspect. 2009 Apr;117(4):568-73 [19440495] Environ Health Perspect. 2009 Nov;117(11):1773-9 [20049131] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.envres.2014.03.020 ER - TY - JOUR T1 - A phase II study of dose-dense and dose-intense ABVD (ABVDDD-DI ) without consolidation radiotherapy in patients with advanced Hodgkin lymphoma. AN - 1535632396; 24673727 AB - We explored activity and safety of a dose-dense/dose-intense adriamycin, bleomycin, vinblastine and dacarbazine regimen (ABVDDD-DI ) in 82 patients with advanced Hodgkin Lymphoma. Patients entered a two-stage Bryant-Day Phase II study to receive six cycles of ABVDDD-DI without consolidation radiotherapy. Cycles were supported with granulocyte colony-stimulating factor and delivered every 21 d; drugs were administered on days 1 and 11 at the same doses of standard ABVD except for doxorubicin (35 mg/m2; first four cycles only). Co-primary endpoints were complete response (CR) rate and severe acute cardiopulmonary toxicity; secondary endpoints were event-free (EFS) and disease-free survival (DFS). All patients received the four doxorubicin-intensified courses and 96% concluded all six cycles (82.3% within the intended 18 weeks). This translated into a 66.9% increase of received dose-intensity for doxorubicin and 31.8% for the other agents over standard ABVD. The CR rate was 95.1% (78/82) and 87.8% (72/82) achieved a metabolic CR after two cycles. Cardiopulmonary toxicity never exceeded grade 2 and affected 14.6% of patients. Most frequent toxicities were grade 4 neutropenia (10%) and anaemia (9%), grade 3 infection (17%) and grade 2 mucocutaneous changes (30%). Five-year EFS and DFS was 88.3% and 93.7%, respectively. ABVDDD-DI regimen was well-tolerated and ensured substantial CR and EFS rates without radiotherapy. © 2014 John Wiley & Sons Ltd. JF - British journal of haematology AU - Russo, Filippo AU - Corazzelli, Gaetano AU - Frigeri, Ferdinando AU - Capobianco, Gaetana AU - Aloj, Luigi AU - Volzone, Francesco AU - De Chiara, Annarosaria AU - Bonelli, Annamaria AU - Gatani, Tindaro AU - Marcacci, Gianpaolo AU - Donnarumma, Daniela AU - Becchimanzi, Cristina AU - de Lutio, Elisabetta AU - Ionna, Franco AU - De Filippi, Rosaria AU - Lastoria, Secondo AU - Pinto, Antonello AD - Haematology-Oncology and Stem Cell Transplantation Unit, National Cancer Institute, Fondazione 'G. Pascale', IRCCS, Naples, Italy. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 118 EP - 129 VL - 166 IS - 1 KW - Bleomycin KW - 11056-06-7 KW - Vinblastine KW - 5V9KLZ54CY KW - Dacarbazine KW - 7GR28W0FJI KW - Doxorubicin KW - 80168379AG KW - Index Medicus KW - doxorubicin KW - dose intensity KW - Hodgkin lymphoma KW - radiotherapy KW - ABVD KW - Young Adult KW - Humans KW - Vinblastine -- therapeutic use KW - Adult KW - Treatment Outcome KW - Vinblastine -- administration & dosage KW - Dacarbazine -- administration & dosage KW - Adolescent KW - Bleomycin -- therapeutic use KW - Male KW - Doxorubicin -- adverse effects KW - Drug Administration Schedule KW - Neoplasm Staging KW - Dose-Response Relationship, Drug KW - Bleomycin -- administration & dosage KW - Doxorubicin -- administration & dosage KW - Dacarbazine -- adverse effects KW - Bleomycin -- adverse effects KW - Kaplan-Meier Estimate KW - Dacarbazine -- therapeutic use KW - Radiotherapy, Adjuvant KW - Doxorubicin -- therapeutic use KW - Follow-Up Studies KW - Middle Aged KW - Vinblastine -- adverse effects KW - Female KW - Hodgkin Disease -- pathology KW - Hodgkin Disease -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535632396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+haematology&rft.atitle=A+phase+II+study+of+dose-dense+and+dose-intense+ABVD+%28ABVDDD-DI+%29+without+consolidation+radiotherapy+in+patients+with+advanced+Hodgkin+lymphoma.&rft.au=Russo%2C+Filippo%3BCorazzelli%2C+Gaetano%3BFrigeri%2C+Ferdinando%3BCapobianco%2C+Gaetana%3BAloj%2C+Luigi%3BVolzone%2C+Francesco%3BDe+Chiara%2C+Annarosaria%3BBonelli%2C+Annamaria%3BGatani%2C+Tindaro%3BMarcacci%2C+Gianpaolo%3BDonnarumma%2C+Daniela%3BBecchimanzi%2C+Cristina%3Bde+Lutio%2C+Elisabetta%3BIonna%2C+Franco%3BDe+Filippi%2C+Rosaria%3BLastoria%2C+Secondo%3BPinto%2C+Antonello&rft.aulast=Russo&rft.aufirst=Filippo&rft.date=2014-07-01&rft.volume=166&rft.issue=1&rft.spage=118&rft.isbn=&rft.btitle=&rft.title=British+journal+of+haematology&rft.issn=1365-2141&rft_id=info:doi/10.1111%2Fbjh.12862 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-10 N1 - Date created - 2014-06-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/bjh.12862 ER - TY - JOUR T1 - As a novel p53 direct target, bidirectional gene HspB2/αB-crystallin regulates the ROS level and Warburg effect. AN - 1535631909; 24859470 AB - Many mammalian genes are composed of bidirectional gene pairs with the two genes separated by less than 1.0kb. The transcriptional regulation and function of these bidirectional genes remain largely unclear. Here, we report that bidirectional gene pair HspB2/αB-crystallin, both of which are members of the small heat shock protein gene family, is a novel direct target gene of p53. Two potential binding sites of p53 are present in the intergenic region of HspB2/αB-crystallin. p53 up-regulated the bidirectional promoter activities of HspB2/αB-crystallin. Actinomycin D (ActD), an activator of p53, induces the promoter and protein activities of HspB2/αB-crystallin. p53 binds to two p53 binding sites in the intergenic region of HspB2/αB-crystallin in vitro and in vivo. Moreover, the products of bidirectional gene pair HspB2/αB-crystallin regulate glucose metabolism, intracellular reactive oxygen species (ROS) level and the Warburg effect by affecting metabolic genes, including the synthesis of cytochrome c oxidase 2 (SCO2), hexokinase II (HK2), and TP53-induced glycolysis and apoptosis regulator (TIGAR). The ROS level and the Warburg effect are affected after the depletion of p53, HspB2 and αB-crystallin respectively. Finally, we show that both HspB2 and αB-crystallin are linked with human renal carcinogenesis. These findings provide novel insights into the role of p53 as a regulator of bidirectional gene pair HspB2/αB-crystallin-mediated ROS and the Warburg effect. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biochimica et biophysica acta AU - Liu, Shuang AU - Yan, Bin AU - Lai, Weiwei AU - Chen, Ling AU - Xiao, Desheng AU - Xi, Sichuan AU - Jiang, Yiqun AU - Dong, Xin AU - An, Jing AU - Chen, Xiang AU - Cao, Ya AU - Tao, Yongguang AD - Center for Medicine Research, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China; Cancer Research Institute, Central South University, Changsha, Hunan 410078, China; Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China. ; Cancer Research Institute, Central South University, Changsha, Hunan 410078, China; Center for Molecular Imaging, Central South University, Changsha, Hunan 410078, China; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan 410078, China; Key Laboratory of Carcinogenesis, Ministry of Health, Hunan 410078, China. ; Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan 410078, China. ; Thoracic Oncology Section, Surgery Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892 USA. ; State Key Laboratory of Medical Genetics, Central South University, Changsha, Hunan 4010078, China. ; Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China. ; Cancer Research Institute, Central South University, Changsha, Hunan 410078, China; Center for Molecular Imaging, Central South University, Changsha, Hunan 410078, China; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Hunan 410078, China; Key Laboratory of Carcinogenesis, Ministry of Health, Hunan 410078, China. Electronic address: taoyong@csu.edu.cn. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 592 EP - 603 VL - 1839 IS - 7 SN - 0006-3002, 0006-3002 KW - HSP27 Heat-Shock Proteins KW - 0 KW - HSPB2 protein, human KW - Reactive Oxygen Species KW - Tumor Suppressor Protein p53 KW - alpha-Crystallin B Chain KW - Index Medicus KW - Renal cell carcinoma KW - p53 KW - HspB2 KW - αB-crystallin KW - Bidirectional promoter KW - Warburg effect KW - Gene Expression Regulation, Neoplastic KW - Reactive Oxygen Species -- metabolism KW - Promoter Regions, Genetic KW - Humans KW - Protein Binding -- genetics KW - Cell Line, Tumor KW - Binding Sites -- genetics KW - Transcriptional Activation KW - Carcinoma, Renal Cell -- pathology KW - HSP27 Heat-Shock Proteins -- metabolism KW - Carcinoma, Renal Cell -- metabolism KW - alpha-Crystallin B Chain -- metabolism KW - HSP27 Heat-Shock Proteins -- genetics KW - alpha-Crystallin B Chain -- genetics KW - Tumor Suppressor Protein p53 -- genetics KW - Tumor Suppressor Protein p53 -- metabolism KW - Carcinoma, Renal Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535631909?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=As+a+novel+p53+direct+target%2C+bidirectional+gene+HspB2%2F%CE%B1B-crystallin+regulates+the+ROS+level+and+Warburg+effect.&rft.au=Liu%2C+Shuang%3BYan%2C+Bin%3BLai%2C+Weiwei%3BChen%2C+Ling%3BXiao%2C+Desheng%3BXi%2C+Sichuan%3BJiang%2C+Yiqun%3BDong%2C+Xin%3BAn%2C+Jing%3BChen%2C+Xiang%3BCao%2C+Ya%3BTao%2C+Yongguang&rft.aulast=Liu&rft.aufirst=Shuang&rft.date=2014-07-01&rft.volume=1839&rft.issue=7&rft.spage=592&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbagrm.2014.05.017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-11 N1 - Date created - 2014-06-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbagrm.2014.05.017 ER - TY - JOUR T1 - Effects of Helicobacter pylori treatment on gastric cancer incidence and mortality in subgroups. AN - 1535627557; 24925350 AB - Among 2258 Helicobacter pylori-seropositive subjects randomly assigned to receive one-time H. pylori treatment with amoxicillin-omeprazole or its placebo, we evaluated the 15-year effect of treatment on gastric cancer incidence and mortality in subgroups defined by age, baseline gastric histopathology, and post-treatment infection status. We used conditional logistic and Cox regressions for covariable adjustments in incidence and mortality analyses, respectively. Treatment was associated with a statistically significant decrease in gastric cancer incidence (odds ratio = 0.36; 95% confidence interval [CI] = 0.17 to 0.79) and mortality (hazard ratio = 0.26; 95% CI = 0.09 to 0.79) at ages 55 years and older and a statistically significant decrease in incidence among those with intestinal metaplasia or dysplasia at baseline (odds ratio = 0.56; 95% CI = 0.34 to 0.91). Treatment benefits for incidence and mortality among those with and without post-treatment infection were similar. Thus H. pylori treatment can benefit older members and those with advanced baseline histopathology, and benefits are present even with post-treatment infection, suggesting treatment can benefit an entire population, not just the young or those with mild histopathology. Published by Oxford University Press 2014. JF - Journal of the National Cancer Institute AU - Li, Wen-Qing AU - Ma, Jun-Ling AU - Zhang, Lian AU - Brown, Linda M AU - Li, Ji-You AU - Shen, Lin AU - Pan, Kai-Feng AU - Liu, Wei-Dong AU - Hu, Yuanreng AU - Han, Zhong-Xiang AU - Crystal-Mansour, Susan AU - Pee, David AU - Blot, William J AU - Fraumeni, Joseph F AU - You, Wei-Cheng AU - Gail, Mitchell H AD - Affiliations of authors: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (W-QL, JFF, MHG); Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Cancer Epidemiology, Peking University Cancer Hospital and Institute, Beijing, China (W-QL, J-LM, LZ, J-YL, LS, K-FP, W-CY); RTI International, Rockville, MD (LMB); Linqu County Public Health Bureau, Shandong, China (W-DL, Z-XH); Westat, Rockville, MD (SC-M); Information Management Services, Rockville, MD (DP); International Epidemiology Institute, Rockville, MD (WJB); Department of Medicine (Epidemiology), Vanderbilt University, Nashville, TN (WJB). ; Affiliations of authors: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (W-QL, JFF, MHG); Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Cancer Epidemiology, Peking University Cancer Hospital and Institute, Beijing, China (W-QL, J-LM, LZ, J-YL, LS, K-FP, W-CY); RTI International, Rockville, MD (LMB); Linqu County Public Health Bureau, Shandong, China (W-DL, Z-XH); Westat, Rockville, MD (SC-M); Information Management Services, Rockville, MD (DP); International Epidemiology Institute, Rockville, MD (WJB); Department of Medicine (Epidemiology), Vanderbilt University, Nashville, TN (WJB). gailm@mail.nih.gov weichengyou@yahoo.com. Y1 - 2014/07// PY - 2014 DA - July 2014 VL - 106 IS - 7 KW - Anti-Bacterial Agents KW - 0 KW - Amoxicillin KW - 804826J2HU KW - Omeprazole KW - KG60484QX9 KW - Index Medicus KW - Randomized Controlled Trials as Topic KW - Odds Ratio KW - Age Factors KW - Humans KW - Aged KW - Drug Therapy, Combination KW - Amoxicillin -- therapeutic use KW - Logistic Models KW - Adult KW - Treatment Outcome KW - Omeprazole -- therapeutic use KW - Incidence KW - Follow-Up Studies KW - Middle Aged KW - Female KW - Male KW - Proportional Hazards Models KW - Stomach Neoplasms -- microbiology KW - Anti-Bacterial Agents -- therapeutic use KW - Precancerous Conditions -- microbiology KW - Stomach Neoplasms -- mortality KW - Helicobacter Infections -- drug therapy KW - Helicobacter Infections -- complications KW - Helicobacter pylori -- drug effects KW - Precancerous Conditions -- drug therapy KW - Stomach Neoplasms -- prevention & control KW - Stomach Neoplasms -- epidemiology KW - Precancerous Conditions -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535627557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+Helicobacter+pylori+treatment+on+gastric+cancer+incidence+and+mortality+in+subgroups.&rft.au=Li%2C+Wen-Qing%3BMa%2C+Jun-Ling%3BZhang%2C+Lian%3BBrown%2C+Linda+M%3BLi%2C+Ji-You%3BShen%2C+Lin%3BPan%2C+Kai-Feng%3BLiu%2C+Wei-Dong%3BHu%2C+Yuanreng%3BHan%2C+Zhong-Xiang%3BCrystal-Mansour%2C+Susan%3BPee%2C+David%3BBlot%2C+William+J%3BFraumeni%2C+Joseph+F%3BYou%2C+Wei-Cheng%3BGail%2C+Mitchell+H&rft.aulast=Li&rft.aufirst=Wen-Qing&rft.date=2014-07-01&rft.volume=106&rft.issue=7&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju116 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-11 N1 - Date created - 2014-06-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Cancer. 1999 Nov 26;83(5):615-9 [10521796] Gut. 2013 May;62(5):676-82 [22698649] JAMA. 2013 Feb 13;309(6):578-86 [23403682] Biometrics. 2002 Mar;58(1):21-9 [11890317] JAMA. 2004 Jan 14;291(2):187-94 [14722144] JAMA. 1991 Jul 3;266(1):93-8 [2046134] Cancer Res. 1993 Mar 15;53(6):1317-21 [8443811] Lancet. 1994 Jan 22;343(8891):243-4 [7904707] Control Clin Trials. 1998 Aug;19(4):352-69 [9683311] Aliment Pharmacol Ther. 2013 May;37(10):969-78 [23550594] J Natl Cancer Inst. 2006 Jul 19;98(14):974-83 [16849680] Gut. 2007 May;56(5):631-6 [17142647] Helicobacter. 2007 Oct;12(5):575-8 [17760729] Lancet. 2008 Aug 2;372(9636):392-7 [18675689] World J Gastroenterol. 2011 Nov 7;17(41):4596-601 [22147965] J Natl Cancer Inst. 2012 Mar 21;104(6):488-92 [22271764] Comment In: J Natl Cancer Inst. 2014 Nov;106(11). pii: dju352. doi: 10.1093/jnci/dju352 [25381392] J Natl Cancer Inst. 2014 Nov;106(11). pii: dju348. doi: 10.1093/jnci/dju348 [25381391] J Natl Cancer Inst. 2014 Jul;106(7). pii: dju148. doi: 10.1093/jnci/dju148 [24925352] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/dju116 ER - TY - JOUR T1 - Physical activity and cancer-specific mortality in the NIH-AARP Diet and Health Study cohort AN - 1534817168; 19846980 AB - Higher physical activity levels have been associated with a lower risk of developing various cancers and all-cancer mortality, but the impact of pre-diagnosis physical activity on cancer-specific death has not been fully characterized. In the prospective National Institutes of Health-AARP Diet and Health Study with 293,511 men and women, we studied prediagnosis moderate to vigorous intensity leisure time physical activity (MVPA) in the past 10 years and cancer-specific mortality. Over a median 12.1 years, we observed 15,001 cancer deaths. Using Cox proportional hazards regression, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for MVPA with cancer mortality overall and by 20 specific cancer sites, adjusting for relevant risk factors. Compared to participants reporting never/rare MVPA, those reporting >7 hr/week MVPA had a lower risk of total cancer mortality (HR=0.89, 95% CI 0.84-0.94; p-trend 7 hr/week of MVPA to those reporting never/rare MVPA, we observed a lower risk of death from colon (HR=0.70; 95% CI 0.57-0.85; p-trend <0.001), liver (0.71; 0.52-0.98; p-trend=0.012) and lung cancer (0.84; 0.77-0.92; p-trend <0.001) and a significant p-trend for non-Hodgkins lymphoma (0.80; 0.62-1.04; p-trend=0.017). An unexpected increased mortality p-trend with increasing MVPA was observed for death from kidney cancer (1.42; 0.98-2.03; p-trend=0.016). Our findings suggest that higher prediagnosis leisure time physical activity is associated with lower risk of overall cancer mortality and mortality from multiple cancer sites. Future studies should confirm observed associations and further explore timing of physical activity and underlying biological mechanisms. What's new? Despite evidence that physical activity reduces risk of multiple chronic diseases, including cancer, as much as one-third of the U.S. population is inactive. In this study, the authors explored associations between pre-diagnosis physical activity and cancer mortality. They found that higher pre-diagnosis leisure-time physical activity is associated with a decreased risk of overall cancer mortality, and particularly mortality from cancers of the colon, liver, lung, and non-Hodgkin's lymphoma. JF - International Journal of Cancer AU - Arem, Hannah AU - Moore, Steve C AU - Park, Yikyung AU - Ballard-Barbash, Rachel AU - Hollenbeck, Albert AU - Leitzmann, Michael AU - Matthews, Charles E AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD. Y1 - 2014/07// PY - 2014 DA - Jul 2014 SP - 423 EP - 431 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 135 IS - 2 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Diets KW - Mortality KW - Health risks KW - Non-Hodgkin's lymphoma KW - USA KW - Physical activity KW - Risk factors KW - Liver KW - Kidney KW - Risk reduction 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/1534817168?accountid=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=Physical+activity+and+cancer-specific+mortality+in+the+NIH-AARP+Diet+and+Health+Study+cohort&rft.au=Arem%2C+Hannah%3BMoore%2C+Steve+C%3BPark%2C+Yikyung%3BBallard-Barbash%2C+Rachel%3BHollenbeck%2C+Albert%3BLeitzmann%2C+Michael%3BMatthews%2C+Charles+E&rft.aulast=Arem&rft.aufirst=Hannah&rft.date=2014-07-01&rft.volume=135&rft.issue=2&rft.spage=423&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28659 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Diets; Non-Hodgkin's lymphoma; Health risks; Mortality; Risk factors; Physical activity; Kidney; Liver; Risk reduction; Lung cancer; USA DO - http://dx.doi.org/10.1002/ijc.28659 ER - TY - JOUR T1 - Mitochondrial genome maintenance in health and disease. AN - 1534471332; 24780559 AB - Human mitochondria harbor an essential, high copy number, 16,569 base pair, circular DNA genome that encodes 13 gene products required for electron transport and oxidative phosphorylation. Mutation of this genome can compromise cellular respiration, ultimately resulting in a variety of progressive metabolic diseases collectively known as 'mitochondrial diseases'. Mutagenesis of mtDNA and the persistence of mtDNA mutations in cells and tissues is a complex topic, involving the interplay of DNA replication, DNA damage and repair, purifying selection, organelle dynamics, mitophagy, and aging. We briefly review these general elements that affect maintenance of mtDNA, and we focus on nuclear genes encoding the mtDNA replication machinery that can perturb the genetic integrity of the mitochondrial genome. Published by Elsevier B.V. JF - DNA repair AU - Copeland, William C AU - Longley, Matthew J AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, Durham, NC 27709, USA. Electronic address: copelan1@niehs.nih.gov. ; Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, Durham, NC 27709, USA. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 190 EP - 198 VL - 19 KW - DNA, Mitochondrial KW - 0 KW - Index Medicus KW - Mitochondrial DNA replication KW - POLG KW - mtDNA KW - Mutagenesis KW - Mitochondrial disease KW - Humans KW - Oxidative Phosphorylation KW - Mutation KW - DNA, Mitochondrial -- genetics KW - Mitochondrial Diseases -- pathology KW - Mitochondrial Diseases -- genetics KW - DNA Replication -- genetics KW - Genome, Mitochondrial KW - DNA Damage -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534471332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mitochondrial+genome+maintenance+in+health+and+disease.&rft.au=Copeland%2C+William+C%3BLongley%2C+Matthew+J&rft.aulast=Copeland&rft.aufirst=William&rft.date=2014-07-01&rft.volume=19&rft.issue=&rft.spage=190&rft.isbn=&rft.btitle=&rft.title=DNA+repair&rft.issn=1568-7856&rft_id=info:doi/10.1016%2Fj.dnarep.2014.03.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-12 N1 - Date created - 2014-06-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4135-40 [21368114] PLoS Genet. 2011 Mar;7(3):e1002028 [21455489] J Biol Chem. 2011 May 13;286(19):16992-6 [21454602] Cold Spring Harb Perspect Biol. 2013 May;5(5):a012641 [23637283] Genetics. 2013 Jun;194(2):519-22 [23589460] Toxicol Sci. 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Mol Cell. 2012 Sep 28;47(6):980-6 [22864116] Nat Genet. 2013 Feb;45(2):214-9 [23313956] Am J Hum Genet. 2013 Feb 7;92(2):293-300 [23352259] Nucleic Acids Res. 2013 Mar 1;41(5):3144-61 [23358826] Cold Spring Harb Perspect Biol. 2013 Apr;5(4):a011395 [23545419] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.dnarep.2014.03.010 ER - TY - JOUR T1 - The clinical and financial burden of pre-emptive management of cytomegalovirus disease after allogeneic stem cell transplantation-implications for preventative treatment approaches. AN - 1534468888; 24831837 AB - Although cytomegalovirus (CMV) infection after allogeneic stem cell transplantation (SCT) is rarely fatal, the management of CMV by pre-emptive medication for viral reactivation has toxicity and carries a financial burden. New strategies to prevent CMV reactivation with vaccines and antiviral T cells may represent an advance over pre-emptive strategies but have yet to be justified in terms of transplantation outcome and cost. We compared outcomes and post-transplantation treatment cost in 44 patients who never required pre-emptive CMV treatment with 90 treated patients undergoing SCT at our institute between 2006 and 2012. Eighty-one subjects received CD34+ selected myeloablative SCT, 12 umbilical cord blood transplants, and 41 T-replete non-myeloablative SCT. One hundred nineteen patients (89%) were at risk for CMV because either the donor or recipient was seropositive. Of these, 90 patients (75.6%) reactivated CMV at a median of 30 (range 8-105) days after transplantation and received antivirals. There was no difference in standard transplantation risk factors between the two groups. In multivariate modeling, CMV reactivation >250 copies/mL (odds ratio = 3, P < 0.048), total duration of inpatient IV antiviral therapy (odds ratio = 1.04, P < 0.001), type of transplantation (T-deplete vs. T-replete; odds ratio = 4.65, P < 0.017) were found to be significantly associated with increased non-relapse mortality. The treated group incurred an additional cost of antiviral medication and longer hospitalization within the first 6 months after SCT of $58,000 to $74,000 per patient. Our findings suggest that to prevent CMV reactivation, treatment should be given within 1 week of SCT. Preventative treatment may improve outcome and have significant cost savings. Published by Elsevier Inc. JF - Cytotherapy AU - Jain, Natasha A AU - Lu, Kit AU - Ito, Sawa AU - Muranski, Pawel AU - Hourigan, Christopher S AU - Haggerty, Janice AU - Chokshi, Puja D AU - Ramos, Catalina AU - Cho, Elena AU - Cook, Lisa AU - Childs, Richard AU - Battiwalla, Minoo AU - Barrett, A John AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: minoo.battiwalla@nih.gov. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 927 EP - 933 VL - 16 IS - 7 KW - Index Medicus KW - pre-emptive therapy KW - antiviral cellular therapy KW - economic cost KW - CMV reactivation KW - Humans KW - Aged KW - Child KW - T-Lymphocytes -- pathology KW - Tissue Donors KW - Cost of Illness KW - Risk Factors KW - Adult KW - Virus Activation -- genetics KW - Middle Aged KW - Adolescent KW - T-Lymphocytes -- virology KW - Female KW - Male KW - T-Lymphocytes -- immunology KW - Hematologic Neoplasms -- therapy KW - Hematologic Neoplasms -- pathology KW - Cytomegalovirus Infections -- economics KW - Hematopoietic Stem Cell Transplantation -- economics KW - Cytomegalovirus -- pathogenicity KW - Transplantation, Homologous -- adverse effects KW - Cytomegalovirus -- genetics KW - Cytomegalovirus Infections -- virology KW - Cytomegalovirus Infections -- pathology KW - Transplantation, Homologous -- economics KW - Hematopoietic Stem Cell Transplantation -- adverse effects KW - Hematologic Neoplasms -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534468888?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytotherapy&rft.atitle=The+clinical+and+financial+burden+of+pre-emptive+management+of%C2%A0cytomegalovirus+disease+after+allogeneic+stem+cell+transplantation-implications+for+preventative+treatment+approaches.&rft.au=Jain%2C+Natasha+A%3BLu%2C+Kit%3BIto%2C+Sawa%3BMuranski%2C+Pawel%3BHourigan%2C+Christopher+S%3BHaggerty%2C+Janice%3BChokshi%2C+Puja+D%3BRamos%2C+Catalina%3BCho%2C+Elena%3BCook%2C+Lisa%3BChilds%2C+Richard%3BBattiwalla%2C+Minoo%3BBarrett%2C+A+John&rft.aulast=Jain&rft.aufirst=Natasha&rft.date=2014-07-01&rft.volume=16&rft.issue=7&rft.spage=927&rft.isbn=&rft.btitle=&rft.title=Cytotherapy&rft.issn=1477-2566&rft_id=info:doi/10.1016%2Fj.jcyt.2014.02.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-12 N1 - Date created - 2014-06-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Blood. 2012 Aug 23;120(8):1545-51 [22700725] Mol Ther. 2012 Aug;20(8):1622-32 [22801446] Biol Blood Marrow Transplant. 2012 Nov;18(11):1687-99 [22683614] Blood. 2013 May 2;121(18):3745-58 [23435462] Blood. 2013 Jun 27;121(26):5113-23 [23610374] Blood. 2013 Aug 15;122(7):1316-24 [23744585] Bone Marrow Transplant. 2013 Oct;48(10):1313-6 [23562969] Mol Ther. 2013 Nov;21(11):2113-21 [23783429] Hematology Am Soc Hematol Educ Program. 2013;2013:342-7 [24319202] Cytotherapy. 2014 Feb;16(2):149-59 [24438896] Bone Marrow Transplant. 2000 Apr;25(7):757-63 [10745262] Bone Marrow Transplant. 2000 Jul;26(1):23-9 [10918402] Blood. 2001 Feb 15;97(4):867-74 [11159510] Br J Haematol. 2001 Jan;112(1):228-36 [11167809] J Infect Dis. 2002 Feb 1;185(3):273-82 [11807708] Clin Infect Dis. 2002 Apr 15;34(8):1094-7 [11914998] Blood. 2002 Jun 1;99(11):3916-22 [12010789] Clin Infect Dis. 2002 Sep 15;35(6):703-12 [12203168] Bone Marrow Transplant. 2003 Oct;32(7):703-7 [13130318] Lancet. 2003 Oct 25;362(9393):1375-7 [14585640] Br J Haematol. 2003 Nov;123(4):662-70 [14616970] Blood. 2003 Dec 15;102(13):4255-60 [12933590] Biol Blood Marrow Transplant. 2004 Jan;10(1):49-57 [14752779] Blood. 2004 Mar 15;103(6):2003-8 [14644993] Clin Infect Dis. 1992 Apr;14(4):831-5 [1315585] Science. 1992 Jul 10;257(5067):238-41 [1352912] Blood. 1995 Oct 1;86(7):2815-20 [7670117] N Engl J Med. 1995 Oct 19;333(16):1038-44 [7675046] Blood. 1996 Nov 15;88(10):4063-71 [8916975] Bone Marrow Transplant. 1996 Nov;18 Suppl 2:110-4 [8932810] Blood. 1997 Sep 15;90(6):2502-8 [9310503] Blood. 1999 Mar 1;93(5):1781-2 [10084817] J Exp Med. 2005 Aug 1;202(3):379-86 [16061727] Haematologica. 2005 Sep;90(9):1290-2 [16154862] Blood. 2006 Sep 1;108(5):1770-3 [16675712] Nat Med. 2006 Oct;12(10):1160-6 [16998485] Biol Blood Marrow Transplant. 2007 May;13(5):577-83 [17448917] Biol Blood Marrow Transplant. 2007 Jun;13(6):707-14 [17531781] Biol Blood Marrow Transplant. 2007 Jul;13(7):765-70 [17580254] J Infect Dis. 2007 Sep 1;196(5):699-704 [17674311] Blood Cells Mol Dis. 2008 Jan-Feb;40(1):63-7 [17869548] Eur J Haematol. 2008 Mar;80(3):251-7 [18081702] Herpes. 2008 Oct;15(1):4-12 [18983762] Herpes. 2009 Jan;15(3):44-5 [19306601] Biol Blood Marrow Transplant. 2009 May;15(5):564-73 [19361748] Blood. 2010 Sep 9;116(10):1655-62 [20508161] Clin Infect Dis. 2011 Jan 1;52(1):49-57 [21148519] Blood. 2011 Aug 4;118(5):1402-12 [21540462] J Infect Dis. 2012 Apr 15;205(8):1294-304 [22402037] Lancet Infect Dis. 2012 Apr;12(4):290-9 [22237175] J Immunother. 2012 Oct;35(8):621-8 [22996368] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jcyt.2014.02.010 ER - TY - JOUR T1 - Prevalence of suicide attempters in emergency departments in Japan: a systematic review and meta-analysis. AN - 1526128857; 24836085 AB - The number of hospital admissions related to suicide attempts is increasing worldwide. The Emergency Department (ED) is recognized in Japan as an opportunity to intervene with suicide attempters however, the prevalence of suicide attempters in the ED is unknown. Therefore, a meta-analysis was conducted to provide this information. We conducted searches of databases (PubMed, PsycINFO, CINAHL, ICHUSHI, CiNii) to identify studies about suicide attempters in the ED in Japan. A meta-analysis was used to calculate the pooled prevalence proportion of suicide attempters in the ED, and their prevalence proportion of psychiatric disorder and method of suicide in suicide attempters. The search of Japanese studies identified 3338 records, of which 70 were included in the meta-analysis. A total of 25 studies reported the psychiatric diagnosis and 62 studies reported the method of suicide. The pooled prevalence proportion of suicide attempters was 4.7%. Mood disorders were the most frequent psychiatric disorders (ICD: 30%, DSM: 35%), and poisoning was the most frequent method of attempting suicide (52%). There might be a publication bias because only published studies were included. There also might be an information bias, such as reporting bias or misclassification, because most of studies included in the analysis used retrospective designs. The results provide clear evidence of the prevalence of suicide attempters in the ED in Japan. The results indicate that suicide attempters in the ED have a higher proportion of mood disorders, and that the most common method of suicide is poisoning. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Journal of affective disorders AU - Kawashima, Yoshitaka AU - Yonemoto, Naohiro AU - Inagaki, Masatoshi AU - Yamada, Mitsuhiko AD - Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1, Ogawahigashimachi, Kodaira, Tokyo 187-8553, Japan. Electronic address: kawashima@ncnp.go.jp. ; Department of Epidemiology and Biostatistics, Translational Medical Center, National Centre of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Electronic address: nyonemoto@gmail.com. ; Department of Neuropsychiatry, Okayama University Hospital, Kita-ku, Okayama, Japan. Electronic address: masatoshiinagaki@okayama-u.ac.jp. ; Department of Neuropsychopharmacology, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1, Ogawahigashimachi, Kodaira, Tokyo 187-8553, Japan. Electronic address: mitsu@ncnp.go.jp. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 33 EP - 39 VL - 163 KW - Index Medicus KW - Meta-analysis KW - Suicide KW - Self-harm KW - Systematic review KW - Emergency medicine KW - Japan -- epidemiology KW - Hospitalization KW - Mental Disorders -- epidemiology KW - Humans KW - Retrospective Studies KW - Emergency Service, Hospital KW - Drug Overdose -- epidemiology KW - Prevalence KW - Suicide, Attempted -- statistics & numerical data KW - Suicide, Attempted -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1526128857?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+affective+disorders&rft.atitle=Prevalence+of+suicide+attempters+in+emergency+departments+in+Japan%3A+a+systematic+review+and+meta-analysis.&rft.au=Kawashima%2C+Yoshitaka%3BYonemoto%2C+Naohiro%3BInagaki%2C+Masatoshi%3BYamada%2C+Mitsuhiko&rft.aulast=Kawashima&rft.aufirst=Yoshitaka&rft.date=2014-07-01&rft.volume=163&rft.issue=&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Journal+of+affective+disorders&rft.issn=1573-2517&rft_id=info:doi/10.1016%2Fj.jad.2014.03.025 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-14 N1 - Date created - 2014-05-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jad.2014.03.025 ER - TY - JOUR T1 - FGFR3 induces degradation of BMP type I receptor to regulate skeletal development. AN - 1522680006; 24657641 AB - Fibroblast growth factors (FGFs) and their receptors (FGFRs) play significant roles in vertebrate organogenesis and morphogenesis. FGFR3 is a negative regulator of chondrogenesis and multiple mutations with constitutive activity of FGFR3 result in achondroplasia, one of the most common dwarfisms in humans, but the molecular mechanism remains elusive. In this study, we found that chondrocyte-specific deletion of BMP type I receptor a (Bmpr1a) rescued the bone overgrowth phenotype observed in Fgfr3 deficient mice by reducing chondrocyte differentiation. Consistently, using in vitro chondrogenic differentiation assay system, we demonstrated that FGFR3 inhibited BMPR1a-mediated chondrogenic differentiation. Furthermore, we showed that FGFR3 hyper-activation resulted in impaired BMP signaling in chondrocytes of mouse growth plates. We also found that FGFR3 inhibited BMP-2- or constitutively activated BMPR1-induced phosphorylation of Smads through a mechanism independent of its tyrosine kinase activity. We found that FGFR3 facilitates BMPR1a to degradation through Smurf1-mediated ubiquitination pathway. We demonstrated that down-regulation of BMP signaling by BMPR1 inhibitor dorsomorphin led to the retardation of chondrogenic differentiation, which mimics the effect of FGF-2 on chondrocytes and BMP-2 treatment partially rescued the retarded growth of cultured bone rudiments from thanatophoric dysplasia type II mice. Our findings reveal that FGFR3 promotes the degradation of BMPR1a, which plays an important role in the pathogenesis of FGFR3-related skeletal dysplasia. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biochimica et biophysica acta AU - Qi, Huabing AU - Jin, Min AU - Duan, Yaqi AU - Du, Xiaolan AU - Zhang, Yuanquan AU - Ren, Fangli AU - Wang, Yinyin AU - Tian, Qingyun AU - Wang, Xiaofeng AU - Wang, Quan AU - Zhu, Ying AU - Xie, Yangli AU - Liu, Chuanju AU - Cao, Xu AU - Mishina, Yuji AU - Chen, Di AU - Deng, Chu-xia AU - Chang, Zhijie AU - Chen, Lin AD - Center of Bone Metabolism and Repair (CBMR), Trauma Center, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China. ; Center of Bone Metabolism and Repair (CBMR), Trauma Center, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China; State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400042, China. ; State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Medicine, Tsinghua University, Beijing 100084, China. ; Department of Cell Biology, New York University School of Medicine, New York, NY 10016, USA; Department of Orthopaedic Surgery, New York University School of Medicine and NYU Hospital for Joint Diseases, New York, NY 10003, USA. ; Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. ; Department of Biologic & Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI 48109, USA. ; Department of Biochemistry, Rush University, Chicago, IL 60612, USA. ; Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, 10/9N105, National Institutes of Health, Bethesda, MD 20892, USA. ; State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Medicine, Tsinghua University, Beijing 100084, China. Electronic address: zhijiec@tsinghua.edu.cn. ; Center of Bone Metabolism and Repair (CBMR), Trauma Center, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China; State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400042, China; Department of Rehabilitation Medicine, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing 400042, China. Electronic address: linchen70@163.com. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 1237 EP - 1247 VL - 1843 IS - 7 SN - 0006-3002, 0006-3002 KW - (6-(4-(2-piperidin-1-ylethoxy)phenyl))-3-pyridin-4-ylpyrazolo(1,5-a)pyrimidine KW - 0 KW - Bmp2 protein, mouse KW - Bone Morphogenetic Protein 2 KW - Pyrazoles KW - Pyrimidines KW - Smad Proteins KW - Fibroblast Growth Factor 2 KW - 103107-01-3 KW - Smurf1 protein, mouse KW - EC 2.3.2.26 KW - Ubiquitin-Protein Ligases KW - EC 2.3.2.27 KW - Fgfr3 protein, mouse KW - EC 2.7.10.1 KW - Receptor, Fibroblast Growth Factor, Type 3 KW - Bmpr1a protein, mouse KW - EC 2.7.11.30 KW - Bone Morphogenetic Protein Receptors, Type I KW - Index Medicus KW - Achondroplasia KW - Smurf1 KW - FGFR3 KW - Chondrocyte KW - BMPR1 KW - Smad Proteins -- genetics KW - Fibroblast Growth Factor 2 -- metabolism KW - Fibroblast Growth Factor 2 -- pharmacology KW - Animals KW - Morphogenesis -- genetics KW - Humans KW - Pyrimidines -- pharmacology KW - Cell Differentiation KW - Mice KW - Phosphorylation -- drug effects KW - Bone Morphogenetic Protein 2 -- pharmacology KW - Mice, Knockout KW - Smad Proteins -- metabolism KW - Pyrazoles -- pharmacology KW - Bone Morphogenetic Protein 2 -- metabolism KW - Ubiquitination -- drug effects KW - Ubiquitin-Protein Ligases -- genetics KW - Ubiquitin-Protein Ligases -- metabolism KW - Embryo, Mammalian KW - Signal Transduction KW - Gene Expression Regulation, Developmental KW - Receptor, Fibroblast Growth Factor, Type 3 -- deficiency KW - Growth Plate -- cytology KW - Receptor, Fibroblast Growth Factor, Type 3 -- genetics KW - Chondrocytes -- drug effects KW - Chondrocytes -- cytology KW - Bone Morphogenetic Protein Receptors, Type I -- genetics KW - Achondroplasia -- metabolism KW - Growth Plate -- metabolism KW - Bone Morphogenetic Protein Receptors, Type I -- metabolism KW - Chondrocytes -- metabolism KW - Achondroplasia -- genetics KW - Growth Plate -- growth & development KW - Achondroplasia -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1522680006?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=FGFR3+induces+degradation+of+BMP+type+I+receptor+to+regulate+skeletal+development.&rft.au=Qi%2C+Huabing%3BJin%2C+Min%3BDuan%2C+Yaqi%3BDu%2C+Xiaolan%3BZhang%2C+Yuanquan%3BRen%2C+Fangli%3BWang%2C+Yinyin%3BTian%2C+Qingyun%3BWang%2C+Xiaofeng%3BWang%2C+Quan%3BZhu%2C+Ying%3BXie%2C+Yangli%3BLiu%2C+Chuanju%3BCao%2C+Xu%3BMishina%2C+Yuji%3BChen%2C+Di%3BDeng%2C+Chu-xia%3BChang%2C+Zhijie%3BChen%2C+Lin&rft.aulast=Qi&rft.aufirst=Huabing&rft.date=2014-07-01&rft.volume=1843&rft.issue=7&rft.spage=1237&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbamcr.2014.03.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-30 N1 - Date created - 2014-05-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Development. 1998 Dec;125(24):4977-88 [9811582] Genes Dev. 1999 Jun 1;13(11):1361-6 [10364154] Hum Mol Genet. 1999 Jan;8(1):35-44 [9887329] Genes Dev. 1999 Jun 15;13(12):1601-13 [10385628] J Clin Invest. 1999 Aug;104(4):399-407 [10449432] Nature. 1999 Aug 12;400(6745):687-93 [10458166] Nature. 1999 Sep 30;401(6752):480-5 [10519551] J Cell Sci. 2005 Feb 1;118(Pt 3):643-50 [15657086] Exp Cell Res. 2005 Apr 1;304(2):417-31 [15748888] Proc Natl Acad Sci U S A. 2005 Apr 5;102(14):5062-7 [15781876] Cytokine Growth Factor Rev. 2005 Apr;16(2):205-13 [15863035] Proc Natl Acad Sci U S A. 2005 Dec 13;102(50):18023-7 [16322106] Ann N Y Acad Sci. 2006 Apr;1068:1-13 [16831900] Ann N Y Acad Sci. 2006 Apr;1068:26-40 [16831903] Dev Biol. 2006 Aug 15;296(2):315-28 [16815385] Development. 2006 Dec;133(23):4667-78 [17065231] Mol Cell. 2007 Feb 9;25(3):441-54 [17289590] Lancet. 2007 Jul 14;370(9582):162-72 [17630040] Cell. 2007 Nov 30;131(5):980-93 [18045539] Nat Chem Biol. 2008 Jan;4(1):33-41 [18026094] Bone. 2008 Apr;42(4):631-43 [18242159] Nat Cell Biol. 2008 Aug;10(8):994-1002 [18641638] Annu Rev Genomics Hum Genet. 2008;9:183-96 [18767962] Development. 2008 Oct;135(19):3247-57 [18776145] Mol Cell. 2008 Sep 26;31(6):918-24 [18922473] PLoS One. 2008;3(12):e3961 [19088846] Hum Mol Genet. 2009 Jan 15;18(2):227-40 [18923003] Development. 2009 Apr;136(7):1093-104 [19224984] EMBO J. 2009 Jul 22;28(14):2028-41 [19536134] Hum Mol Genet. 2010 Apr 1;19(7):1199-210 [20053668] Development. 2010 May;137(10):1601-11 [20392740] J Clin Invest. 2010 Jul;120(7):2457-73 [20551513] J Biol Chem. 2010 Sep 24;285(39):30103-14 [20624921] Circ Res. 2010 Nov 12;107(10):1209-19 [20847311] Nat Rev Mol Cell Biol. 2009 Jun;10(6):398-409 [19436320] J Clin Invest. 1999 Dec;104(11):1517-25 [10587515] Development. 2000 Feb;127(3):621-30 [10631182] Hum Mol Genet. 2000 Jul 1;9(11):1603-13 [10861287] Hum Mol Genet. 2000 Aug 12;9(13):2001-8 [10942429] Annu Rev Cell Dev Biol. 2000;16:191-220 [11031235] Hum Mol Genet. 2001 Mar 1;10(5):457-65 [11181569] Mol Cell. 2000 Dec;6(6):1365-75 [11163210] Nat Rev Mol Cell Biol. 2001 Apr;2(4):294-307 [11283727] J Biol Chem. 2001 Apr 20;276(16):12477-80 [11278251] Hum Mol Genet. 2001 Jun 1;10(12):1255-64 [11406607] Genesis. 2002 Feb;32(2):69-72 [11857780] J Bone Miner Res. 2002 May;17(5):898-906 [12009021] Yi Chuan Xue Bao. 2002 May;29(5):424-9 [12043570] Dev Cell. 2002 Sep;3(3):439-49 [12361605] Nature. 2003 Apr 10;422(6932):625-9 [12687003] Nature. 2003 May 15;423(6937):332-6 [12748651] Cell. 2003 Jun 13;113(6):685-700 [12809600] J Bone Miner Res. 2003 Nov;18(11):2043-51 [14606518] Genes Dev. 2004 Feb 1;18(3):290-305 [14871928] Biochem Biophys Res Commun. 2004 Oct 8;323(1):91-7 [15351706] Genes Dev. 1994 Feb 1;8(3):277-89 [8314082] Nature. 1994 Sep 15;371(6494):252-4 [8078586] Am J Hum Genet. 1995 Feb;56(2):368-73 [7847369] Genes Dev. 1995 Dec 15;9(24):3027-37 [8543149] Cell. 1996 Mar 22;84(6):911-21 [8601314] Nat Genet. 1996 Apr;12(4):390-7 [8630492] Nat Genet. 1996 Jun;13(2):233-7 [8640234] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):5860-5 [8650183] Genes Dev. 1997 Apr 15;11(8):984-95 [9136927] J Cell Biochem. 1997 Jun 1;65(3):325-39 [9138089] Genes Cells. 1998 Apr;3(4):257-64 [9663660] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbamcr.2014.03.011 ER - TY - JOUR T1 - Menopausal hormone therapy and risk of endometrial cancer. AN - 1521912978; 23680641 AB - Endometrial cancer is clearly a hormonally responsive tumor, with a critical role played by estrogens unopposed by progestins. Numerous epidemiologic studies have shown substantial risk increases associated with use of unopposed estrogens, especially among thin women. This risk, however, can be reduced if progestins are added to the therapy. The manner in which progestins are prescribed is a critical determinant of risk. Most studies show that women who have ever used progestins continuously (>25 days/months) are at somewhat reduced risk relative to non-users (meta-analysis relative risk, RR, based on observational studies=0.78, 95 confidence intervals, CI, 0.72-0.86). The reduced risk in greatest among heavy women. In contrast, women who have ever used progestins sequentially for <10 days each month are at increased risk, with meta-analysis results showing on overall RR of 1.76 (1.51-2.05); in contrast, progestins given for 10-24 days/month appear unrelated to risk (RR=1.07, 0.92-1.24). These risks were based on varying patterns of usage, with little information available regarding how endometrial cancer risk is affected by duration of use, type and/or dose of estrogen or progestin, or mode of administration. Effects may also vary by clinical characteristics (e.g., differences for Type I vs. II tumors). Further resolution of many of these relationships may be dependent on pooling data from multiple studies to derive sufficient power for subgroups of users. With changing clinical practices, it will be important for future studies to monitor a wide range of exposures and to account for divergent effects of different usage patterns. This article is part of a Special Issue entitled 'Menopause'. Published by Elsevier Ltd. JF - The Journal of steroid biochemistry and molecular biology AU - Brinton, Louise A AU - Felix, Ashley S AD - Hormonal and Reproductive Epidemiology Branch, National Cancer Institute, Rockville, MD 20852-7234, United States. Electronic address: brinton@nih.gov. ; Hormonal and Reproductive Epidemiology Branch, National Cancer Institute, Rockville, MD 20852-7234, United States. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 83 EP - 89 VL - 142 KW - Progestins KW - 0 KW - Index Medicus KW - Risk KW - Epidemiology KW - Endometrial cancer KW - Menopausal hormone therapy KW - Humans KW - Progestins -- administration & dosage KW - Menopause KW - Female KW - Endometrial Neoplasms -- chemically induced KW - Estrogen Replacement Therapy -- adverse effects KW - Estrogen Replacement Therapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521912978?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+steroid+biochemistry+and+molecular+biology&rft.atitle=Menopausal+hormone+therapy+and+risk+of+endometrial+cancer.&rft.au=Brinton%2C+Louise+A%3BFelix%2C+Ashley+S&rft.aulast=Brinton&rft.aufirst=Louise&rft.date=2014-07-01&rft.volume=142&rft.issue=&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+steroid+biochemistry+and+molecular+biology&rft.issn=1879-1220&rft_id=info:doi/10.1016%2Fj.jsbmb.2013.05.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-19 N1 - Date created - 2014-05-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Postgrad Med J. 1978;54 Suppl 2:59-64 [740582] Obstet Gynecol. 1979 Sep;54(3):269-77 [471366] J R Soc Med. 1979 May;72(5):322-7 [552525] Gynecol Oncol. 1980 Oct;10(2):173-87 [7461483] Gynecol Oncol. 1983 Feb;15(1):10-7 [6822361] Maturitas. 1985 Jul;7(2):147-59 [4033448] Obstet Gynecol. 1987 Sep;70(3 Pt 1):289-93 [3627576] Br J Cancer. 1988 Feb;57(2):205-12 [3358913] Maturitas. 1988 Dec;10(4):271-82 [3226337] BMJ. 1989 Jan 21;298(6667):147-51 [2538173] Br J Cancer. 1989 Mar;59(3):445-7 [2930713] Am J Obstet Gynecol. 1990 Jan;162(1):148-54 [2301483] Obstet Gynecol. 1993 Feb;81(2):265-71 [8380913] Obstet Gynecol. 1995 Feb;85(2):304-13 [7824251] Cancer Causes Control. 1996 Nov;7(6):575-80 [8932917] J Natl Cancer Inst. 1997 Aug 6;89(15):1110-6 [9262248] Epidemiology. 1998 Jan;9(1):99-101 [9430277] J Natl Cancer Inst. 1999 Jul 7;91(13):1131-7 [10393721] Drug Saf. 2005;28(3):241-9 [15733028] Lancet. 2005 Apr 30-May 6;365(9470):1543-51 [15866308] Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1724-31 [16030108] Am J Epidemiol. 2006 Oct 15;164(8):775-86 [16997897] Cancer. 2007 Apr 1;109(7):1303-11 [17315161] Cancer Causes Control. 2007 Nov;18(9):1001-7 [17653829] Am J Obstet Gynecol. 2007 Aug;197(2):139.e1-7 [17689625] Lancet. 2008 Feb 16;371(9612):569-78 [18280327] Int J Cancer. 2010 Jan 1;126(1):208-16 [19551854] Obstet Gynecol. 2009 Dec;114(6):1197-204 [19935019] Cancer Epidemiol Biomarkers Prev. 2010 Feb;19(2):475-83 [20086105] Am J Epidemiol. 2010 Dec 15;172(12):1394-403 [20961969] Cancer Epidemiol Biomarkers Prev. 2010 Dec;19(12):3119-30 [21030602] Int J Cancer. 2011 Apr 1;128(7):1644-51 [21280035] Cancer Causes Control. 2011 Dec;22(12):1639-46 [21909949] Hematol Oncol Clin North Am. 2012 Feb;26(1):1-12 [22244658] Cochrane Database Syst Rev. 2012;8:CD000402 [22895916] Int J Cancer. 2013 Jan 15;132(2):417-26 [22553145] Am J Epidemiol. 2013 Jan 15;177(2):142-51 [23171881] J Clin Epidemiol. 2000 Apr;53(4):385-91 [10785569] Am J Obstet Gynecol. 2000 Dec;183(6):1456-61 [11120510] Ann N Y Acad Sci. 2001 Sep;943:296-315 [11594550] Cancer Causes Control. 2001 Nov;12(9):829-35 [11714111] Maturitas. 2002 Feb 26;41(2):115-21 [11836042] JAMA. 2002 Jul 3;288(1):58-66 [12090863] Cancer Causes Control. 2003 Mar;14(2):195-201 [12749724] JAMA. 2003 Oct 1;290(13):1739-48 [14519708] Eur J Endocrinol. 2004 Feb;150(2):161-71 [14763914] Gynecol Oncol. 2004 May;93(2):568-70 [15099984] Cochrane Database Syst Rev. 2004;(3):CD000402 [15266429] Am J Obstet Gynecol. 2004 Oct;191(4):1146-51 [15507934] N Engl J Med. 1976 Jun 3;294(23):1259-62 [1264151] Br Med J. 1978 Dec 9;2(6152):1643-4 [728765] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jsbmb.2013.05.001 ER - TY - JOUR T1 - miR-126 contributes to Parkinson's disease by dysregulating the insulin-like growth factor/phosphoinositide 3-kinase signaling. AN - 1514433929; 24559646 AB - Dopamine (DA) neurons in sporadic Parkinson's disease (PD) display dysregulated gene expression networks and signaling pathways that are implicated in PD pathogenesis. Micro (mi)RNAs are regulators of gene expression, which could be involved in neurodegenerative diseases. We determined the miRNA profiles in laser microdissected DA neurons from postmortem sporadic PD patients' brains and age-matched controls. DA neurons had a distinctive miRNA signature and a set of miRNAs was dysregulated in PD. Bioinformatics analysis provided evidence for correlations of miRNAs with signaling pathways relevant to PD, including an association of miR-126 with insulin/IGF-1/PI3K signaling. In DA neuronal cell systems, enhanced expression of miR-126 impaired IGF-1 signaling and increased vulnerability to the neurotoxin 6-OHDA by downregulating factors in IGF-1/PI3K signaling, including its targets p85β, IRS-1, and SPRED1. Blocking of miR-126 function increased IGF-1 trophism and neuroprotection to 6-OHDA. Our data imply that elevated levels of miR-126 may play a functional role in DA neurons and in PD pathogenesis by downregulating IGF-1/PI3K/AKT signaling and that its inhibition could be a mechanism of neuroprotection. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Neurobiology of aging AU - Kim, Woori AU - Lee, Yenarae AU - McKenna, Noah D AU - Yi, Ming AU - Simunovic, Filip AU - Wang, Yulei AU - Kong, Benjamin AU - Rooney, Robert J AU - Seo, Hyemyung AU - Stephens, Robert M AU - Sonntag, Kai C AD - Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA; Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA. ; Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA. ; Bioinformatics Support Group, Advanced Biomedical Computing Center, NCI-Frederick, Frederick, MD, USA. ; Life Technologies, Foster City, CA, USA. ; Genome Explorations Inc, Memphis, TN, USA. ; Division of Molecular & Life Sciences, College of Science & Technology, Hanyang University, Seoul, Korea. ; Department of Psychiatry, McLean Hospital, Harvard Medical School, Belmont, MA, USA. Electronic address: ksonntag@mclean.harvard.edu. Y1 - 2014/07// PY - 2014 DA - July 2014 SP - 1712 EP - 1721 VL - 35 IS - 7 KW - MIRN126 microRNA, human KW - 0 KW - MicroRNAs KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Oxidopamine KW - 8HW4YBZ748 KW - Phosphatidylinositol 3-Kinases KW - EC 2.7.1.- KW - Index Medicus KW - Dopamine neurons KW - 6-OHDA neurotoxicity KW - Postmortem KW - Laser capture microdissection KW - Cell systems KW - Parkinson's disease KW - IGF-1 signaling KW - PI3K KW - miR-126 KW - miRNAs KW - Insulin KW - Oxidopamine -- toxicity KW - Cells, Cultured KW - Humans KW - Brain -- metabolism KW - Down-Regulation -- drug effects KW - Signal Transduction -- physiology KW - Phosphatidylinositol 3-Kinases -- metabolism KW - Signal Transduction -- drug effects KW - Parkinson Disease -- metabolism KW - Signal Transduction -- genetics KW - Insulin-Like Growth Factor I -- metabolism KW - Dopaminergic Neurons -- metabolism KW - MicroRNAs -- physiology KW - Parkinson Disease -- genetics KW - Gene Expression Regulation -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514433929?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=miR-126+contributes+to+Parkinson%27s+disease+by+dysregulating+the+insulin-like+growth+factor%2Fphosphoinositide+3-kinase+signaling.&rft.au=Kim%2C+Woori%3BLee%2C+Yenarae%3BMcKenna%2C+Noah+D%3BYi%2C+Ming%3BSimunovic%2C+Filip%3BWang%2C+Yulei%3BKong%2C+Benjamin%3BRooney%2C+Robert+J%3BSeo%2C+Hyemyung%3BStephens%2C+Robert+M%3BSonntag%2C+Kai+C&rft.aulast=Kim&rft.aufirst=Woori&rft.date=2014-07-01&rft.volume=35&rft.issue=7&rft.spage=1712&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+aging&rft.issn=1558-1497&rft_id=info:doi/10.1016%2Fj.neurobiolaging.2014.01.021 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-17 N1 - Date created - 2014-04-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Gene Ther. 2002 Sep;9(17):1155-62 [12170379] Mov Disord. 2011 May;26(6):1049-55 [21626550] J Biol Chem. 2004 Apr 30;279(18):18776-82 [14761948] Neurotox Res. 2004;5(8):579-98 [15111235] Ann Neurol. 2004 Sep;56(3):319-28 [15349858] Nat Biotechnol. 1997 Sep;15(9):871-5 [9306402] J Virol. 1998 Dec;72(12):9873-80 [9811723] Cell. 2005 Jan 14;120(1):15-20 [15652477] Hum Mol Genet. 2005 Jul 1;14(13):1709-25 [15888489] Nat Methods. 2006 Nov;3(11):881-6 [17060911] PLoS One. 2007;2(2):e238 [17327906] Neurobiol Dis. 2007 Jun;26(3):606-14 [17412603] Proc Natl Acad Sci U S A. 2007 Jun 12;104(24):10164-9 [17553960] Mol Cell. 2007 Jul 6;27(1):91-105 [17612493] Science. 2007 Aug 31;317(5842):1220-4 [17761882] Brain Pathol. 2008 Jan;18(1):130-8 [18226108] Am J Hum Genet. 2008 Feb;82(2):283-9 [18252210] Neurology. 2008 May 13;70(20):1916-25 [18474848] Cancer Res. 2008 May 15;68(10):3566-72 [18483236] Acta Neuropathol. 2011 Jul;122(1):75-86 [21541762] Hum Mol Genet. 2011 Aug 1;20(15):3067-78 [21558425] Methods Mol Biol. 2011;755:327-43 [21761317] Aging Cell. 2011 Dec;10(6):1080-8 [21967153] J Bioinform Comput Biol. 2011 Dec;9(6):795-812 [22084014] Methods Mol Biol. 2012;822:261-72 [22144205] Curr Alzheimer Res. 2012 Jan;9(1):35-66 [22329651] Trends Endocrinol Metab. 2012 Mar;23(3):133-41 [22245457] Exp Neurol. 2012 Jun;235(2):427-35 [22178324] J Clin Invest. 2012 Apr;122(4):1316-38 [22476197] J Clin Invest. 2012 Apr;122(4):1339-53 [22476196] Biochem Biophys Res Commun. 2008 Sep 5;373(4):607-12 [18602365] Dev Cell. 2008 Aug;15(2):261-71 [18694565] Dev Cell. 2008 Aug;15(2):272-84 [18694566] J Gerontol A Biol Sci Med Sci. 2012 Jun;67(6):611-25 [22503992] J Neurosci. 2012 Aug 8;32(32):10887-94 [22875923] Clin Exp Pharmacol Physiol. 2009 Sep;36(9):e32-9 [19473196] Neurosci Bull. 2013 Dec;29(6):745-51 [23740209] Genes Chromosomes Cancer. 2008 Nov;47(11):939-46 [18663744] Biochem Biophys Res Commun. 2008 Dec 5;377(1):136-40 [18834857] Nucleic Acids Res. 2009 Jan;37(Database issue):D105-10 [18996891] Genome Res. 2009 Jan;19(1):92-105 [18955434] Cell. 2009 Jan 23;136(2):215-33 [19167326] Clin Exp Pharmacol Physiol. 2009 Feb;36(2):181-8 [18986336] Brain. 2009 Jul;132(Pt 7):1795-809 [19052140] BMC Bioinformatics. 2009;10:200 [19563622] Genome Biol. 2009;10(6):R64 [19531210] Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):13052-7 [19628698] Nat Rev Neurosci. 2009 Dec;10(12):837-41 [19904280] PLoS One. 2010;5(1):e8856 [20111594] PLoS One. 2010;5(2):e9011 [20126402] J Immunol. 2010 Feb 15;184(4):1702-9 [20083669] Biochim Biophys Acta. 2010 Apr;1802(4):396-405 [20079433] Dev Neurobiol. 2010 Apr;70(5):384-96 [20186710] J Biol Chem. 2010 Apr 23;285(17):12726-34 [20106983] Brain Res. 2010 Jun 18;1338:48-57 [20380815] Mol Cell Biochem. 2011 May;351(1-2):157-64 [21249429] PLoS One. 2011;6(3):e17343 [21464990] Eur J Epidemiol. 2011 Jun;26 Suppl 1:S1-58 [21626386] J Mol Cell Biol. 2011 Jun;3(3):176-80 [21278200] Lancet Neurol. 2004 Mar;3(3):169-78 [14980532] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.neurobiolaging.2014.01.021 ER - TY - JOUR T1 - Mapping topoisomerase sites in mitochondrial DNA with a poisonous mitochondrial topoisomerase I (Top1mt). AN - 1549631722; 24798329 AB - Mitochondrial topoisomerase I (Top1mt) is a type IB topoisomerase present in vertebrates and exclusively targeted to mitochondria. Top1mt relaxes mitochondrial DNA (mtDNA) supercoiling by introducing transient cleavage complexes wherein the broken DNA strand swivels around the intact strand. Top1mt cleavage complexes (Top1mtcc) can be stabilized in vitro by camptothecin (CPT). However, CPT does not trap Top1mtcc efficiently in cells and is highly cytotoxic due to nuclear Top1 targeting. To map Top1mtcc on mtDNA in vivo and to overcome the limitations of CPT, we designed two substitutions (T546A and N550H) in Top1mt to stabilize Top1mtcc. We refer to the double-mutant enzyme as Top1mt*. Using retroviral transduction and ChIP-on-chip assays with Top1mt* in Top1mt knock-out murine embryonic fibroblasts, we demonstrate that Top1mt* forms high levels of cleavage complexes preferentially in the noncoding regulatory region of mtDNA, accumulating especially at the heavy strand replication origin OH, in the ribosomal genes (12S and 16S) and at the light strand replication origin OL. Expression of Top1mt* also caused rapid mtDNA depletion without affecting mitochondria mass, suggesting the existence of specific mitochondrial pathways for the removal of damaged mtDNA. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Dalla Rosa, Ilaria AU - Huang, Shar-Yin N AU - Agama, Keli AU - Khiati, Salim AU - Zhang, Hongliang AU - Pommier, Yves AD - From the Laboratory of Molecular Pharmacology, Developmental Therapeutics Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892. ; From the Laboratory of Molecular Pharmacology, Developmental Therapeutics Branch, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892 pommier@nih.gov. Y1 - 2014/06/27/ PY - 2014 DA - 2014 Jun 27 SP - 18595 EP - 18602 VL - 289 IS - 26 KW - DNA, Mitochondrial KW - 0 KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - Index Medicus KW - DNA Topoisomerase KW - Mitochondrial DNA (mtDNA) KW - Mitochondrial Metabolism KW - DNA Topology KW - Chromatin Immunoprecipitation (ChiP) KW - mtDNA Transcription KW - Top1mt KW - Regulatory Sequences, Nucleic Acid KW - Animals KW - DNA Damage KW - Mice KW - Mice, Knockout KW - Mitochondria -- enzymology KW - DNA, Mitochondrial -- metabolism KW - DNA, Mitochondrial -- chemistry KW - DNA Topoisomerases, Type I -- genetics KW - Mitochondria -- genetics KW - DNA Topoisomerases, Type I -- metabolism KW - DNA, Mitochondrial -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549631722?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mapping+topoisomerase+sites+in+mitochondrial+DNA+with+a+poisonous+mitochondrial+topoisomerase+I+%28Top1mt%29.&rft.au=Dalla+Rosa%2C+Ilaria%3BHuang%2C+Shar-Yin+N%3BAgama%2C+Keli%3BKhiati%2C+Salim%3BZhang%2C+Hongliang%3BPommier%2C+Yves&rft.aulast=Dalla+Rosa&rft.aufirst=Ilaria&rft.date=2014-06-27&rft.volume=289&rft.issue=26&rft.spage=18595&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.555367 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-16 N1 - Date created - 2014-07-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 1985 Nov 25;260(27):14873-8 [2997227] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6116-20 [6273850] Gene. 1989 Apr 15;77(1):61-8 [2744488] Nucleic Acids Res. 1991 Mar 25;19(6):1235-41 [1851553] J Biol Chem. 1991 Oct 25;266(30):20418-23 [1657924] J Mol Biol. 1993 May 5;231(1):6-18 [8388476] Biochemistry. 1993 May 25;32(20):5352-64 [8499440] J Biol Chem. 1994 Jan 21;269(3):2068-74 [8294458] J Natl Cancer Inst. 1994 Jun 1;86(11):836-42 [8182764] J Biol Chem. 1997 May 9;272(19):12801-8 [9139740] J Biol Chem. 2004 Dec 24;279(52):54069-78 [15489506] J Med Chem. 2005 Jul 28;48(15):4803-14 [16033260] Nat Rev Cancer. 2006 Oct;6(10):789-802 [16990856] Mol Cell. 2006 Dec 28;24(6):813-25 [17189185] Annu Rev Biochem. 2007;76:679-99 [17408359] Hum Mutat. 2008 Feb;29(2):330-1 [18205204] Nat Protoc. 2008;3(11):1736-50 [18927559] Biochemistry. 2008 Oct 28;47(43):11196-203 [18826252] EMBO Rep. 2009 Aug;10(8):887-93 [19557000] Nucleic Acids Res. 2009 Oct;37(19):6414-28 [19720733] Chem Biol. 2010 May 28;17(5):421-33 [20534341] Clin Chem. 2010 Jul;56(7):1119-27 [20448188] Genes Dev. 2010 Jul 15;24(14):1546-58 [20634320] Cell. 2010 Aug 20;142(4):519-30 [20723754] Mol Cell Biol. 2011 Feb;31(3):482-94 [21098118] J Cell Biol. 2011 Nov 28;195(5):739-49 [22123861] Nat Rev Drug Discov. 2012 Jan;11(1):25-36 [22173432] Mol Cell. 2012 Apr 27;46(2):115-24 [22541554] Proc Natl Acad Sci U S A. 2012 Oct 2;109(40):16125-30 [22991469] Nucleic Acids Res. 2013 Nov;41(21):9848-57 [23982517] Nucleic Acids Res. 2014 Jun;42(11):7259-67 [24803675] Clin Cancer Res. 2014 Sep 15;20(18):4873-81 [24714774] J Biol Chem. 2000 May 19;275(20):15246-53 [10809761] Biochim Biophys Acta. 2012 Sep-Oct;1819(9-10):970-8 [22207204] PLoS One. 2012;7(7):e41094 [22911747] Biol Chem. 2012 Jul;393(7):547-64 [22944659] Nat Rev Mol Cell Biol. 2012 Oct;13(10):659-71 [22992591] Adv Cancer Res. 2001;80:189-216 [11034544] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10608-13 [11526219] Annu Rev Biochem. 2001;70:369-413 [11395412] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15387-92 [12426403] Biochem Pharmacol. 2004 Mar 15;67(6):1035-45 [15006540] Nucleic Acids Res. 2004;32(7):2087-92 [15096574] J Mol Biol. 1978 Feb 15;119(1):49-68 [633368] Proc Natl Acad Sci U S A. 1978 Feb;75(2):677-81 [273230] Nature. 1981 Apr 9;290(5806):457-65 [7219534] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7024-7 [2823250] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.555367 ER - TY - JOUR T1 - 4-amino-1-hydroxy-2-oxo-1,8-naphthyridine-containing compounds having high potency against raltegravir-resistant integrase mutants of HIV-1. AN - 1541371201; 24901667 AB - There are currently three HIV-1 integrase (IN) strand transfer inhibitors (INSTIs) approved by the FDA for the treatment of AIDS. However, the emergence of drug-resistant mutants emphasizes the need to develop additional agents that have improved efficacies against the existent resistant mutants. As reported herein, we modified our recently disclosed 1-hydroxy-2-oxo-1,2-dihydro-1,8-naphthyridine-3-carboxamides IN inhibitors to develop compounds that have improved efficacies against recombinant IN in biochemical assays. These new compounds show single-digit nanomolar antiviral potencies against HIV vectors that carry wild-type (WT) IN in a single round replication assay and have improved potency against vectors harboring the major forms of drug resistant IN mutants. These compounds also have low toxicity for cultured cells, which in several cases, results in selectivity indices (CC50/EC50) of greater than 10000. The compounds have the potential, with additional structural modifications, to yield clinical agents that are effective against the known strains of resistant viruses. JF - Journal of medicinal chemistry AU - Zhao, Xue Zhi AU - Smith, Steven J AU - Métifiot, Mathieu AU - Marchand, Christophe AU - Boyer, Paul L AU - Pommier, Yves AU - Hughes, Stephen H AU - Burke, Terrence R AD - Chemical Biology Laboratory, and ‡HIV Drug Resistance Program, Center for Cancer Research, NCI at Frederick, National Institutes of Health , Building 376, Boyles Street, P.O. Box B, Frederick, Maryland 21702, United States. Y1 - 2014/06/26/ PY - 2014 DA - 2014 Jun 26 SP - 5190 EP - 5202 VL - 57 IS - 12 KW - HIV Integrase Inhibitors KW - 0 KW - Naphthyridines KW - Pyrrolidinones KW - Recombinant Proteins KW - Raltegravir Potassium KW - 43Y000U234 KW - HIV Integrase KW - EC 2.7.7.- KW - Index Medicus KW - Stereoisomerism KW - Drug Resistance, Viral KW - Virus Replication -- drug effects KW - Humans KW - HEK293 Cells KW - Cell Line, Tumor KW - Recombinant Proteins -- chemistry KW - Mutation KW - Structure-Activity Relationship KW - HIV-1 -- genetics KW - HIV Integrase Inhibitors -- chemical synthesis KW - Naphthyridines -- pharmacology KW - HIV Integrase Inhibitors -- chemistry KW - HIV Integrase -- genetics KW - HIV Integrase Inhibitors -- pharmacology KW - HIV-1 -- enzymology KW - Naphthyridines -- chemical synthesis KW - Pyrrolidinones -- pharmacology KW - HIV-1 -- drug effects KW - Naphthyridines -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541371201?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=4-amino-1-hydroxy-2-oxo-1%2C8-naphthyridine-containing+compounds+having+high+potency+against+raltegravir-resistant+integrase+mutants+of+HIV-1.&rft.au=Zhao%2C+Xue+Zhi%3BSmith%2C+Steven+J%3BM%C3%A9tifiot%2C+Mathieu%3BMarchand%2C+Christophe%3BBoyer%2C+Paul+L%3BPommier%2C+Yves%3BHughes%2C+Stephen+H%3BBurke%2C+Terrence+R&rft.aulast=Zhao&rft.aufirst=Xue&rft.date=2014-06-26&rft.volume=57&rft.issue=12&rft.spage=5190&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Fjm5001908 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-05 N1 - Date created - 2014-06-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Genet Genomics. 2004 Sep;272(2):216-26 [15316769] J Med Chem. 2004 Oct 21;47(22):5336-9 [15481971] Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6320-4 [7687065] Bioorg Med Chem Lett. 2005 Mar 15;15(6):1577-82 [15745800] J Med Chem. 2006 Nov 16;49(23):6646-9 [17154493] J Med Chem. 2008 Jan 24;51(2):251-9 [18095643] Antimicrob Agents Chemother. 2008 Apr;52(4):1351-8 [18227187] Bioorg Med Chem Lett. 2009 May 15;19(10):2714-7 [19364649] Curr Top Med Chem. 2009;9(11):1016-37 [19747122] Antimicrob Agents Chemother. 2010 Jan;54(1):491-501 [19901095] Drugs. 2010 Mar 26;70(5):631-42 [20329808] Biochemistry. 2010 May 4;49(17):3715-22 [20334344] J Virol. 2010 Aug;84(15):7625-33 [20484498] Bioorg Med Chem Lett. 2010 Nov 15;20(22):6754-7 [20869872] Curr Opin Struct Biol. 2011 Apr;21(2):249-56 [21277766] Chem Biol Drug Des. 2012 Feb;79(2):157-65 [22107736] Expert Opin Investig Drugs. 2012 Mar;21(3):395-401 [22321026] Expert Opin Investig Drugs. 2012 Apr;21(4):523-30 [22380682] Curr Opin HIV AIDS. 2012 Sep;7(5):401-8 [22789986] J Med Chem. 2012 Oct 25;55(20):8735-44 [22963135] Curr Opin Infect Dis. 2012 Dec;25(6):677-86 [23086187] ACS Chem Biol. 2013 Jan 18;8(1):209-17 [23075516] J Med Chem. 2013 Feb 14;56(3):1124-35 [23316884] Drugs. 2013 Sep;73(14):1627-37 [24052331] J Med Chem. 2013 Jul 25;56(14):5901-16 [23845180] J Med Chem. 2013 Nov 14;56(21):8588-98 [24124919] Antivir Chem Chemother. 2014;23(4):129-44 [24150519] J Med Chem. 2014 Feb 27;57(4):1573-82 [24471816] Chem Biol Drug Des. 2014 May;83(5):521-31 [24405985] Erratum In: J Med Chem. 2014 Aug 14;57(15):6885 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/jm5001908 ER - TY - JOUR T1 - Chloroquine synergizes sunitinib cytotoxicity via modulating autophagic, apoptotic and angiogenic machineries. AN - 1526129822; 24751611 AB - Tyrosine kinases play a pivotal role in oncogenesis. Although tyrosine kinase inhibitors as sunitinib malate are used in cancer therapy, emerging studies report compromised cytotoxicity when used as monotherapy and thus combinations with other anti-cancer agents is recommended. Chloroquine is a clinically available anti-malarial agent which has been shown to exhibit anti-cancer activity. In the current study, we questioned whether chloroquine can modulate sunitinib cytotoxicity. We found that chloroquine synergistically augmented sunitinib cytotoxicity on human breast (MCF-7 and T-47D), cervical (Hela), colorectal (Caco-2 and HCT116), hepatocellular (HepG2), laryngeal (HEp-2) and prostate (PC3) cancer cell lines as indicated by combination and concentration reduction indices. These results were also consistent with that of Ehrlich ascites carcinoma (EAC) Swiss albino mice models as confirmed by tumor volume, weight, histopathological examination and PCNA expression. Sunitinib induced autophagy via upregulating beclin-1 expression which was blocked by chloroquine as evidenced by accumulated SQTSM1/p62 level. Furthermore, chloroquine augmented sunitinib-induced apoptosis by decreasing survivin level and increasing caspase 3 activity. Chloroquine also enhanced the antiangiogenic capacity of sunitinib as indicated by decreased CD34 expression and peritoneal/skin angiogenesis. Sunitinib when combined with chloroquine also increased reactive nitrogen species production via increasing inducible nitric oxide synthase expression and nitric oxide level whilst reduced reactive oxygen species production by increasing GSH level, activities of glutathione peroxidase and catalase and reducing lipid peroxides compared to sunitinib-only treated group. Taken together, these findings suggest that chloroquine enhanced sunitinib cytotoxicity in a synergistic manner via inducing apoptosis while switching off autophagic and angiogenic machineries. Nevertheless, further studies are required to elucidate the efficacy and safety profile of such combination. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Chemico-biological interactions AU - Abdel-Aziz, Amal Kamal AU - Shouman, Samia AU - El-Demerdash, Ebtehal AU - Elgendy, Mohamed AU - Abdel-Naim, Ashraf B AD - Pharmacology and Toxicology Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt; Department of Experimental Oncology, European Institute of Oncology, Milan, Italy. ; Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt. ; Pharmacology and Toxicology Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt. ; Department of Experimental Oncology, European Institute of Oncology, Milan, Italy. ; Pharmacology and Toxicology Department, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt. Electronic address: abnaim@pharma.asu.edu.eg. Y1 - 2014/06/25/ PY - 2014 DA - 2014 Jun 25 SP - 28 EP - 40 VL - 217 KW - Antineoplastic Agents KW - 0 KW - Indoles KW - Pyrroles KW - Chloroquine KW - 886U3H6UFF KW - sunitinib KW - V99T50803M KW - Index Medicus KW - Apoptosis KW - Sunitinib KW - Oxidative stress KW - Autophagy KW - Angiogenesis KW - Animals KW - HeLa Cells KW - Humans KW - Mice KW - Caco-2 Cells KW - Cell Line, Tumor KW - HCT116 Cells KW - Blotting, Western KW - Neovascularization, Pathologic -- drug therapy KW - Cell Survival -- drug effects KW - Hep G2 Cells KW - Apoptosis -- drug effects KW - MCF-7 Cells KW - Drug Synergism KW - Immunohistochemistry KW - Female KW - Carcinoma, Ehrlich Tumor -- blood supply KW - Chloroquine -- pharmacology KW - Carcinoma, Ehrlich Tumor -- pathology KW - Carcinoma, Ehrlich Tumor -- drug therapy KW - Indoles -- pharmacology KW - Pyrroles -- pharmacology KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1526129822?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemico-biological+interactions&rft.atitle=Chloroquine+synergizes+sunitinib+cytotoxicity+via+modulating+autophagic%2C+apoptotic+and+angiogenic+machineries.&rft.au=Abdel-Aziz%2C+Amal+Kamal%3BShouman%2C+Samia%3BEl-Demerdash%2C+Ebtehal%3BElgendy%2C+Mohamed%3BAbdel-Naim%2C+Ashraf+B&rft.aulast=Abdel-Aziz&rft.aufirst=Amal&rft.date=2014-06-25&rft.volume=217&rft.issue=&rft.spage=28&rft.isbn=&rft.btitle=&rft.title=Chemico-biological+interactions&rft.issn=1872-7786&rft_id=info:doi/10.1016%2Fj.cbi.2014.04.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-01 N1 - Date created - 2014-05-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.cbi.2014.04.007 ER - TY - JOUR T1 - IP6K structure and the molecular determinants of catalytic specificity in an inositol phosphate kinase family. AN - 1540112972; 24956979 AB - Inositol trisphosphate kinases (IP3Ks) and inositol hexakisphosphate kinases (IP6Ks) each regulate specialized signalling activities by phosphorylating either InsP3 or InsP6 respectively. The molecular basis for these different kinase activities can be illuminated by a structural description of IP6K. Here we describe the crystal structure of an Entamoeba histolytica hybrid IP6K/IP3K, an enzymatic parallel to a 'living fossil'. Through molecular modelling and mutagenesis, we extrapolated our findings to human IP6K2, which retains vestigial IP3K activity. Two structural elements, an α-helical pair and a rare, two-turn 310 helix, together forge a substrate-binding pocket with an open clamshell geometry. InsP6 forms substantial contacts with both structural elements. Relative to InsP6, enzyme-bound InsP3 rotates 55° closer to the α-helices, which provide most of the protein's interactions with InsP3. These data reveal the molecular determinants of IP6K activity, and suggest an unusual evolutionary trajectory for a primordial kinase that could have favored efficient bifunctionality, before propagation of separate IP3Ks and IP6Ks. JF - Nature communications AU - Wang, Huanchen AU - DeRose, Eugene F AU - London, Robert E AU - Shears, Stephen B AD - Inositol Signaling Group, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, NC 27709, USA. ; Nuclear Magnetic Resonance Group, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, NC 27709, USA. Y1 - 2014/06/24/ PY - 2014 DA - 2014 Jun 24 SP - 4178 VL - 5 KW - Inositol Phosphates KW - 0 KW - Protozoan Proteins KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Phosphotransferases (Phosphate Group Acceptor) KW - EC 2.7.4.- KW - inositol hexakisphosphate kinase KW - EC 2.7.4.21 KW - Index Medicus KW - Sensitivity and Specificity KW - Multigene Family KW - Humans KW - Adenosine Triphosphate -- metabolism KW - Crystallography, X-Ray KW - Evolution, Molecular KW - Catalysis KW - Binding Sites KW - Adenosine Triphosphate -- chemistry KW - Protozoan Proteins -- chemistry KW - Phosphotransferases (Phosphate Group Acceptor) -- chemistry KW - Protozoan Proteins -- metabolism KW - Inositol Phosphates -- metabolism KW - Protozoan Proteins -- genetics KW - Phosphotransferases (Phosphate Group Acceptor) -- metabolism KW - Entamoeba histolytica -- enzymology KW - Phosphotransferases (Phosphate Group Acceptor) -- genetics KW - Entamoeba histolytica -- chemistry KW - Inositol Phosphates -- chemistry KW - Entamoeba histolytica -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1540112972?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=IP6K+structure+and+the+molecular+determinants+of+catalytic+specificity+in+an+inositol+phosphate+kinase+family.&rft.au=Wang%2C+Huanchen%3BDeRose%2C+Eugene+F%3BLondon%2C+Robert+E%3BShears%2C+Stephen+B&rft.aulast=Wang&rft.aufirst=Huanchen&rft.date=2014-06-24&rft.volume=5&rft.issue=&rft.spage=4178&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms5178 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-16 N1 - Date created - 2014-06-24 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4O4F; PDB; 4O4E; 4O4B; 4O4D; 4O4C N1 - SuppNotes - Cited By: Protein Eng. 1999 Oct;12(10):811-4 [10556239] PLoS Pathog. 2014 Feb;10(2):e1003981 [24586175] J Biol Chem. 1999 Dec 10;274(50):35434-40 [10585413] FEBS Lett. 2000 Feb 18;468(1):28-32 [10683435] Science. 2000 Mar 17;287(5460):2026-9 [10720331] J Biol Chem. 2000 Aug 11;275(32):24686-92 [10827188] Biochem J. 2000 Nov 1;351 Pt 3:551-5 [11042108] J Biol Chem. 2001 Jul 6;276(27):24965-70 [11337497] J Biol Chem. 2001 Oct 19;276(42):39179-85 [11502751] J Biol Chem. 2002 Aug 30;277(35):31857-62 [12084730] J Biol Chem. 2002 Nov 15;277(46):43836-43 [12223481] Methods Enzymol. 2003;374:300-21 [14696379] Biochem J. 2004 Jan 15;377(Pt 2):265-80 [14567754] Mol Cell. 2004 Sep 10;15(5):689-701 [15350214] Mol Cell. 2004 Sep 10;15(5):703-11 [15350215] J Biol Chem. 1989 Nov 25;264(33):19871-8 [2555335] Biochem J. 1996 Feb 15;314 ( Pt 1):227-33 [8660287] Biochem J. 1997 Oct 15;327 ( Pt 2):553-60 [9359429] Proteins. 1997 Dec;29(4):401-16 [9408938] EMBO J. 1998 Mar 16;17(6):1710-6 [9501092] EMBO J. 1998 Nov 16;17(22):6599-607 [9822604] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] J Biol Chem. 2005 Jan 14;280(2):1634-40 [15533939] Mol Cell. 2005 Apr 15;18(2):201-12 [15837423] Cell Mol Life Sci. 2006 Mar;63(5):552-64 [16429326] J Biol Chem. 2006 Dec 8;281(49):38109-16 [17050532] Science. 2007 Apr 6;316(5821):109-12 [17412959] J Biol Chem. 2007 Sep 21;282(38):28117-25 [17616525] Science. 2007 Nov 23;318(5854):1299-302 [18033884] Proc Natl Acad Sci U S A. 2008 Jan 29;105(4):1134-9 [18195352] Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2349-53 [18268345] Chem Biol. 2008 Mar;15(3):274-86 [18355727] J Biol Chem. 2009 Jan 16;284(3):1863-72 [18981179] J Biol Chem. 2009 Apr 17;284(16):10571-82 [19208622] Oncogene. 2009 Jun 25;28(25):2383-92 [19430495] Mol Pharmacol. 2009 Aug;76(2):236-52 [19439500] Cell Mol Life Sci. 2009 Dec;66(24):3851-71 [19714294] Proc Natl Acad Sci U S A. 2010 May 25;107(21):9608-13 [20453199] Annu Rev Biochem. 2010;79:471-505 [20235827] J Gen Physiol. 2010 Dec;136(6):585-92 [21115694] Cell. 2010 Dec 10;143(6):897-910 [21145457] Proc Natl Acad Sci U S A. 2011 Feb 8;108(6):2205-9 [21262846] Mol Biochem Parasitol. 2012 Jan;181(1):49-52 [22001062] Science. 2011 Nov 11;334(6057):802-5 [22076377] Nat Chem Biol. 2012 Jan;8(1):111-6 [22119861] J Biol Chem. 2012 Oct 12;287(42):35360-9 [22896696] J Biol Chem. 2013 Feb 1;288(5):3312-21 [23255604] Biochem J. 2013 Jun 15;452(3):369-79 [23725456] Biochem J. 2013 Aug 1;453(3):413-26 [23682967] Blood. 2013 Aug 22;122(8):1478-86 [23782934] FEBS Lett. 2013 Nov 1;587(21):3464-70 [24021644] Proc Natl Acad Sci U S A. 2013 Nov 19;110(47):18970-5 [24191012] Biosci Rep. 2013;33(2):e00022 [23240582] Curr Biol. 1999 Nov 18;9(22):1323-6 [10574768] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncomms5178 ER - TY - CPAPER T1 - The Adventures of an NIH Program Officer T2 - 33rd Annual Meeting of the American Society for Virology (ASV2014) AN - 1562647230; 6301780 JF - 33rd Annual Meeting of the American Society for Virology (ASV2014) AU - Post, Diane Y1 - 2014/06/21/ PY - 2014 DA - 2014 Jun 21 KW - Virology KW - Microbiology KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562647230?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.atitle=The+Adventures+of+an+NIH+Program+Officer&rft.au=Post%2C+Diane&rft.aulast=Post&rft.aufirst=Diane&rft.date=2014-06-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.issn=&rft_id=info:doi/ L2 - http://asv2014.colostate.edu/meeting-details/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-31 N1 - Last updated - 2014-09-18 ER - TY - CPAPER T1 - Perspectives and current status of poliovirus vaccines T2 - 33rd Annual Meeting of the American Society for Virology (ASV2014) AN - 1562647065; 6301763 JF - 33rd Annual Meeting of the American Society for Virology (ASV2014) AU - Ehrenfeld, Ellie Y1 - 2014/06/21/ PY - 2014 DA - 2014 Jun 21 KW - Poliovirus KW - Disease control KW - Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562647065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.atitle=Perspectives+and+current+status+of+poliovirus+vaccines&rft.au=Ehrenfeld%2C+Ellie&rft.aulast=Ehrenfeld&rft.aufirst=Ellie&rft.date=2014-06-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.issn=&rft_id=info:doi/ L2 - http://asv2014.colostate.edu/meeting-details/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-31 N1 - Last updated - 2014-09-18 ER - TY - CPAPER T1 - A gammaretrovirus isolated from koalas in US zoos with malignant neoplasias T2 - 33rd Annual Meeting of the American Society for Virology (ASV2014) AN - 1562644670; 6301789 JF - 33rd Annual Meeting of the American Society for Virology (ASV2014) AU - Eiden, Maribeth Y1 - 2014/06/21/ PY - 2014 DA - 2014 Jun 21 KW - Neoplasia UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562644670?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.atitle=A+gammaretrovirus+isolated+from+koalas+in+US+zoos+with+malignant+neoplasias&rft.au=Eiden%2C+Maribeth&rft.aulast=Eiden&rft.aufirst=Maribeth&rft.date=2014-06-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=33rd+Annual+Meeting+of+the+American+Society+for+Virology+%28ASV2014%29&rft.issn=&rft_id=info:doi/ L2 - http://asv2014.colostate.edu/scientific-program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-31 N1 - Last updated - 2014-09-18 ER - TY - JOUR T1 - Identification of drivers from cancer genome diversity in hepatocellular carcinoma. AN - 1540130046; 24955791 AB - Hepatocellular carcinoma (HCC) is one of the most common cancers with a dismal outcome. The complicated molecular pathogenesis of HCC caused by tumor heterogeneity makes it difficult to identify druggable targets useful for treating HCC patients. One approach that has a potential for the improvement of patient prognosis is the identification of cancer driver genes that play a critical role in the development of HCC. Recent technological advances of high-throughput methods, such as gene expression profiles, DNA copy number alterations and somatic mutations, have expanded our understanding of the comprehensive genetic profiles of HCC. Integrative analysis of these omics profiles enables us to classify the molecular subgroups of HCC patients. As each subgroup classified according to genetic profiles has different clinical features, such as recurrence rate and prognosis, the tumor subclassification tools are useful in clinical practice. Furthermore, a global genetic analysis, including genome-wide RNAi functional screening, makes it possible to identify cancer vulnerable genes. Identification of common cancer driver genes in HCC leads to the development of an effective molecular target therapy. JF - International journal of molecular sciences AU - Takai, Atsushi AU - Dang, Hien T AU - Wang, Xin W AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. atsushi.takai@nih.gov. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. hien.dang@nih.gov. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. xw3u@nih.gov. Y1 - 2014/06/20/ PY - 2014 DA - 2014 Jun 20 SP - 11142 EP - 11160 VL - 15 IS - 6 KW - Biomarkers, Tumor KW - 0 KW - RNA, Small Interfering KW - Index Medicus KW - Biomarkers, Tumor -- metabolism KW - Animals KW - Polymorphism, Single Nucleotide KW - Humans KW - Transcriptome KW - RNA, Small Interfering -- metabolism KW - Genetic Variation KW - Liver Neoplasms -- pathology KW - Carcinoma, Hepatocellular -- metabolism KW - Carcinoma, Hepatocellular -- genetics KW - Carcinoma, Hepatocellular -- pathology KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1540130046?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+molecular+sciences&rft.atitle=Identification+of+drivers+from+cancer+genome+diversity+in+hepatocellular+carcinoma.&rft.au=Takai%2C+Atsushi%3BDang%2C+Hien+T%3BWang%2C+Xin+W&rft.aulast=Takai&rft.aufirst=Atsushi&rft.date=2014-06-20&rft.volume=15&rft.issue=6&rft.spage=11142&rft.isbn=&rft.btitle=&rft.title=International+journal+of+molecular+sciences&rft.issn=1422-0067&rft_id=info:doi/10.3390%2Fijms150611142 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-04 N1 - Date created - 2014-06-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hepatology. 2006 Feb;43(2 Suppl 1):S99-S112 [16447287] Nat Genet. 2006 Apr;38(4):421-30 [16518402] Nat Med. 2006 Apr;12(4):410-6 [16532004] FEBS Lett. 2006 Jun 26;580(15):3571-81 [16750200] 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Nov;43(5):863-74 [16139920] Hepatology. 2005 Nov;42(5):1109-17 [16250053] Carcinogenesis. 2005 Dec;26(12):2050-7 [16000397] JAMA. 2006 Jan 4;295(1):65-73 [16391218] Cell. 2012 Sep 14;150(6):1107-20 [22980975] Cancer Res. 2004 Oct 15;64(20):7263-70 [15492245] J Viral Hepat. 2004 Nov;11(6):502-10 [15500550] Science. 1976 Oct 1;194(4260):23-8 [959840] Nature. 1991 Apr 4;350(6317):427-8 [1849234] Nature. 1991 Apr 4;350(6317):429-31 [1672732] Cancer Res. 1991 Oct 15;51(20):5520-5 [1655254] Lancet. 1991 Nov 30;338(8779):1356-9 [1682737] Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9622-6 [1329103] Cancer Res. 1992 Nov 15;52(22):6358-64 [1330291] Cancer Res. 1993 Jun 15;53(12):2884-7 [8389246] Trends Genet. 1993 Apr;9(4):138-41 [8516849] Science. 1994 May 27;264(5163):1317-9 [8191284] Hepatology. 1995 Dec;22(6):1702-7 [7489977] Hum Pathol. 1996 Apr;27(4):342-9 [8617476] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3390/ijms150611142 ER - TY - JOUR T1 - New strategies in ewing sarcoma: lost in translation? AN - 1535622225; 24756371 AB - Ewing sarcoma is the second most common pediatric malignant bone tumor. Aggressive multimodality therapy has led to an improvement in outcomes, particularly in patients with localized disease. However, therapy-related toxicities are not trivial, and the prognosis for patients with relapsed and/or metastatic disease continues to be poor. In this article, we outline some of the promising therapies that have the potential to change the Ewing sarcoma therapeutic paradigm in the not-too-distant future: insulin-like growth factor receptor inhibitors, targeting of the fusion protein, epigenetic manipulation, PARP inhibitors, and immunotherapy. ©2014 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Arnaldez, Fernanda I AU - Helman, Lee J AD - Authors' Affiliation: Pediatric Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland arnaldezf@mail.nih.gov. ; Authors' Affiliation: Pediatric Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland. Y1 - 2014/06/15/ PY - 2014 DA - 2014 Jun 15 SP - 3050 EP - 3056 VL - 20 IS - 12 SN - 1078-0432, 1078-0432 KW - Antineoplastic Agents KW - 0 KW - Enzyme Inhibitors KW - Poly(ADP-ribose) Polymerase Inhibitors KW - Receptors, Somatomedin KW - PARP1 protein, human KW - EC 2.4.2.30 KW - Poly (ADP-Ribose) Polymerase-1 KW - Index Medicus KW - Receptors, Somatomedin -- antagonists & inhibitors KW - Humans KW - Sarcoma, Ewing -- immunology KW - Enzyme Inhibitors -- therapeutic use KW - Bone Neoplasms -- immunology KW - Immunotherapy KW - Bone Neoplasms -- metabolism KW - Sarcoma, Ewing -- metabolism KW - Molecular Targeted Therapy KW - Bone Neoplasms -- therapy KW - Antineoplastic Agents -- therapeutic use KW - Sarcoma, Ewing -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535622225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=New+strategies+in+ewing+sarcoma%3A+lost+in+translation%3F&rft.au=Arnaldez%2C+Fernanda+I%3BHelman%2C+Lee+J&rft.aulast=Arnaldez&rft.aufirst=Fernanda&rft.date=2014-06-15&rft.volume=20&rft.issue=12&rft.spage=3050&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-13-0633 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-15 N1 - Date created - 2014-06-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Med Pediatr Oncol. 2003 May;40(5):276-87 [12652615] Cancer. 1973 Apr;31(4):889-93 [4267530] Cancer Res. 1990 Jan 1;50(1):38-43 [2104538] Int J Cancer. 2011 Jan 1;128(1):216-26 [20648560] Pediatr Blood Cancer. 2011 Apr;56(4):595-603 [21298745] Neoplasia. 2011 Feb;13(2):145-53 [21403840] PLoS One. 2011;6(4):e18424 [21494688] PLoS One. 2011;6(4):e19305 [21559395] J Natl Cancer Inst. 2011 Jun 22;103(12):962-78 [21653923] Cancer Genet. 2011 Jul;204(7):351-65 [21872822] J Clin Oncol. 2011 Dec 1;29(34):4541-7 [22025149] J Clin Oncol. 2011 Dec 1;29(34):4534-40 [22025154] J Clin Oncol. 2012 Jan 20;30(3):256-62 [22184397] Annu Rev Pathol. 2012;7:145-59 [21942527] Eur J Cancer. 2012 Mar;48(4):579-85 [22088484] Oncotarget. 2012 Feb;3(2):172-82 [22383402] Br J Cancer. 2012 Mar 13;106(6):1123-33 [22374462] Nat Genet. 2012 Apr;44(4):461-6 [22387997] Nature. 2012 Mar 29;483(7391):570-5 [22460902] Cancer Res. 2012 Apr 1;72(7):1608-13 [22287547] Clin Cancer Res. 2012 May 1;18(9):2625-31 [22465830] Cancer Biol Ther. 2012 Apr;13(6):417-24 [22313685] N Engl J Med. 2012 Jun 28;366(26):2443-54 [22658127] Crit Rev Oncol Hematol. 2012 Aug;83(2):184-93 [22112692] Int J Cancer. 2012 Nov 1;131(9):2153-64 [22323082] Mol Endocrinol. 2012 Sep;26(9):1603-16 [22798295] Cancer Metastasis Rev. 2012 Dec;31(3-4):753-61 [22711031] J Clin Oncol. 2012 Nov 20;30(33):4141-7 [23071222] J Clin Oncol. 2012 Nov 20;30(33):4148-54 [23091096] N Engl J Med. 2013 Apr 18;368(16):1509-18 [23527958] J Mol Recognit. 2013 Jul;26(7):318-29 [23657987] N Engl J Med. 2013 Jul 11;369(2):134-44 [23724846] Br J Cancer. 2013 Aug 6;109(3):658-66 [23839490] Oncogene. 2013 Oct 17;32(42):5089-100 [23178492] Br J Cancer. 2001 May 18;84(10):1424-31 [11355958] Oncogene. 2002 Apr 25;21(18):2890-5 [11973649] Cancer Res. 2002 Nov 1;62(21):6108-15 [12414635] Nature. 1992 Sep 10;359(6391):162-5 [1522903] Genomics. 1996 Jan 1;31(1):58-64 [8808280] J Biol Chem. 1997 Dec 5;272(49):30822-7 [9388225] Expert Opin Ther Targets. 2005 Aug;9(4):825-30 [16083345] Nature. 2005 Aug 25;436(7054):1186-90 [15995699] J Clin Oncol. 2006 Jan 1;24(1):152-9 [16382125] Cancer Cell. 2006 May;9(5):405-16 [16697960] Cancer Res. 2006 Jun 1;66(11):5574-81 [16740692] Clin Cancer Res. 2006 Nov 15;12(22):6781-90 [17121899] Clin Cancer Res. 2007 Feb 15;13(4):1322-30 [17317844] PLoS Med. 2007 Apr;4(4):e122 [17425403] Cell Cycle. 2008 Jan 15;7(2):250-6 [18256529] Cancer Res. 2008 Apr 1;68(7):2176-85 [18381423] PLoS One. 2008;3(4):e1965 [18414662] J Pediatr Hematol Oncol. 2008 Jun;30(6):425-30 [18525458] Pediatr Blood Cancer. 2008 Sep;51(3):334-8 [18506764] PLoS One. 2008;3(7):e2634 [18648544] Clin Cancer Res. 2008 Aug 1;14(15):4850-8 [18676758] Mol Immunol. 2008 Sep;45(15):3917-25 [18657862] J Clin Oncol. 2008 Sep 20;26(27):4385-93 [18802150] Pediatr Blood Cancer. 2009 Mar;52(3):324-7 [18989890] Proc Natl Acad Sci U S A. 2009 Mar 31;106(13):5324-9 [19289832] Br J Cancer. 2009 Jul 7;101(1):80-90 [19491900] Nat Med. 2009 Jul;15(7):750-6 [19584866] Clin Cancer Res. 2010 Apr 15;16(8):2363-74 [20371692] Pediatr Blood Cancer. 2010 Jul 1;54(7):921-6 [20166202] Mol Cancer Ther. 2010 May;9(5):1396-407 [20423994] Clin Cancer Res. 2010 Aug 1;16(15):3901-9 [20542985] J Clin Oncol. 2010 Aug 1;28(22):3623-9 [20606092] N Engl J Med. 2003 Feb 20;348(8):694-701 [12594313] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-0633 ER - TY - JOUR T1 - Noninvasive urinary metabolomic profiling identifies diagnostic and prognostic markers in lung cancer. AN - 1535621967; 24736543 AB - Lung cancer remains the most common cause of cancer deaths worldwide, yet there is currently a lack of diagnostic noninvasive biomarkers that could guide treatment decisions. Small molecules (<1,500 Da) were measured in urine collected from 469 patients with lung cancer and 536 population controls using unbiased liquid chromatography/mass spectrometry. Clinical putative diagnostic and prognostic biomarkers were validated by quantitation and normalized to creatinine levels at two different time points and further confirmed in an independent sample set, which comprises 80 cases and 78 population controls, with similar demographic and clinical characteristics when compared with the training set. Creatine riboside (IUPAC name: 2-{2-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)-oxolan-2-yl]-1-methylcarbamimidamido}acetic acid), a novel molecule identified in this study, and N-acetylneuraminic acid (NANA) were each significantly (P < 0.00001) elevated in non-small cell lung cancer and associated with worse prognosis [HR = 1.81 (P = 0.0002), and 1.54 (P = 0.025), respectively]. Creatine riboside was the strongest classifier of lung cancer status in all and stage I-II cases, important for early detection, and also associated with worse prognosis in stage I-II lung cancer (HR = 1.71, P = 0.048). All measurements were highly reproducible with intraclass correlation coefficients ranging from 0.82 to 0.99. Both metabolites were significantly (P < 0.03) enriched in tumor tissue compared with adjacent nontumor tissue (N = 48), thus revealing their direct association with tumor metabolism. Creatine riboside and NANA may be robust urinary clinical metabolomic markers that are elevated in tumor tissue and associated with early lung cancer diagnosis and worse prognosis. ©2014 American Association for Cancer Research. JF - Cancer research AU - Mathé, Ewy A AU - Patterson, Andrew D AU - Haznadar, Majda AU - Manna, Soumen K AU - Krausz, Kristopher W AU - Bowman, Elise D AU - Shields, Peter G AU - Idle, Jeffrey R AU - Smith, Philip B AU - Anami, Katsuhiro AU - Kazandjian, Dickran G AU - Hatzakis, Emmanuel AU - Gonzalez, Frank J AU - Harris, Curtis C AD - Authors' Affiliations: Laboratory of Molecular Immunogenomics, Genomic and Immunity Section, NIAMS/NIH; Laboratories of Human Carcinogenesis, and Metabolism, National Cancer Institute, NIH, Bethesda, Maryland; Department of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis; Metabolomics Core Facility; Nuclear Magnetic Resonance Spectroscopy, The Pennsylvania State University, University Park, Pennsylvania; Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Clinical Research, University of Bern, Bern, SwitzerlandAuthors' Affiliations: Laboratory of Molecular Immunogenomics, Genomic and Immunity Section, NIAMS/NIH; Laboratories of Human Carcinogenesis, and Metabolism, National Cancer Institute, NIH, Bethesda, Maryland; Department of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis; Metabolomics Core Facility; Nuclear Magnetic Resonance Spectroscopy, The Pennsylvania State University, University Park, Pennsylvania; Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Clinical Research, University of Bern, Bern, Switzerland. ; Authors' Affiliations: Laboratory of Molecular Immunogenomics, Genomic and Immunity Section, NIAMS/NIH; Laboratories of Human Carcinogenesis, and Metabolism, National Cancer Institute, NIH, Bethesda, Maryland; Department of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis; Metabolomics Core Facility; Nuclear Magnetic Resonance Spectroscopy, The Pennsylvania State University, University Park, Pennsylvania; Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Clinical Research, University of Bern, Bern, Switzerland. ; Authors' Affiliations: Laboratory of Molecular Immunogenomics, Genomic and Immunity Section, NIAMS/NIH; Laboratories of Human Carcinogenesis, and Metabolism, National Cancer Institute, NIH, Bethesda, Maryland; Department of Veterinary and Biomedical Sciences and Center for Molecular Toxicology and Carcinogenesis; Metabolomics Core Facility; Nuclear Magnetic Resonance Spectroscopy, The Pennsylvania State University, University Park, Pennsylvania; Ohio State University Comprehensive Cancer Center, Columbus, Ohio; and Department of Clinical Research, University of Bern, Bern, Switzerland Curtis_Harris@nih.gov. Y1 - 2014/06/15/ PY - 2014 DA - 2014 Jun 15 SP - 3259 EP - 3270 VL - 74 IS - 12 KW - 2-(2-(3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl)-1-methylcarbamimidamido)acetic acid KW - 0 KW - Biomarkers, Tumor KW - Ribonucleosides KW - N-Acetylneuraminic Acid KW - GZP2782OP0 KW - Creatine KW - MU72812GK0 KW - Index Medicus KW - Kaplan-Meier Estimate KW - Smoking -- urine KW - Metabolome KW - ROC Curve KW - Humans KW - Prognosis KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Male KW - Female KW - Proportional Hazards Models KW - Ribonucleosides -- urine KW - Lung Neoplasms -- diagnosis KW - Lung Neoplasms -- urine KW - Carcinoma, Non-Small-Cell Lung -- mortality KW - Creatine -- analogs & derivatives KW - Biomarkers, Tumor -- urine KW - Lung Neoplasms -- mortality KW - Creatine -- urine KW - Carcinoma, Non-Small-Cell Lung -- urine KW - Carcinoma, Non-Small-Cell Lung -- diagnosis KW - N-Acetylneuraminic Acid -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535621967?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Noninvasive+urinary+metabolomic+profiling+identifies+diagnostic+and+prognostic+markers+in+lung+cancer.&rft.au=Math%C3%A9%2C+Ewy+A%3BPatterson%2C+Andrew+D%3BHaznadar%2C+Majda%3BManna%2C+Soumen+K%3BKrausz%2C+Kristopher+W%3BBowman%2C+Elise+D%3BShields%2C+Peter+G%3BIdle%2C+Jeffrey+R%3BSmith%2C+Philip+B%3BAnami%2C+Katsuhiro%3BKazandjian%2C+Dickran+G%3BHatzakis%2C+Emmanuel%3BGonzalez%2C+Frank+J%3BHarris%2C+Curtis+C&rft.aulast=Math%C3%A9&rft.aufirst=Ewy&rft.date=2014-06-15&rft.volume=74&rft.issue=12&rft.spage=3259&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-0109 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-08 N1 - Date created - 2014-06-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Rapid Commun Mass Spectrom. 2009 Jun;23(11):1543-9 [19399767] J Nutrigenet Nutrigenomics. 2012;5(2):I-II [22965161] PLoS One. 2010;5(1):e8819 [20111698] J Sep Sci. 2010 Jun;33(10):1495-503 [20309903] J Natl Compr Canc Netw. 2010 Jul;8(7):740-801 [20679538] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Ann Oncol. 2012 Sep;23 Suppl 10:x320-7 [22987984] Cancer Prev Res (Phila). 2012 Aug;5(8):992-1006 [22689914] Cancer. 2013 Jan 15;119(2):356-62 [22810899] J Proteome Res. 2013 Feb 1;12(2):679-91 [23240883] J Natl Cancer Inst. 2013 Feb 6;105(3):175-201 [23297039] N Engl J Med. 2013 Apr 18;368(16):1477-88 [23506003] Cancer Lett. 2013 Jun 28;334(1):34-8 [22824243] Biomed Chromatogr. 2000 Nov;14(7):459-63 [11113924] Radiology. 2004 May;231(2):440-5 [15128988] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413] Br Med J. 1973 Feb 10;1(5849):328-30 [4685623] Pharmacology. 1976;14(1):47-51 [183223] Cancer Res. 1977 Sep;37(9):3362-6 [884680] Cancer Res. 1981 Jul;41(7):2773-7 [6265067] Cancer Lett. 1981 May;12(4):335-41 [7306937] Int J Biol Markers. 1988 Jan-Mar;3(1):19-22 [3249044] J Clin Endocrinol Metab. 1999 May;84(5):1729-36 [10323408] Science. 1956 Feb 24;123(3191):309-14 [13298683] Curr Opin Mol Ther. 2004 Dec;6(6):584-92 [15663322] Biomed Chromatogr. 2005 May;19(4):312-28 [15651085] N Engl J Med. 2005 Jun 23;352(25):2589-97 [15972865] Clin Chem. 2006 Jun;52(6):1089-95 [16627561] Cancer Res. 2006 Nov 15;66(22):10795-804 [17108116] Anal Biochem. 2007 Apr 15;363(2):185-95 [17316536] J Clin Oncol. 2007 Dec 1;25(34):5506-18 [17954710] Future Oncol. 2008 Feb;4(1):93-102 [18241004] Trends Endocrinol Metab. 2008 Jul;19(5):175-80 [18394919] J Clin Oncol. 2008 Jul 20;26(21):3552-9 [18506026] Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):260-6 [19124507] J Natl Cancer Inst. 2009 Jan 7;101(1):8-10 [19116386] Nature. 2009 Feb 12;457(7231):910-4 [19212411] Clin Chim Acta. 2009 Apr;402(1-2):31-7 [19135043] BMC Cancer. 2009;9:104 [19344524] N Engl J Med. 2011 Aug 4;365(5):395-409 [21714641] Am J Clin Pathol. 2011 Oct;136(4):609-16 [21917684] Toxicol Lett. 2011 Nov 30;207(2):173-81 [21907771] Cancer Res. 2011 Nov 1;71(21):6749-57 [22028322] Annu Rev Pharmacol Toxicol. 2012;52:37-56 [21819238] J Thorac Cardiovasc Surg. 2012 Jul;144(1):33-8 [22710039] N Engl J Med. 2009 Sep 3;361(10):947-57 [19692680] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0109 ER - TY - JOUR T1 - Druggable oncogene fusions in invasive mucinous lung adenocarcinoma. AN - 1535621629; 24727320 AB - To identify druggable oncogenic fusions in invasive mucinous adenocarcinoma (IMA) of the lung, a malignant type of lung adenocarcinoma in which KRAS mutations frequently occur. From an IMA cohort of 90 cases, consisting of 56 cases (62%) with KRAS mutations and 34 cases without (38%), we conducted whole-transcriptome sequencing of 32 IMAs, including 27 cases without KRAS mutations. We used the sequencing data to identify gene fusions, and then performed functional analyses of the fusion gene products. We identified oncogenic fusions that occurred mutually exclusively with KRAS mutations: CD74-NRG1, SLC3A2-NRG1, EZR-ERBB4, TRIM24-BRAF, and KIAA1468-RET. NRG1 fusions were present in 17.6% (6/34) of KRAS-negative IMAs. The CD74-NRG1 fusion activated HER2:HER3 signaling, whereas the EZR-ERBB4 and TRIM24-BRAF fusions constitutively activated the ERBB4 and BRAF kinases, respectively. Signaling pathway activation and fusion-induced anchorage-independent growth/tumorigenicity of NIH3T3 cells expressing these fusions were suppressed by tyrosine kinase inhibitors approved for clinical use. Oncogenic fusions act as driver mutations in IMAs without KRAS mutations, and thus represent promising therapeutic targets for the treatment of such IMAs. ©2014 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Nakaoku, Takashi AU - Tsuta, Koji AU - Ichikawa, Hitoshi AU - Shiraishi, Kouya AU - Sakamoto, Hiromi AU - Enari, Masato AU - Furuta, Koh AU - Shimada, Yoko AU - Ogiwara, Hideaki AU - Watanabe, Shun-ichi AU - Nokihara, Hiroshi AU - Yasuda, Kazuki AU - Hiramoto, Masaki AU - Nammo, Takao AU - Ishigame, Teruhide AU - Schetter, Aaron J AU - Okayama, Hirokazu AU - Harris, Curtis C AU - Kim, Young Hak AU - Mishima, Michiaki AU - Yokota, Jun AU - Yoshida, Teruhiko AU - Kohno, Takashi AD - Authors' Affiliations: Divisions of Genome Biology, Genetics, and Refractory Cancer Research, National Cancer Center Research Institute, Divisions of Pathology and Clinical Laboratories, Thoracic Surgery, and Thoracic Oncology, National Cancer Center Hospital, Chuo-ku; Department of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo; Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland; and The Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Barcelona, SpainAuthors' Affiliations: Divisions of Genome Biology, Genetics, and Refractory Cancer Research, National Cancer Center Research Institute, Divisions of Pathology and Clinical Laboratories, Thoracic Surgery, and Thoracic Oncology, National Cancer Center Hospital, Chuo-ku; Department of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo; Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland; and The Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Barcelona, Spain. ; Authors' Affiliations: Divisions of Genome Biology, Genetics, and Refractory Cancer Research, National Cancer Center Research Institute, Divisions of Pathology and Clinical Laboratories, Thoracic Surgery, and Thoracic Oncology, National Cancer Center Hospital, Chuo-ku; Department of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo; Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland; and The Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Barcelona, Spain. ; Authors' Affiliations: Divisions of Genome Biology, Genetics, and Refractory Cancer Research, National Cancer Center Research Institute, Divisions of Pathology and Clinical Laboratories, Thoracic Surgery, and Thoracic Oncology, National Cancer Center Hospital, Chuo-ku; Department of Metabolic Disorder, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo; Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, Japan; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland; and The Institute of Predictive and Personalized Medicine of Cancer (IMPPC), Barcelona, Spain tkkohno@ncc.go.jp. Y1 - 2014/06/15/ PY - 2014 DA - 2014 Jun 15 SP - 3087 EP - 3093 VL - 20 IS - 12 SN - 1078-0432, 1078-0432 KW - KRAS protein, human KW - 0 KW - Oncogene Proteins, Fusion KW - Protein Kinase Inhibitors KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - ras Proteins KW - Index Medicus KW - Neoplasm Invasiveness KW - Animals KW - Cell Transformation, Neoplastic -- pathology KW - Neoplasm Staging KW - Humans KW - Prognosis KW - Aged KW - Cell Transformation, Neoplastic -- drug effects KW - Mice KW - Mice, Nude KW - NIH 3T3 Cells KW - Signal Transduction -- drug effects KW - Follow-Up Studies KW - Middle Aged KW - Female KW - Male KW - ras Proteins -- genetics KW - Adenocarcinoma, Mucinous -- genetics KW - Protein Kinase Inhibitors -- therapeutic use KW - Oncogene Proteins, Fusion -- genetics KW - Lung Neoplasms -- drug therapy KW - Mutation -- genetics KW - Lung Neoplasms -- genetics KW - Adenocarcinoma, Mucinous -- drug therapy KW - Proto-Oncogene Proteins -- genetics KW - Adenocarcinoma, Mucinous -- pathology KW - Oncogene Proteins, Fusion -- antagonists & inhibitors KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535621629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Druggable+oncogene+fusions+in+invasive+mucinous+lung+adenocarcinoma.&rft.au=Nakaoku%2C+Takashi%3BTsuta%2C+Koji%3BIchikawa%2C+Hitoshi%3BShiraishi%2C+Kouya%3BSakamoto%2C+Hiromi%3BEnari%2C+Masato%3BFuruta%2C+Koh%3BShimada%2C+Yoko%3BOgiwara%2C+Hideaki%3BWatanabe%2C+Shun-ichi%3BNokihara%2C+Hiroshi%3BYasuda%2C+Kazuki%3BHiramoto%2C+Masaki%3BNammo%2C+Takao%3BIshigame%2C+Teruhide%3BSchetter%2C+Aaron+J%3BOkayama%2C+Hirokazu%3BHarris%2C+Curtis+C%3BKim%2C+Young+Hak%3BMishima%2C+Michiaki%3BYokota%2C+Jun%3BYoshida%2C+Teruhiko%3BKohno%2C+Takashi&rft.aulast=Nakaoku&rft.aufirst=Takashi&rft.date=2014-06-15&rft.volume=20&rft.issue=12&rft.spage=3087&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-0107 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-15 N1 - Date created - 2014-06-14 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-0107 ER - TY - JOUR T1 - Voriconazole metabolism, toxicity, and the effect of cytochrome P450 2C19 genotype. AN - 1530953712; 24403552 AB - Prospective evaluation of the antifungal drug, voriconazole, is needed to determine whether drug toxicity correlates with CYP2C19 genotype or serum concentrations of voriconazole or its metabolites. We conducted a prospective study of 95 patients to determine voriconazole toxicity and its relationship to genotype and serum levels of voriconazole and its two metabolites. Efficacy was not evaluated because, in most cases, the drug was given for empirical or prophylactic therapy. Hallucinations occurred in 16 patients (16.8%), visual changes in 17 (17.9%), photosensitivity in 10 (10.5%), and hepatotoxicity in 6 (6.3%). There was no correlation between photosensitivity or hepatotoxicity and levels of voriconazole or metabolites. Patients with hallucinations had higher average voriconazole levels (4.5 vs 2.5 μg/mL) but with extensive overlap. The recommended oral dose of 200 mg did not provide consistently detectable serum voriconazole levels in adults. CYP2C19 and CYP2C9 genotypes had a minor influence over levels, though the 4 patients homozygous for the 2C19*2 genotype had higher average levels for voriconazole (4.3 vs 2.5 μg/mL) and lower N-oxide levels (1.6 vs 2.5 μg/mL). CYP2C19 and 2C9 genotypes were not major determinants of voriconazole metabolism. No toxic serum level of voriconazole or its metabolites could be identified. Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - The Journal of infectious diseases AU - Zonios, Dimitrios AU - Yamazaki, Hiroshi AU - Murayama, Norie AU - Natarajan, Ven AU - Palmore, Tara AU - Childs, Richard AU - Skinner, Jeff AU - Bennett, John E AD - National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), Bethesda, Maryland. ; Showa Pharmaceutical University, Machida, Tokyo 194-8543, Japan. ; SAIC-Frederick Inc, National Cancer Institute at Frederick, Maryland. ; National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland. Y1 - 2014/06/15/ PY - 2014 DA - 2014 Jun 15 SP - 1941 EP - 1948 VL - 209 IS - 12 KW - Antifungal Agents KW - 0 KW - Pyrimidines KW - Triazoles KW - CYP2C9 protein, human KW - EC 1.14.13.- KW - Cytochrome P-450 CYP2C9 KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - CYP2C19 protein, human KW - Cytochrome P-450 CYP2C19 KW - Voriconazole KW - JFU09I87TR KW - Abridged Index Medicus KW - Index Medicus KW - metabolites KW - toxicity KW - CYP2C19 KW - voriconazole KW - Young Adult KW - Homozygote KW - Dose-Response Relationship, Drug KW - Humans KW - Aged KW - Liver -- metabolism KW - Prospective Studies KW - Liver -- drug effects KW - Adult KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Antifungal Agents -- toxicity KW - Triazoles -- toxicity KW - Hallucinations -- chemically induced KW - Pyrimidines -- toxicity KW - Triazoles -- blood KW - Pyrimidines -- blood KW - Antifungal Agents -- administration & dosage KW - Aryl Hydrocarbon Hydroxylases -- genetics KW - Pyrimidines -- administration & dosage KW - Antifungal Agents -- blood KW - Triazoles -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1530953712?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Voriconazole+metabolism%2C+toxicity%2C+and+the+effect+of+cytochrome+P450+2C19+genotype.&rft.au=Zonios%2C+Dimitrios%3BYamazaki%2C+Hiroshi%3BMurayama%2C+Norie%3BNatarajan%2C+Ven%3BPalmore%2C+Tara%3BChilds%2C+Richard%3BSkinner%2C+Jeff%3BBennett%2C+John+E&rft.aulast=Zonios&rft.aufirst=Dimitrios&rft.date=2014-06-15&rft.volume=209&rft.issue=12&rft.spage=1941&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjiu017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-14 N1 - Date created - 2014-05-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Transplant. 2009 Dec;9(12):2845-50 [19845595] Br J Clin Pharmacol. 2009 Dec;68(6):906-15 [20002085] Ther Drug Monit. 2011 Feb;33(1):86-93 [21192313] Pharmacogenomics. 2011 Jun;12(6):861-72 [21692616] Clin Infect Dis. 2012 Aug;55(3):381-90 [22610925] Antimicrob Agents Chemother. 2012 Sep;56(9):4793-9 [22751544] Antimicrob Agents Chemother. 2000 May;44(5):1209-13 [10770753] Br J Clin Pharmacol. 2003 Dec;56 Suppl 1:37-44 [14616412] Pharmacogenetics. 2004 Aug;14(8):527-37 [15284535] Bone Marrow Transplant. 2005 Mar;35(5):509-13 [15654347] J Antimicrob Chemother. 2006 Jun;57(6):1248-50 [16556632] Clin Pharmacokinet. 2006;45(7):649-63 [16802848] Swiss Med Wkly. 2006 Nov 11;136(45-46):739-42 [17183438] Biochem Pharmacol. 2007 Jun 15;73(12):2020-6 [17433262] Clin Infect Dis. 2008 Jan 15;46(2):201-11 [18171251] Clin Infect Dis. 2008 Jul 1;47(1):e7-e10 [18491963] J Clin Pharmacol. 2009 Feb;49(2):196-204 [19033450] Biol Blood Marrow Transplant. 2009 Mar;15(3):370-6 [19203729] Eur J Clin Pharmacol. 2009 Mar;65(3):281-5 [18982321] J Heart Lung Transplant. 2010 Nov;29(11):1240-4 [20591690] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/infdis/jiu017 ER - TY - JOUR T1 - Medial vascular calcification revisited: review and perspectives. AN - 1548630094; 24740885 AB - Vascular calcifications (VCs) are actively regulated biological processes associated with crystallization of hydroxyapatite in the extracellular matrix and in cells of the media (VCm) or intima (VCi) of the arterial wall. Both patterns of VC often coincide and occur in patients with type II diabetes, chronic kidney disease, and other less frequent disorders; VCs are also typical in senile degeneration. In this article, we review the current state of knowledge about the pathology, molecular biology, and nosology of VCm, expand on potential mechanisms responsible for poor prognosis, and expose some of the directions for future research in this area. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2014. For permissions please email: journals.permissions@oup.com. JF - European heart journal AU - Lanzer, Peter AU - Boehm, Manfred AU - Sorribas, Victor AU - Thiriet, Marc AU - Janzen, Jan AU - Zeller, Thomas AU - St Hilaire, Cynthia AU - Shanahan, Catherine AD - Division of Cardiovascular Disease, Department of Internal Medicine, Health Care Center Bitterfeld, Bitterfeld-Wolfen gGmbH, Friedrich-Ludwig-Jahn-Straße 2, D-06749 Bitterfeld-Wolfen, Germany planzer@gzbiwo.de. ; Center for Molecular Medicine, National Institutes of Health, Bethesda, MD, USA. ; Laboratory of Molecular Toxicology, University of Zaragoza, Zaragoza, Spain. ; National Institute for Research in Computer Science and Control, Paris, France. ; VascPath, Bern, Switzerland. ; University Heart Center Freiburg, Bad Krozingen, Germany. ; Cardiovascular Division, King's College London, London, UK. Y1 - 2014/06/14/ PY - 2014 DA - 2014 Jun 14 SP - 1515 EP - 1525 VL - 35 IS - 23 KW - Biomarkers KW - 0 KW - Calcium-Binding Proteins KW - Phosphates KW - Index Medicus KW - Vascular function KW - Vascular molecular biology and genetics KW - Mönckeberg's media sclerosis KW - Vascular calcifications KW - Monckeberg Medial Calcific Sclerosis -- therapy KW - Renal Insufficiency, Chronic -- physiopathology KW - Hyperphosphatemia -- physiopathology KW - Tunica Media -- physiopathology KW - Phosphates -- physiology KW - Humans KW - Tunica Intima -- physiopathology KW - Prognosis KW - Monckeberg Medial Calcific Sclerosis -- pathology KW - Terminology as Topic KW - Diabetes Mellitus, Type 2 -- physiopathology KW - Tunica Media -- pathology KW - Arteriosclerosis -- pathology KW - Arteriosclerosis -- physiopathology KW - Monckeberg Medial Calcific Sclerosis -- physiopathology KW - Diabetes Mellitus, Type 2 -- pathology KW - Adult KW - Diabetic Angiopathies -- physiopathology KW - Biomarkers -- metabolism KW - Calcium-Binding Proteins -- physiology KW - Tunica Intima -- pathology KW - Male KW - Female KW - Diabetic Angiopathies -- pathology KW - Vascular Calcification -- therapy KW - Vascular Calcification -- physiopathology KW - Vascular Calcification -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548630094?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+heart+journal&rft.atitle=Medial+vascular+calcification+revisited%3A+review+and+perspectives.&rft.au=Lanzer%2C+Peter%3BBoehm%2C+Manfred%3BSorribas%2C+Victor%3BThiriet%2C+Marc%3BJanzen%2C+Jan%3BZeller%2C+Thomas%3BSt+Hilaire%2C+Cynthia%3BShanahan%2C+Catherine&rft.aulast=Lanzer&rft.aufirst=Peter&rft.date=2014-06-14&rft.volume=35&rft.issue=23&rft.spage=1515&rft.isbn=&rft.btitle=&rft.title=European+heart+journal&rft.issn=1522-9645&rft_id=info:doi/10.1093%2Feurheartj%2Fehu163 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-02 N1 - Date created - 2014-06-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hypertension. 2010 Oct;56(4):555-62 [20733089] Angiology. 2002 Jul-Aug;53(4):483-6 [12143958] Circ Res. 2008 Aug 29;103(5):e28-34 [18669918] 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http://dx.doi.org/10.1093/eurheartj/ehu163 ER - TY - JOUR T1 - Simplagrin, a Platelet Aggregation Inhibitor from Simulium nigrimanum Salivary Glands Specifically Binds to the Von Willebrand Factor Receptor in Collagen and Inhibits Carotid Thrombus Formation In Vivo AN - 1611613031; 20168513 AB - Blood feeding arthropods-like mosquitoes and black flies-have evolved salivary secretions rich in molecules that affect hemostasis, including vasodilators and inhibitors of blood clotting and platelet aggregation. Among the platelet inhibitors, antagonists of collagen-induced platelet aggregation and adhesion have been found in salivary glands of blood feeders. Here we report the first collagen-binding protein from salivary glands of a black fly. This molecule prevents thrombosis in mice without causing significant bleeding, making it an attractive candidate as an antithrombotic agent. Because blackflies and mosquitoes shared a common blood feeding ancestor approximately 250 million years ago, it appears that collagen-binding activity in salivary glands was an evolutionary innovation present in an ancient dipteran ancestor. Our work highlights the central role of inhibition of platelet aggregation as a vital salivary function in blood feeding arthropods. JF - PLoS Neglected Tropical Diseases AU - Chagas, Andrezza C AU - McPhie, Peter AU - San, Hong AU - Narum, David AU - Reiter, Karine AU - Tokomasu, Fuyuki AU - Brayner, Fabio A AU - Alves, Luiz C AU - Ribeiro, Jose MC AU - Calvo, Eric AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Rockville, Maryland, United States of America Y1 - 2014/06/12/ PY - 2014 DA - 2014 Jun 12 PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States VL - 8 IS - 6 SN - 1935-2727, 1935-2727 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources KW - Simulium KW - Arthropoda KW - Glands KW - Secretion KW - Receptors KW - Inhibitors KW - Aggregation KW - Aquatic insects KW - Adhesion KW - Public health KW - Collagen 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/1611613031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+Neglected+Tropical+Diseases&rft.atitle=Simplagrin%2C+a+Platelet+Aggregation+Inhibitor+from+Simulium+nigrimanum+Salivary+Glands+Specifically+Binds+to+the+Von+Willebrand+Factor+Receptor+in+Collagen+and+Inhibits+Carotid+Thrombus+Formation+In+Vivo&rft.au=Chagas%2C+Andrezza+C%3BMcPhie%2C+Peter%3BSan%2C+Hong%3BNarum%2C+David%3BReiter%2C+Karine%3BTokomasu%2C+Fuyuki%3BBrayner%2C+Fabio+A%3BAlves%2C+Luiz+C%3BRibeiro%2C+Jose+MC%3BCalvo%2C+Eric&rft.aulast=Chagas&rft.aufirst=Andrezza&rft.date=2014-06-12&rft.volume=8&rft.issue=6&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0002947 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-10-01 N1 - Last updated - 2015-06-26 N1 - SubjectsTermNotLitGenreText - Secretion; Glands; Receptors; Aggregation; Inhibitors; Adhesion; Aquatic insects; Collagen; Public health; Simulium; Arthropoda DO - http://dx.doi.org/10.1371/journal.pntd.0002947 ER - TY - JOUR T1 - Macrophage Models of Gaucher Disease for Evaluating Disease Pathogenesis and Candidate Drugs AN - 1823946437; PQ0001725961 AB - Gaucher disease is caused by an inherited deficiency of glucocerebrosidase that manifests with storage of glycolipids in lysosomes, particularly in macrophages. Available cell lines modeling Gaucher disease do not demonstrate lysosomal storage of glycolipids; therefore, we set out to develop two macrophage models of Gaucher disease that exhibit appropriate substrate accumulation. We used these cellular models both to investigate altered macrophage biology in Gaucher disease and to evaluate candidate drugs for its treatment. We generated and characterized monocyte-derived macrophages from 20 patients carrying different Gaucher disease mutations. In addition, we created induced pluripotent stem cell (iPSC)-derived macrophages from five fibroblast lines taken from patients with type 1 or type 2 Gaucher disease. Macrophages derived from patient monocytes or iPSCs showed reduced glucocerebrosidase activity and increased storage of glucocerebroside and glucosylsphingosine in lysosomes. These macrophages showed efficient phagocytosis of bacteria but reduced production of intracellular reactive oxygen species and impaired chemotaxis. The disease phenotype was reversed with a noninhibitory small-molecule chaperone drug that enhanced glucocerebrosidase activity in the macrophages, reduced glycolipid storage, and normalized chemotaxis and production of reactive oxygen species. Macrophages differentiated from patient monocytes or patient-derived iPSCs provide cellular models that can be used to investigate disease pathogenesis and facilitate drug development. JF - Science Translational Medicine AU - Aflaki, Elma AU - Stubblefield, Barbara K AU - Maniwang, Emerson AU - Lopez, Grisel AU - Moaven, Nima AU - Goldin, Ehud AU - Marugan, Juan AU - Patnaik, Samarjit AU - Dutra, Amalia AU - Southall, Noel AU - Zheng, Wei AU - Tayebi, Nahid AU - Sidransky, Ellen AD - Section on Molecular Neurogenetics, Medical Genetics Branch, National Institutes of Health, Bethesda, MD 20892, USA, sidranse@mail.nih.gov Y1 - 2014/06/11/ PY - 2014 DA - 2014 Jun 11 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 6 IS - 240 SN - 1946-6234, 1946-6234 KW - Biotechnology and Bioengineering Abstracts KW - Macrophages KW - Translation KW - Inhibitory postsynaptic potentials KW - Drug development KW - Glucosylceramidase KW - Chemotaxis KW - Fibroblasts KW - Glycolipids KW - Stem cells KW - Reactive oxygen species KW - Gaucher's disease KW - Chaperones KW - Monocytes KW - Phagocytosis KW - Drugs KW - Mutation KW - Lysosomes KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1823946437?accountid=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=Macrophage+Models+of+Gaucher+Disease+for+Evaluating+Disease+Pathogenesis+and+Candidate+Drugs&rft.au=Aflaki%2C+Elma%3BStubblefield%2C+Barbara+K%3BManiwang%2C+Emerson%3BLopez%2C+Grisel%3BMoaven%2C+Nima%3BGoldin%2C+Ehud%3BMarugan%2C+Juan%3BPatnaik%2C+Samarjit%3BDutra%2C+Amalia%3BSouthall%2C+Noel%3BZheng%2C+Wei%3BTayebi%2C+Nahid%3BSidransky%2C+Ellen&rft.aulast=Aflaki&rft.aufirst=Elma&rft.date=2014-06-11&rft.volume=6&rft.issue=240&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Science+Translational+Medicine&rft.issn=19466234&rft_id=info:doi/10.1126%2Fscitranslmed.3008659 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-09-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Macrophages; Translation; Inhibitory postsynaptic potentials; Drug development; Glucosylceramidase; Chemotaxis; Fibroblasts; Glycolipids; Stem cells; Reactive oxygen species; Gaucher's disease; Chaperones; Monocytes; Phagocytosis; Mutation; Drugs; Lysosomes DO - http://dx.doi.org/10.1126/scitranslmed.3008659 ER - TY - JOUR T1 - Removing T-cell epitopes with computational protein design. AN - 1535630293; 24843166 AB - Immune responses can make protein therapeutics ineffective or even dangerous. We describe a general computational protein design method for reducing immunogenicity by eliminating known and predicted T-cell epitopes and maximizing the content of human peptide sequences without disrupting protein structure and function. We show that the method recapitulates previous experimental results on immunogenicity reduction, and we use it to disrupt T-cell epitopes in GFP and Pseudomonas exotoxin A without disrupting function. JF - Proceedings of the National Academy of Sciences of the United States of America AU - King, Chris AU - Garza, Esteban N AU - Mazor, Ronit AU - Linehan, Jonathan L AU - Pastan, Ira AU - Pepper, Marion AU - Baker, David AD - Institute for Protein Design, Department of Biochemistry and chrisk1@uw.edu. ; Department of Immunology, University of Washington, Seattle, WA 98195; and. ; National Cancer Institute and. ; National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892. ; Institute for Protein Design, Department of Biochemistry and. Y1 - 2014/06/10/ PY - 2014 DA - 2014 Jun 10 SP - 8577 EP - 8582 VL - 111 IS - 23 KW - Bacterial Toxins KW - 0 KW - Epitopes, T-Lymphocyte KW - Exotoxins KW - HLA Antigens KW - Immunotoxins KW - Proteins KW - Virulence Factors KW - Green Fluorescent Proteins KW - 147336-22-9 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Rosetta KW - machine learning KW - biotherapeutics KW - immunotoxin KW - deimmunization KW - Animals KW - Spectrometry, Fluorescence KW - Virulence Factors -- chemistry KW - Humans KW - ADP Ribose Transferases -- genetics KW - Green Fluorescent Proteins -- genetics KW - Bacterial Toxins -- genetics KW - ADP Ribose Transferases -- chemistry KW - Support Vector Machine KW - Green Fluorescent Proteins -- immunology KW - Molecular Sequence Data KW - Computer-Aided Design KW - Flow Cytometry KW - Sequence Homology, Amino Acid KW - Exotoxins -- genetics KW - HLA Antigens -- genetics KW - Green Fluorescent Proteins -- chemistry KW - ADP Ribose Transferases -- immunology KW - Models, Molecular KW - Virulence Factors -- genetics KW - Exotoxins -- chemistry KW - Cell Line, Tumor KW - Mice KW - Exotoxins -- immunology KW - Bacterial Toxins -- immunology KW - Virulence Factors -- immunology KW - Immunization KW - HLA Antigens -- immunology KW - Mice, Inbred C57BL KW - Bacterial Toxins -- chemistry KW - Protein Structure, Tertiary KW - Immunotoxins -- chemistry KW - Proteins -- chemistry KW - Immunotoxins -- immunology KW - Protein Engineering -- methods KW - Immunotoxins -- genetics KW - Epitopes, T-Lymphocyte -- immunology KW - Proteins -- genetics KW - Proteins -- immunology KW - Epitopes, T-Lymphocyte -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535630293?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Removing+T-cell+epitopes+with+computational+protein+design.&rft.au=King%2C+Chris%3BGarza%2C+Esteban+N%3BMazor%2C+Ronit%3BLinehan%2C+Jonathan+L%3BPastan%2C+Ira%3BPepper%2C+Marion%3BBaker%2C+David&rft.aulast=King&rft.aufirst=Chris&rft.date=2014-06-10&rft.volume=111&rft.issue=23&rft.spage=8577&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.1321126111 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-30 N1 - Date created - 2014-06-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Bioinformatics. 2001 Dec;17(12):1236-7 [11751237] Proc Natl Acad Sci U S A. 2011 Apr 26;108(17):6981-6 [21478437] Methods Mol Biol. 2004;248:503-18 [14970517] Cell. 1993 Jul 16;74(1):197-203 [8334703] J Immunol. 1998 Apr 1;160(7):3363-73 [9531296] Nat Med. 1998 Oct;4(10):1201-5 [9771757] Clin Ther. 1999 Feb;21(2):309-18 [10211534] J Immunol. 2005 Mar 15;174(6):3187-96 [15749848] Stem Cells. 2005 Oct;23(9):1251-65 [16109764] Mol Cancer Ther. 2005 Nov;4(11):1791-800 [16276001] Nat Biotechnol. 2006 Jan;24(1):79-88 [16369541] PLoS One. 2011;6(6):e20161 [21731610] Cancer Res. 2011 Oct 15;71(20):6300-9 [21998010] Nucleic Acids Res. 2012 Jan;40(Database issue):D84-90 [22086963] J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053] Proc Natl Acad Sci U S A. 2012 Dec 18;109(51):E3597-603 [23213206] J Comput Chem. 2013 Apr 5;34(10):879-91 [23299435] Expert Rev Clin Pharmacol. 2013 Nov;6(6):651-62 [24164613] Proteins. 2014 May;82(5):858-66 [24265170] J Mol Recognit. 2007 Mar-Apr;20(2):75-82 [17205610] Immunity. 2007 Aug;27(2):203-13 [17707129] 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] Adv Drug Deliv Rev. 2009 Sep 30;61(11):977-85 [19679153] Nucleic Acids Res. 2010 Jan;38(Database issue):D854-62 [19906713] BMC Bioinformatics. 2010;11:180 [20380721] Immunology. 2010 Jul;130(3):319-28 [20408898] Curr Drug Saf. 2010 Oct;5(4):308-13 [20615174] Proc Natl Acad Sci U S A. 2011 Jan 25;108(4):1272-7 [21209329] J Bioinform Comput Biol. 2011 Apr;9(2):207-29 [21523929] Springer Semin Immunopathol. 2001 Dec;23(4):405-19 [11826617] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1321126111 ER - TY - JOUR T1 - NADPH oxidases: a perspective on reactive oxygen species production in tumor biology. AN - 1526730787; 24156355 AB - Reactive oxygen species (ROS) promote genomic instability, altered signal transduction, and an environment that can sustain tumor formation and growth. The NOX family of NADPH oxidases, membrane-bound epithelial superoxide and hydrogen peroxide producers, plays a critical role in the maintenance of immune function, cell growth, and apoptosis. The impact of NOX enzymes in carcinogenesis is currently being defined and may directly link chronic inflammation and NOX ROS-mediated tumor formation. Increased interest in the function of NOX enzymes in tumor biology has spurred a surge of investigative effort to understand the variability of NOX expression levels in tumors and the effect of NOX activity on tumor cell proliferation. These initial efforts have demonstrated a wide variance in NOX distribution and expression levels across numerous cancers as well as in common tumor cell lines, suggesting that much remains to be discovered about the unique role of NOX-related ROS production within each system. Progression from in vitro cell line studies toward in vivo tumor tissue screening and xenograft models has begun to provide evidence supporting the importance of NOX expression in carcinogenesis. A lack of universally available, isoform-specific antibodies and animal tumor models of inducible knockout or over-expression of NOX isoforms has hindered progress toward the completion of in vivo studies. In vivo validation experiments and the use of large, existing gene expression data sets should help define the best model systems for studying the NOX homologues in the context of cancer. JF - Antioxidants & redox signaling AU - Meitzler, Jennifer L AU - Antony, Smitha AU - Wu, Yongzhong AU - Juhasz, Agnes AU - Liu, Han AU - Jiang, Guojian AU - Lu, Jiamo AU - Roy, Krishnendu AU - Doroshow, James H AD - 1 Laboratory of Molecular Pharmacology of the Center for Cancer Research, National Cancer Institute, National Institutes of Health , Bethesda, Maryland. Y1 - 2014/06/10/ PY - 2014 DA - 2014 Jun 10 SP - 2873 EP - 2889 VL - 20 IS - 17 KW - Reactive Oxygen Species KW - 0 KW - Superoxides KW - 11062-77-4 KW - Hydrogen Peroxide KW - BBX060AN9V KW - NADPH Oxidase KW - EC 1.6.3.1 KW - Index Medicus KW - Oxidation-Reduction KW - Reactive Oxygen Species -- metabolism KW - Superoxides -- metabolism KW - Apoptosis -- genetics KW - Hydrogen Peroxide -- metabolism KW - Humans KW - Cell Cycle -- genetics KW - NADPH Oxidase -- metabolism KW - Signal Transduction -- genetics KW - Neoplasms -- physiopathology KW - Cell Proliferation -- genetics KW - Neoplasms -- therapy KW - NADPH Oxidase -- genetics KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1526730787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antioxidants+%26+redox+signaling&rft.atitle=NADPH+oxidases%3A+a+perspective+on+reactive+oxygen+species+production+in+tumor+biology.&rft.au=Meitzler%2C+Jennifer+L%3BAntony%2C+Smitha%3BWu%2C+Yongzhong%3BJuhasz%2C+Agnes%3BLiu%2C+Han%3BJiang%2C+Guojian%3BLu%2C+Jiamo%3BRoy%2C+Krishnendu%3BDoroshow%2C+James+H&rft.aulast=Meitzler&rft.aufirst=Jennifer&rft.date=2014-06-10&rft.volume=20&rft.issue=17&rft.spage=2873&rft.isbn=&rft.btitle=&rft.title=Antioxidants+%26+redox+signaling&rft.issn=1557-7716&rft_id=info:doi/10.1089%2Fars.2013.5603 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-30 N1 - Date created - 2014-05-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Thyroid. 2001 Nov;11(11):1017-23 [11762710] Arch Biochem Biophys. 2002 Jan 15;397(2):342-4 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DNA Repair (Amst). 2010 Jun 4;9(6):604-16 [20399712] Surg Oncol. 2002 May;10(4):153-69 [12020670] N Engl J Med. 2002 Jul 11;347(2):95-102 [12110737] Gut. 2003 Feb;52(2):231-6 [12524405] J Biol Chem. 2003 Feb 7;278(6):3510-3 [12473664] Carcinogenesis. 2003 Mar;24(3):353-62 [12663492] J Immunol. 2003 Jul 1;171(1):299-306 [12817011] J Biol Chem. 2003 Jul 4;278(27):25234-46 [12716910] Am J Physiol Cell Physiol. 2003 Aug;285(2):C353-69 [12686516] Immunity. 2003 Nov;19(5):725-37 [14614859] J Immunol. 2004 Mar 1;172(5):3051-8 [14978110] Drug Resist Updat. 2004 Apr;7(2):97-110 [15158766] Nat Genet. 2004 Oct;36(10):1090-8 [15448693] J Biol Chem. 2004 Oct 29;279(44):46065-72 [15326186] Jpn J Infect Dis. 2004 Oct;57(5):S28-9 [15507765] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1089/ars.2013.5603 ER - TY - CPAPER T1 - Public Health Researcher's Perspective on CECs, Public Health and Inter-Disciplinary T2 - 2014 Annual Conference of the American Water Works Association (ACE 2014) AN - 1548628240; 6290475 JF - 2014 Annual Conference of the American Water Works Association (ACE 2014) AU - Weis, Christopher Y1 - 2014/06/08/ PY - 2014 DA - 2014 Jun 08 KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1548628240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Conference+of+the+American+Water+Works+Association+%28ACE+2014%29&rft.atitle=Public+Health+Researcher%27s+Perspective+on+CECs%2C+Public+Health+and+Inter-Disciplinary&rft.au=Weis%2C+Christopher&rft.aulast=Weis&rft.aufirst=Christopher&rft.date=2014-06-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Conference+of+the+American+Water+Works+Association+%28ACE+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.awwa.org/conferences-education/conferences/annual-conference/program/ace14-online-program.aspx# LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-30 N1 - Last updated - 2014-07-28 ER - TY - JOUR T1 - Allosteric inhibitors of the Eya2 phosphatase are selective and inhibit Eya2-mediated cell migration. AN - 1549631473; 24755226 AB - Eya proteins are essential co-activators of the Six family of transcription factors and contain a unique tyrosine phosphatase domain belonging to the haloacid dehalogenase family of phosphatases. The phosphatase activity of Eya is important for the transcription of a subset of Six1-target genes, and also directs cells to the repair rather than apoptosis pathway upon DNA damage. Furthermore, Eya phosphatase activity has been shown to mediate transformation, invasion, migration, and metastasis of breast cancer cells, making it a potential new drug target for breast cancer. We have previously identified a class of N-arylidenebenzohydrazide compounds that specifically inhibit the Eya2 phosphatase. Herein, we demonstrate that these compounds are reversible inhibitors that selectively inhibit the phosphatase activity of Eya2, but not Eya3. Our mutagenesis results suggest that this class of compounds does not bind to the active site and the binding does not require the coordination with Mg(2+). Moreover, these compounds likely bind within a site on the opposite face of the active site, and function as allosteric inhibitors. We also demonstrate that this class of compounds inhibits Eya2 phosphatase-mediated cell migration, setting the foundation for these molecules to be developed into chemical probes for understanding the specific function of the Eya2 phosphatase and to serve as a prototype for the development of Eya2 phosphatase specific anti-cancer drugs. © 2014 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Krueger, Aaron B AU - Drasin, David J AU - Lea, Wendy A AU - Patrick, Aaron N AU - Patnaik, Samarjit AU - Backos, Donald S AU - Matheson, Christopher J AU - Hu, Xin AU - Barnaeva, Elena AU - Holliday, Michael J AU - Blevins, Melanie A AU - Robin, Tyler P AU - Eisenmesser, Elan Z AU - Ferrer, Marc AU - Simeonov, Anton AU - Southall, Noel AU - Reigan, Philip AU - Marugan, Juan AU - Ford, Heide L AU - Zhao, Rui AD - From the Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, Colorado 80045. ; the Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado 80045. ; the National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland 20892, and. ; the Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado School of Pharmacy, Aurora, Colorado 80045. ; the National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland 20892, and maruganj@mail.nih.gov. ; the Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado 80045, heide.ford@ucdenver.edu. ; From the Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, Colorado 80045, rui.zhao@ucdenver.edu. Y1 - 2014/06/06/ PY - 2014 DA - 2014 Jun 06 SP - 16349 EP - 16361 VL - 289 IS - 23 KW - Enzyme Inhibitors KW - 0 KW - Intracellular Signaling Peptides and Proteins KW - Nuclear Proteins KW - EYA2 protein, human KW - EC 3.1.3.48 KW - Protein Tyrosine Phosphatases KW - Magnesium KW - I38ZP9992A KW - Index Medicus KW - Transcription Coactivator KW - Enzyme Inhibitor KW - Phosphatase KW - Migration KW - Anticancer Drug KW - Humans KW - Spectrophotometry, Ultraviolet KW - Amino Acid Sequence KW - Protein Binding KW - Magnesium -- metabolism KW - Molecular Docking Simulation KW - Nuclear Magnetic Resonance, Biomolecular KW - Molecular Sequence Data KW - Calorimetry KW - Enzyme Inhibitors -- pharmacology KW - Allosteric Regulation KW - Crystallography, X-Ray KW - Sequence Homology, Amino Acid KW - Cell Line KW - Intracellular Signaling Peptides and Proteins -- chemistry KW - Protein Tyrosine Phosphatases -- metabolism KW - Protein Tyrosine Phosphatases -- physiology KW - Nuclear Proteins -- antagonists & inhibitors KW - Intracellular Signaling Peptides and Proteins -- antagonists & inhibitors KW - Intracellular Signaling Peptides and Proteins -- metabolism KW - Cell Movement -- physiology KW - Nuclear Proteins -- chemistry KW - Intracellular Signaling Peptides and Proteins -- physiology KW - Nuclear Proteins -- metabolism KW - Nuclear Proteins -- physiology KW - Protein Tyrosine Phosphatases -- chemistry KW - Protein Tyrosine Phosphatases -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1549631473?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Allosteric+inhibitors+of+the+Eya2+phosphatase+are+selective+and+inhibit+Eya2-mediated+cell+migration.&rft.au=Krueger%2C+Aaron+B%3BDrasin%2C+David+J%3BLea%2C+Wendy+A%3BPatrick%2C+Aaron+N%3BPatnaik%2C+Samarjit%3BBackos%2C+Donald+S%3BMatheson%2C+Christopher+J%3BHu%2C+Xin%3BBarnaeva%2C+Elena%3BHolliday%2C+Michael+J%3BBlevins%2C+Melanie+A%3BRobin%2C+Tyler+P%3BEisenmesser%2C+Elan+Z%3BFerrer%2C+Marc%3BSimeonov%2C+Anton%3BSouthall%2C+Noel%3BReigan%2C+Philip%3BMarugan%2C+Juan%3BFord%2C+Heide+L%3BZhao%2C+Rui&rft.aulast=Krueger&rft.aufirst=Aaron&rft.date=2014-06-06&rft.volume=289&rft.issue=23&rft.spage=16349&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.566729 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-07 N1 - Date created - 2014-07-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncogene. 2010 Jan 21;29(3):368-79 [19901965] J Biol Chem. 2009 Jun 12;284(24):16066-70 [19351884] Oncogene. 2010 Jun 24;29(25):3715-22 [20418914] Anticancer Agents Med Chem. 2011 Jan;11(1):141-50 [21288196] ACS Chem Biol. 2011 May 20;6(5):511-9 [21348431] Blood. 2011 Jun 23;117(25):6895-905 [21518926] Chem Biol Drug Des. 2011 Oct;78(4):642-50 [21777393] Oncogene. 2012 Feb 2;31(5):552-62 [21706047] Nat Chem Biol. 2012 May;8(5):437-46 [22426112] PLoS One. 2012;7(4):e34806 [22545090] J Biomol Screen. 2013 Jan;18(1):85-96 [22820394] ACS Chem Biol. 2013 Jan 18;8(1):36-45 [23214403] FEBS J. 2013 Jan;280(2):549-71 [22607316] Nat Struct Mol Biol. 2013 Apr;20(4):447-53 [23435380] J Am Chem Soc. 2013 May 8;135(18):6838-41 [23611635] Cell Rep. 2013 Jun 27;3(6):2127-41 [23727239] Cancer Res. 2013 Jul 15;73(14):4488-99 [23636126] Am J Pathol. 2002 Jun;160(6):2181-90 [12057921] Development. 2002 Jul;129(13):3033-44 [12070080] Development. 2003 Sep;130(17):3989-4000 [12874121] Nature. 2003 Nov 20;426(6964):247-54 [14628042] Nature. 2003 Nov 20;426(6964):295-8 [14628052] Nature. 2003 Nov 20;426(6964):299-302 [14628053] Curr Opin Struct Biol. 2004 Apr;14(2):217-24 [15093837] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6478-83 [15123840] Proc Natl Acad Sci U S A. 2004 May 25;101(21):8090-5 [15141091] J Assoc Res Otolaryngol. 2004 Sep;5(3):295-304 [15492887] J Mol Biol. 1993 Sep 5;233(1):123-38 [8377180] J Biol Chem. 1996 Dec 20;271(51):32729-36 [8955106] Genome Res. 1997 Feb;7(2):128-41 [9049631] Hum Mol Genet. 1997 Dec;6(13):2247-55 [9361030] Nat Genet. 1999 Sep;23(1):113-7 [10471511] Cancer Res. 2005 Feb 1;65(3):925-32 [15705892] Lancet. 2005 Feb 19-25;365(9460):671-9 [15721472] Trends Genet. 2005 Mar;21(3):163-71 [15734575] Development. 2005 May;132(9):2235-49 [15788460] Cancer Res. 2007 Apr 1;67(7):3036-42 [17409410] Dev Biol. 2007 Oct 15;310(2):416-29 [17714699] Dev Biol. 2007 Nov 1;311(1):53-68 [17880938] J Chem Inf Model. 2008 Oct;48(10):1965-73 [18816046] Nature. 2009 Apr 2;458(7238):591-6 [19234442] FASEB J. 2010 Feb;24(2):560-9 [19858093] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.566729 ER - TY - JOUR T1 - Dopamine D(3) receptors contribute to methamphetamine-induced alterations in dopaminergic neuronal function: role of hyperthermia. AN - 1521333684; 24685638 AB - Methamphetamine administration causes long-term deficits to dopaminergic systems that, in humans, are thought to be associated with motor slowing and memory impairment. Methamphetamine interacts with the dopamine transporter (DAT) and increases extracellular concentrations of dopamine that, in turn, binds to a number of dopamine receptor subtypes. Although the relative contribution of each receptor subtype to the effects of methamphetamine is not fully known, non-selective dopamine D2/D3 receptor antagonists can attenuate methamphetamine-induced changes to dopamine systems. The present study extended these findings by testing the role of the dopamine D3 receptor subtype in mediating the long-term dopaminergic, and for comparison serotonergic, deficits caused by methamphetamine. Results indicate that the dopamine D3 receptor selective antagonist, PG01037, attenuated methamphetamine-induced decreases in striatal DAT, but not hippocampal serotonin (5HT) transporter (SERT), function, as assessed 7 days after treatment. However, PG01037 also attenuated methamphetamine-induced hyperthermia. When methamphetamine-induced hyperthermia was maintained by treating rats in a warm ambient environment, PG01037 failed to attenuate the effects of methamphetamine on DAT uptake. Furthermore, PG01037 did not attenuate methamphetamine-induced decreases in dopamine and 5HT content. Taken together, the present study demonstrates that dopamine D3 receptors mediate, in part, the long-term deficits in DAT function caused by methamphetamine, and that this effect likely involves an attenuation of methamphetamine-induced hyperthermia. Copyright © 2014 Elsevier B.V. All rights reserved. JF - European journal of pharmacology AU - Baladi, Michelle G AU - Newman, Amy H AU - Nielsen, Shannon M AU - Hanson, Glen R AU - Fleckenstein, Annette E AD - Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah, USA. ; Medicinal Chemistry Section, National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD, USA. ; Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah, USA; School of Dentistry, University of Utah, Salt Lake City, Utah, USA. ; Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah, USA. Electronic address: fleckenstein@hsc.utah.edu. Y1 - 2014/06/05/ PY - 2014 DA - 2014 Jun 05 SP - 105 EP - 110 VL - 732 KW - Central Nervous System Stimulants KW - 0 KW - Dopamine Antagonists KW - Receptors, Dopamine D3 KW - Serotonin KW - 333DO1RDJY KW - Methamphetamine KW - 44RAL3456C KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Dopamine transporter KW - Dopamine D(3) receptors KW - PG01037 KW - Serotonin transporter KW - D(3) antagonist KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Synaptosomes -- drug effects KW - Serotonin -- physiology KW - Dopamine Antagonists -- pharmacology KW - Hippocampus -- metabolism KW - Dopamine -- metabolism KW - Synaptosomes -- metabolism KW - Male KW - Hippocampus -- drug effects KW - Dopaminergic Neurons -- drug effects KW - Central Nervous System Stimulants -- toxicity KW - Receptors, Dopamine D3 -- drug effects KW - Fever -- physiopathology KW - Methamphetamine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521333684?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmacology&rft.atitle=Dopamine+D%283%29+receptors+contribute+to+methamphetamine-induced+alterations+in+dopaminergic+neuronal+function%3A+role+of+hyperthermia.&rft.au=Baladi%2C+Michelle+G%3BNewman%2C+Amy+H%3BNielsen%2C+Shannon+M%3BHanson%2C+Glen+R%3BFleckenstein%2C+Annette+E&rft.aulast=Baladi&rft.aufirst=Michelle&rft.date=2014-06-05&rft.volume=732&rft.issue=&rft.spage=105&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=1879-0712&rft_id=info:doi/10.1016%2Fj.ejphar.2014.03.023 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-09 N1 - Date created - 2014-05-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Neurosci. 1995 Feb;15(2):1308-17 [7869099] J Pharmacol Exp Ther. 1995 Feb;272(2):868-75 [7853205] Nat Med. 1996 Jun;2(6):699-703 [8640565] Synapse. 1996 Mar;22(3):217-25 [9132989] Eur J Pharmacol. 2011 May 11;658(2-3):156-9 [21371470] Neurobiol Dis. 2011 Jun;42(3):391-403 [21303698] J Neurochem. 2011 Aug;118(4):668-76 [21668447] Synapse. 2011 Nov;65(11):1144-55 [21584865] J Pharmacol Exp Ther. 2011 Nov;339(2):530-6 [21810934] J Pharmacol Exp Ther. 2012 Feb;340(2):295-303 [22034657] J Pharmacol Exp Ther. 2012 Oct;343(1):214-24 [22815535] Psychopharmacology (Berl). 2013 Feb;225(4):765-80 [23274506] Psychopharmacology (Berl). 2013 Aug;228(4):551-61 [23732837] J Psychopharmacol. 2011 Feb;25(2):263-73 [20142301] J Pharmacol Exp Ther. 1997 Aug;282(2):834-8 [9262348] Brain Res. 1997 Aug 22;766(1-2):113-20 [9359594] J Neurosci. 1998 Oct 15;18(20):8417-22 [9763484] Psychopharmacology (Berl). 1999 Jan;141(3):287-96 [10027510] J Biol Chem. 1951 Nov;193(1):265-75 [14907713] J Med Chem. 2005 Feb 10;48(3):839-48 [15689168] Synapse. 2005 May;56(2):84-93 [15714503] Proc Natl Acad Sci U S A. 2005 Mar 1;102(9):3495-500 [15728379] J Med Chem. 2005 Jun 2;48(11):3663-79 [15916415] Brain Res Brain Res Rev. 2005 Jul;49(1):77-105 [15960988] J Pharmacol Exp Ther. 2005 Jul;314(1):310-9 [15833897] Behav Pharmacol. 2006 May;17(3):239-47 [16572002] Psychopharmacology (Berl). 2007 Aug;193(2):159-70 [17393143] Synapse. 2008 May;62(5):325-36 [18288648] Psychopharmacology (Berl). 2008 Jun;198(3):301-11 [18438646] Neuropsychopharmacology. 2010 Jan;35(1):217-38 [19710631] J Pharmacol Exp Ther. 2010 Jan;332(1):308-15 [19797621] J Pharmacol Exp Ther. 2010 Oct;335(1):207-12 [20622144] J Neurochem. 2000 Oct;75(4):1608-17 [10987842] J Pharmacol Exp Ther. 2000 Dec;295(3):1077-85 [11082443] Am J Psychiatry. 2001 Mar;158(3):377-82 [11229977] Am J Psychiatry. 2001 Aug;158(8):1206-14 [11481152] Brain Res. 2001 Nov 16;919(1):179-83 [11689178] Neuropharmacology. 2003 Jun;44(8):1047-53 [12763098] Eur J Pharmacol. 1976 Apr;36(2):363-71 [6286] Drug Alcohol Depend. 1976 Feb;1(3):215-9 [828106] J Pharmacol Exp Ther. 1979 Feb;208(2):195-202 [216794] Brain Res. 1980 Jan 6;181(1):151-60 [7350950] J Pharmacol Exp Ther. 1986 Sep;238(3):932-7 [2943891] Brain Res. 1990 Oct 8;529(1-2):85-90 [1980848] J Pharmacol Exp Ther. 1992 Feb;260(2):817-24 [1346646] Brain Res. 1991 Nov 15;564(2):256-60 [1810626] Brain Res. 1993 Jan 22;601(1-2):209-12 [8431767] J Neurochem. 1993 May;60(5):1792-9 [8473897] J Pharmacol Exp Ther. 1994 Mar;268(3):1571-80 [8138969] Synapse. 1994 Jul;17(3):203-9 [7974204] J Pharmacol Exp Ther. 1995 Dec;275(3):1104-14 [8531070] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ejphar.2014.03.023 ER - TY - JOUR T1 - Residential Levels of Polybrominated Diphenyl Ethers and Risk of Childhood Acute Lymphoblastic Leukemia in California AN - 1622604891; 20889827 AB - Background: House dust is a major source of exposure to polybrominated diphenyl ethers (PBDEs), which are found at high levels in U.S. homes. Methods: We studied 167 acute lymphoblastic leukemia (ALL) cases 0-7 years of age and 214 birth certificate controls matched on date of birth, sex, and race/ethnicity from the Northern California Childhood Leukemia Study. In 2001-2007, we sampled carpets in the room where the child spent the most time while awake; we used a high-volume small-surface sampler or we took dust from the home vacuum. We measured concentrations of 14 PBDE congeners including penta (28, 47, 99, 100, 153, 154), octa (183, 196, 197, 203), and decaBDEs (206-209). Odds ratios (ORs) were calculated using logistic regression, adjusting for demographics, income, year of dust collection, and sampling method. Results: BDE-47, BDE-99, and BDE-209 were found at the highest concentrations (medians, 1,173, 1,579, and 938 ng/g, respectively). Comparing the highest to lowest quartile, we found no association with ALL for summed pentaBDEs (OR = 0.7; 95% CI: 0.4, 1.3), octaBDEs (OR = 1.3; 95% CI: 0.7, 2.3), or decaBDEs (OR = 1.0; 95% CI: 0.6, 1.8). Comparing homes in the highest concentration (nanograms per gram) tertile to those with no detections, we observed significantly increased ALL risk for BDE-196 (OR = 2.1; 95% CI: 1.1, 3.8), BDE-203 (OR = 2.0; 95% CI: 1.1, 3.6), BDE-206 (OR = 2.1; 95% CI: 1.1, 3.9), and BDE-207 (OR = 2.0; 95% CI: 1.03, 3.8). Conclusion: We found no association with ALL for common PBDEs, but we observed positive associations for specific octa and nonaBDEs. Additional studies with repeated sampling and biological measures would be informative. Citation: Ward MH, Colt JS, Deziel NC, Whitehead TP, Reynolds P, Gunier RB, Nishioka M, Dahl GV, Rappaport SM, Buffler PA, Metayer C. 2014. Residential levels of polybrominated diphenyl ethers and risk of childhood acute lymphoblastic leukemia in California. Environ Health Perspect 122:1110-1116; http://dx.doi.org/10.1289/ehp.1307602 JF - Environmental Health Perspectives AU - Ward, Mary H AU - Colt, Joanne S AU - Deziel, Nicole C AU - Whitehead, Todd P AU - Reynolds, Peggy AU - Gunier, Robert B AU - Nishioka, Marcia AU - Dahl, Gary V AU - Rappaport, Stephen M AU - Buffler, Patricia A AU - Metayer, Catherine AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA Y1 - 2014/06/03/ PY - 2014 DA - 2014 Jun 03 SP - 1110 EP - 1116 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 122 IS - 10 SN - 0091-6765, 0091-6765 KW - Toxicology Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - Age KW - Retinoblastoma protein KW - Dust KW - Income KW - Polybrominated diphenyl ethers KW - Demography KW - Leukemia KW - Carpets KW - Acute lymphatic leukemia KW - Congeners KW - USA, California KW - Sampling KW - Ethnic groups KW - Races KW - Sex KW - Vacuum KW - Children KW - Samplers KW - Birth KW - polybrominated diphenyl ethers KW - House dust KW - Sampling methods KW - H 12000:Epidemiology and Public Health KW - R2 23060:Medical and environmental health KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622604891?accountid=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+Health+Perspectives&rft.atitle=Residential+Levels+of+Polybrominated+Diphenyl+Ethers+and+Risk+of+Childhood+Acute+Lymphoblastic+Leukemia+in+California&rft.au=Ward%2C+Mary+H%3BColt%2C+Joanne+S%3BDeziel%2C+Nicole+C%3BWhitehead%2C+Todd+P%3BReynolds%2C+Peggy%3BGunier%2C+Robert+B%3BNishioka%2C+Marcia%3BDahl%2C+Gary+V%3BRappaport%2C+Stephen+M%3BBuffler%2C+Patricia+A%3BMetayer%2C+Catherine&rft.aulast=Ward&rft.aufirst=Mary&rft.date=2014-06-03&rft.volume=122&rft.issue=10&rft.spage=1110&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1307602 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Retinoblastoma protein; Vacuum; Children; Samplers; Dust; Birth; Demography; polybrominated diphenyl ethers; House dust; Carpets; Acute lymphatic leukemia; Congeners; Sampling; Races; Ethnic groups; Sex; Polybrominated diphenyl ethers; Leukemia; Age; Sampling methods; Income; USA, California DO - http://dx.doi.org/10.1289/ehp.1307602 ER - TY - JOUR T1 - Virus World as an Evolutionary Network of Viruses and Capsidless Selfish Elements AN - 1753468656; 19990207 JF - Microbiology and Molecular Biology Reviews AU - Koonin, Eugene V AU - Dolja, Valerian V AD - National Center for Biotechnology Information, National Library of Medicine, Bethesda, Maryland, USA, koonin@ncbi.nlm.nih.gov. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 278 EP - 303 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 78 IS - 2 SN - 1092-2172, 1092-2172 KW - Microbiology Abstracts B: Bacteriology KW - Evolution KW - J 02310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753468656?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Microbiology+and+Molecular+Biology+Reviews&rft.atitle=Virus+World+as+an+Evolutionary+Network+of+Viruses+and+Capsidless+Selfish+Elements&rft.au=Koonin%2C+Eugene+V%3BDolja%2C+Valerian+V&rft.aulast=Koonin&rft.aufirst=Eugene&rft.date=2014-06-01&rft.volume=78&rft.issue=2&rft.spage=278&rft.isbn=&rft.btitle=&rft.title=Microbiology+and+Molecular+Biology+Reviews&rft.issn=10922172&rft_id=info:doi/10.1128%2FMMBR.00049-13 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 202 N1 - Last updated - 2016-09-14 N1 - SubjectsTermNotLitGenreText - Evolution DO - http://dx.doi.org/10.1128/MMBR.00049-13 ER - TY - JOUR T1 - Central nervous system norcardiosis with granulomatous pachymeningitis and osteomyelitis of skull vault AN - 1722170056; PQ0002098617 AB - A 34-year-old immunocompetent man weighing 95 kg was operated for a small left parietal scalp swelling in the year 2002. He was well until 2008, when he developed chronic diffuse headache, vomiting and drowsiness. The left parietal dura and overlying vault biopsy showed evidence of granulomatous pachymeningitis with osteomyelitis secondary to nocardiosis. He had responded well to inadequate antibiotic therapy. After a dormant period of 3 years, there was recrudescence of severe raised intracranial tension symptoms in 2011. Magnetic resonance imaging showed diffuse pachymeningeal thickening mainly involving the occipital dura, posterior falx, and tentorium cerebelli. In addition, well-defined small nodules with hypointense signals on both Tl- and T2-weighted images were seen in occipital lobes. Patient was treated with three drug regime with good recovery at 3 months follow-up. This is a rare case of central nervous system nocardiosis with skull vault osteomyelitis and a protracted clinical course. JF - Indian Journal of Pathology and Microbiology AU - Nalini, Atchayaram AU - Saini, Jitender AU - Mahadevan, Anita AD - Department of Neurology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 332 EP - 334 PB - Medknow Publications and Media Pvt. Ltd., B-9, Kanara Business Ctr, Off Link Rd, Ghatkopar (E) Mumbai, Maharastra 400 075 India VL - 57 IS - 2 SN - 0377-4929, 0377-4929 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Calcium & Calcified Tissue Abstracts; CSA Neurosciences Abstracts KW - Central nervous system KW - Nocardiosis KW - Vomiting KW - Scalp KW - Magnetic resonance imaging KW - Antibiotics KW - Drowsiness KW - Biopsy KW - Nodules KW - Skull KW - Headache KW - Occipital lobe KW - Drugs KW - Osteomyelitis KW - N3 11027:Neurology & neuropathology KW - T 2025:Bone and Bone Diseases KW - A 01400:Soil Microbes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722170056?accountid=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=Indian+Journal+of+Pathology+and+Microbiology&rft.atitle=Central+nervous+system+norcardiosis+with+granulomatous+pachymeningitis+and+osteomyelitis+of+skull+vault&rft.au=Nalini%2C+Atchayaram%3BSaini%2C+Jitender%3BMahadevan%2C+Anita&rft.aulast=Nalini&rft.aufirst=Atchayaram&rft.date=2014-06-01&rft.volume=57&rft.issue=2&rft.spage=332&rft.isbn=&rft.btitle=&rft.title=Indian+Journal+of+Pathology+and+Microbiology&rft.issn=03774929&rft_id=info:doi/10.4103%2F0377-4929.134735 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Central nervous system; Vomiting; Nocardiosis; Scalp; Magnetic resonance imaging; Biopsy; Drowsiness; Antibiotics; Nodules; Skull; Headache; Occipital lobe; Drugs; Osteomyelitis DO - http://dx.doi.org/10.4103/0377-4929.134735 ER - TY - JOUR T1 - Modelling batched Gaussian longitudinal weight data in mice subject to informative dropout AN - 1683508521 AB - Modelling longitudinal data subject to informative dropout is an active area in statistical research. This article focuses on modelling such longitudinal data when the outcome at each follow-up time is collected in batches rather than individually collected. The problem occurred in a study that compared the weight of mice over time between a control and a treatment group, where animal weight was measured in batches of five animals per cage. We develop both a shared parameter and a pattern mixture modelling approach for accounting for potentially informative dropout due to an animalʼs death. Our methodology suggests that animals receiving the treatment have a lower weight in mid-life, and have a slower decline in weight in the later period of life. Our simulations suggest that both the shared random parameter and pattern mixture modelling approaches work well under a correctly specified model. However, the pattern mixture model is more robust against model misspecification than the shared random parameter model, but the shared random parameter model parameters have a more direct interpretation than those of the pattern mixture modelling approach. JF - Statistical Methods in Medical Research AU - Albert, Paul S AU - Shih, Joanna H AD - Biostatistics and Bioinformatics Branch, Division of Epidemiology, Statistics, and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA ; Biometrics Research Branch, Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD, USA ; Biostatistics and Bioinformatics Branch, Division of Epidemiology, Statistics, and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 203 EP - 217 CY - London PB - Sage Publications Ltd. VL - 23 IS - 3 SN - 0962-2802 KW - Medical Sciences KW - Missing data KW - pattern mixture models KW - repeated measures KW - shared random parameter models KW - Animals KW - Approaches KW - Death KW - Dropping out KW - Methodology KW - Modelling KW - Parameters KW - Weight UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683508521?accountid=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=Statistical+Methods+in+Medical+Research&rft.atitle=Modelling+batched+Gaussian+longitudinal+weight+data+in+mice+subject+to+informative+dropout&rft.au=Albert%2C+Paul+S%3BShih%2C+Joanna+H&rft.aulast=Albert&rft.aufirst=Paul&rft.date=2014-06-01&rft.volume=23&rft.issue=3&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Statistical+Methods+in+Medical+Research&rft.issn=09622802&rft_id=info:doi/10.1177%2F0962280210397886 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-05-12 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1177/0962280210397886 ER - TY - JOUR T1 - Mental Health of HIV-Seropositive Women During Pregnancy and Postpartum Period: A Comprehensive Literature Review AN - 1680149897; 201502965 AB - With growing numbers of HIV-seropositive (HIV+) women of child-bearing age and increased access to effective clinical protocols for preventing mother-to-child transmission (MTCT) of HIV, mental health-related factors have become increasingly relevant due to their potential to affect the women's quality of life, obstetric outcomes and risk of MTCT. This review synthesizes evidence from 53 peer-reviewed publications examining mental health-related variables in pregnant and postpartum HIV+ women. The presentation of results is organized by the level of socioeconomic resources in the countries where studies were conducted (i.e., high-, middle-, and low-income countries). It is concluded that psychiatric symptoms, particularly depression, and mental health vulnerabilities (e.g., inadequate coping skills) are widespread among pregnant HIV+ women globally and have a potential to affect psychological well-being, quality of life and salient clinical outcomes. The current body of evidence provides rationale for developing and evaluating clinical and structural interventions aimed at improving mental health outcomes and their clinical correlates in pregnant HIV+ women. Adapted from the source document. JF - AIDS and Behavior AU - Kapetanovic, Suad AU - Dass-Brailsford, Priscilla AU - Nora, Diana AU - Talisman, Nicholas AD - National Institutes of Health, National Institute of Mental Health, Bethesda, MD, USA suad.kapetanovic@nih.gov Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1152 EP - 1173 PB - Springer, Dordrecht, The Netherlands VL - 18 IS - 6 SN - 1090-7165, 1090-7165 KW - Treatment Outcomes KW - Depression (Psychology) KW - Well Being KW - Acquired Immune Deficiency Syndrome KW - Quality of Life KW - Mental Health KW - Females KW - Literature Reviews KW - Pregnancy KW - article KW - 6126: acquired immune deficiency syndrome (AIDS) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680149897?accountid=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=Mental+Health+of+HIV-Seropositive+Women+During+Pregnancy+and+Postpartum+Period%3A+A+Comprehensive+Literature+Review&rft.au=Kapetanovic%2C+Suad%3BDass-Brailsford%2C+Priscilla%3BNora%2C+Diana%3BTalisman%2C+Nicholas&rft.aulast=Kapetanovic&rft.aufirst=Suad&rft.date=2014-06-01&rft.volume=18&rft.issue=6&rft.spage=1152&rft.isbn=&rft.btitle=&rft.title=AIDS+and+Behavior&rft.issn=10907165&rft_id=info:doi/10.1007%2Fs10461-014-0728-9 LA - English DB - Social Services Abstracts N1 - Date revised - 2015-05-01 N1 - Number of references - 73 N1 - Last updated - 2016-09-28 N1 - CODEN - AIBEFC N1 - SubjectsTermNotLitGenreText - Females; Acquired Immune Deficiency Syndrome; Pregnancy; Treatment Outcomes; Quality of Life; Depression (Psychology); Well Being; Mental Health; Literature Reviews DO - http://dx.doi.org/10.1007/s10461-014-0728-9 ER - TY - JOUR T1 - Challenges in diagnosing a metabolic disorder: error of pyruvate metabolism or drug induced? AN - 1671215324; 23439713 AB - Certain drugs are known to cause metabolic changes resulting in altered metabolic profiles. We report here a case where a combination of antiepileptic drugs resulted in a profile that mimicked a metabolic disorder. A 16month-old female child on antiepileptic drugs (valproate and topiramate) was suspected to have the inherited metabolic disorder, dihydrolipoamide dehydrogenase deficiency, based on clinical symptoms and metabolic profile showing hyperalaninemia, elevated branched-chain amino acids, and lactate-pyruvate ratio. Suspecting that the observed metabolic changes could have also arised from medication, current medication was weaned off and replaced with levetiracetam, clonazepam, and levocarnitine (supportive therapy). Metabolic profiling conducted after 47 days showed normal alanine, branched-chain amino acids, ornithine, and lactate-pyruvate ratio, suggesting that the earlier abnormalities could have been medication induced. We stress that metabolic changes resulting from chronic medication should be considered while interpreting a positive result when investigating an inherited metabolic disorder. © The Author(s) 2013. JF - Journal of child neurology AU - Mampilly, George Tomy AU - Mampilly, Tomy Kochuvareed AU - Christopher, Rita AU - Chandramohan, Neeradha AU - Janaki, Vijayalakshmy AD - Department of Physical Medicine and Rehabilitation, National Institute for Empowerment of Persons with Multiple Disabilities, Muttukadu, Chennai, India. ; Department of Physical Medicine and Rehabilitation, National Institute for Empowerment of Persons with Multiple Disabilities, Muttukadu, Chennai, India tomymampilly@gmail.com. ; Department of Neurochemistry, National Institute of Mental Health and Neurosciences, Bangalore, India. ; Department of Clinical Psychology, National Institute for Empowerment of Persons with Multiple Disabilities, Muttukadu, Chennai, India. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 833 EP - 836 VL - 29 IS - 6 KW - Anticonvulsants KW - 0 KW - topiramate KW - 0H73WJJ391 KW - Fructose KW - 30237-26-4 KW - Valproic Acid KW - 614OI1Z5WI KW - Pyruvic Acid KW - 8558G7RUTR KW - Index Medicus KW - valproate KW - metabolic disorder KW - false positives KW - Infant KW - Fructose -- analogs & derivatives KW - Humans KW - Fructose -- adverse effects KW - Valproic Acid -- adverse effects KW - Female KW - Metabolic Diseases -- chemically induced KW - Anticonvulsants -- adverse effects KW - Pyruvic Acid -- metabolism KW - Metabolic Diseases -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1671215324?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+child+neurology&rft.atitle=Challenges+in+diagnosing+a+metabolic+disorder%3A+error+of+pyruvate+metabolism+or+drug+induced%3F&rft.au=Mampilly%2C+George+Tomy%3BMampilly%2C+Tomy+Kochuvareed%3BChristopher%2C+Rita%3BChandramohan%2C+Neeradha%3BJanaki%2C+Vijayalakshmy&rft.aulast=Mampilly&rft.aufirst=George&rft.date=2014-06-01&rft.volume=29&rft.issue=6&rft.spage=833&rft.isbn=&rft.btitle=&rft.title=Journal+of+child+neurology&rft.issn=1708-8283&rft_id=info:doi/10.1177%2F0883073813477201 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-02 N1 - Date created - 2015-04-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1177/0883073813477201 ER - TY - JOUR T1 - Infectivity of urogenital Chlamydia trachomatis plasmid-deficient, CT135-null, and double-deficient strains in female mice AN - 1654666334; 21296995 AB - Chlamydia trachomatis is the most common cause of human bacterial sexually transmitted infections and is the world's leading cause of infectious preventable blindness. The chlamydial 7.5-kb plasmid and chromosomal gene CT135 have been shown to be important virulence factors in both nonhuman primate and mouse infection models. Chlamydia trachomatis plasmid-deficient urogenital isolates and a predicted CT135 null mutant have been evaluated independently in the female mouse genital tract model and both have been shown to reduce infectivity and virulence. However, these attenuating phenotypes have not been evaluated collectively in the murine model. Here, we test the infectivity of C. trachomatis serovar D strains in the mouse model that are plasmid-deficient, CT135 disrupted, or possess a combination of these attenuating genotypes. We find that the presence of the plasmid results in infections with higher infectious burdens, whereas CT135 facilitates a more protracted or chronic infection. Not unexpectedly, a combination of these genetic deficiencies resulted in a strain with enhanced infection attenuation characteristics. A composite figure showing scanning (left) and transmission (right-center) electron photomicrographs of Chlamydia trachomatis infected epithelial cells. The biosynthesis of glycogen (gold granules among blue developmental forms) is dependent on the chlamydial plasmid which is thought to be an important virulence factor. JF - Pathogens and Disease AU - Sturdevant, Gail L AU - Zhou, Bing AU - Carlson, John H AU - Whitmire, William M AU - Song, Lihua AU - Caldwell, Harlan D AD - Laboratory of Intracellular Parasites, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA. Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 90 EP - 92 PB - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801 England VL - 71 IS - 1 SN - 2049-632X, 2049-632X KW - Microbiology Abstracts B: Bacteriology KW - Granules KW - Epithelial cells KW - virulence factors KW - Animal models KW - Chlamydia trachomatis KW - Genotypes KW - Blindness KW - Pathogens KW - Plasmids KW - Glycogen KW - Infectivity KW - Scanning KW - Chronic infection KW - Gold KW - Genital tract KW - J 02410:Animal Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654666334?accountid=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=Pathogens+and+Disease&rft.atitle=Infectivity+of+urogenital+Chlamydia+trachomatis+plasmid-deficient%2C+CT135-null%2C+and+double-deficient+strains+in+female+mice&rft.au=Sturdevant%2C+Gail+L%3BZhou%2C+Bing%3BCarlson%2C+John+H%3BWhitmire%2C+William+M%3BSong%2C+Lihua%3BCaldwell%2C+Harlan+D&rft.aulast=Sturdevant&rft.aufirst=Gail&rft.date=2014-06-01&rft.volume=71&rft.issue=1&rft.spage=90&rft.isbn=&rft.btitle=&rft.title=Pathogens+and+Disease&rft.issn=2049632X&rft_id=info:doi/10.1111%2F2049-632X.12121 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Granules; Epithelial cells; virulence factors; Animal models; Pathogens; Blindness; Genotypes; Plasmids; Glycogen; Infectivity; Scanning; Chronic infection; Gold; Genital tract; Chlamydia trachomatis DO - http://dx.doi.org/10.1111/2049-632X.12121 ER - TY - JOUR T1 - Regional Variation in the Correlation of Antibody and T-Cell Responses to Trypanosoma cruzi AN - 1647022865; 21189927 AB - Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, is a major cause of morbidity and mortality in Central and South America. Geographic variations in the sensitivity of serologic diagnostic assays to T. cruzi may reflect differences in T. cruzi exposure. We measured parasite-specific T-cell responses among seropositive individuals in two populations from South America with widely varying antibody titers against T. cruzi. Antibody titers among seropositive individuals were significantly lower in Arequipa, Peru compared with Santa Cruz, Bolivia. Similarly, the proportion of seropositive individuals with positive T-cell responses was lower in Peru than Bolivia, resulting in overall lower frequencies of interferon- gamma (IFN gamma )-secreting cells from Peruvian samples. However, the magnitude of the IFN gamma response was similar among the IFN gamma responders in both locations. These data indicate that immunological discrepancies based on geographic region are reflected in T-cell responses as well as antibody responses. JF - American Journal of Tropical Medicine and Hygiene AU - Martin, Diana L AU - Marks, Morgan AU - Galdos-Cardenas, Gerson AU - Gilman, Robert H AU - Goodhew, Brook AU - Ferrufino, Lisbeth AU - Halperin, Anthony AU - Sanchez, Gerardo AU - Verastegui, Manuela AU - Escalante, Patricia AU - Naquira, Cesar AU - Levy, Michael Z AU - Bern, Caryn AD - National Institutes of Health, Bethesda, Maryland; Hospital Universitario Japones, Santa Cruz, Bolivia; Asociacion Benefica PRISMA, Lima, Peru; Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland; Arequipa Ministry of Health, Arequipa, Peru; University of Pennsylvania, Philadelphia, Pennsylvania; Universidad Peruana Cayetano Heredia, Lima, Peru; Division of Parasitic Diseases and Malaria, MS D-65, 1600 Clifton Road NE, Centers for Disease Control and Prevention, Atlanta, GA 30329, hz3@cdc.gov Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1074 EP - 1081 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 90 IS - 6 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality KW - Trypanosoma cruzi KW - gamma -Interferon KW - Mortality KW - Parasites KW - Data processing KW - Morbidity KW - Bolivia KW - Public health KW - Antibodies KW - Lymphocytes T KW - Peru KW - Geographical variations KW - Hygiene KW - Regional variations KW - Mortality causes KW - Chagas' disease KW - K 03350:Immunology KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08502:Methods and instruments KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647022865?accountid=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=Regional+Variation+in+the+Correlation+of+Antibody+and+T-Cell+Responses+to+Trypanosoma+cruzi&rft.au=Martin%2C+Diana+L%3BMarks%2C+Morgan%3BGaldos-Cardenas%2C+Gerson%3BGilman%2C+Robert+H%3BGoodhew%2C+Brook%3BFerrufino%2C+Lisbeth%3BHalperin%2C+Anthony%3BSanchez%2C+Gerardo%3BVerastegui%2C+Manuela%3BEscalante%2C+Patricia%3BNaquira%2C+Cesar%3BLevy%2C+Michael+Z%3BBern%2C+Caryn&rft.aulast=Martin&rft.aufirst=Diana&rft.date=2014-06-01&rft.volume=90&rft.issue=6&rft.spage=1074&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0391 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Parasites; Antibodies; Hygiene; Regional variations; Mortality causes; Public health; Mortality; gamma -Interferon; Data processing; Lymphocytes T; Geographical variations; Morbidity; Chagas' disease; Trypanosoma cruzi; Peru; Bolivia DO - http://dx.doi.org/10.4269/ajtmh.13-0391 ER - TY - JOUR T1 - Mitigating the risk of radiation-induced cancers: limitations and paradigms in drug development AN - 1642619725; 21099727 AB - The United States radiation medical countermeasures (MCM) programme for radiological and nuclear incidents has been focusing on developing mitigators for the acute radiation syndrome (ARS) and delayed effects of acute radiation exposure (DEARE), and biodosimetry technologies to provide radiation dose assessments for guiding treatment. Because a nuclear accident or terrorist incident could potentially expose a large number of people to low to moderate doses of ionising radiation, and thus increase their excess lifetime cancer risk, there is an interest in developing mitigators for this purpose. This article discusses the current status, issues, and challenges regarding development of mitigators against radiation-induced cancers. The challenges of developing mitigators for ARS include: the long latency between exposure and cancer manifestation, limitations of animal models, potential side effects of the mitigator itself, potential need for long-term use, the complexity of human trials to demonstrate effectiveness, and statistical power constraints for measuring health risks (and reduction of health risks after mitigation) following relatively low radiation doses (<0:75 Gy). Nevertheless, progress in the understanding of the molecular mechanisms resulting in radiation injury, along with parallel progress in dose assessment technologies, make this an opportune, if not critical, time to invest in research strategies that result in the development of agents to lower the risk of radiation-induced cancers for populations that survive a significant radiation exposure incident. JF - Journal of Radiological Protection AU - Yoo, Stephen S AU - Jorgensen, Timothy J AU - Kennedy, Ann R AU - Boice, John D, Jr AU - Shapiro, Alla AU - Hu, Tom C-C AU - Moyer, Brian R AU - Grace, Marcy B AU - Kelloff, Gary J AU - Fenech, Michael AU - Prasanna, Pataje GS AU - Coleman, C Norman AD - Radiation Research Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, ccoleman@mail.nih.gov Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - R25 EP - r52 PB - IOP Publishing, The Public Ledger Building, Suite 929 Philadelphia PA 19106 United States VL - 34 IS - 2 SN - 0952-4746, 0952-4746 KW - Risk Abstracts; Health & Safety Science Abstracts KW - radiation-induced cancer KW - radiation mitigator KW - radioprotector KW - radiation risk KW - Risk assessment KW - Mitigation KW - Terrorism KW - Injuries KW - Animal models KW - Cancer KW - Health risks KW - USA KW - Accidents KW - Radiation KW - Ionizing radiation KW - Drugs KW - Research programs KW - Side effects KW - Technology 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/1642619725?accountid=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=Mitigating+the+risk+of+radiation-induced+cancers%3A+limitations+and+paradigms+in+drug+development&rft.au=Yoo%2C+Stephen+S%3BJorgensen%2C+Timothy+J%3BKennedy%2C+Ann+R%3BBoice%2C+John+D%2C+Jr%3BShapiro%2C+Alla%3BHu%2C+Tom+C-C%3BMoyer%2C+Brian+R%3BGrace%2C+Marcy+B%3BKelloff%2C+Gary+J%3BFenech%2C+Michael%3BPrasanna%2C+Pataje+GS%3BColeman%2C+C+Norman&rft.aulast=Yoo&rft.aufirst=Stephen&rft.date=2014-06-01&rft.volume=34&rft.issue=2&rft.spage=R25&rft.isbn=&rft.btitle=&rft.title=Journal+of+Radiological+Protection&rft.issn=09524746&rft_id=info:doi/10.1088%2F0952-4746%2F34%2F2%2FR25 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-04-16 N1 - SubjectsTermNotLitGenreText - Risk assessment; Mitigation; Terrorism; Injuries; Animal models; Cancer; Health risks; Accidents; Radiation; Ionizing radiation; Drugs; Side effects; Research programs; Technology; USA DO - http://dx.doi.org/10.1088/0952-4746/34/2/R25 ER - TY - JOUR T1 - Expanding rare disease drug trials based on shared molecular etiology AN - 1554953467; 20508042 JF - Nature Biotechnology AU - Brooks, Philip J AU - Tagle, Danilo A AU - Groft, Steve AD - Office of Rare Diseases Research, National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 515 EP - 518 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 32 IS - 6 SN - 1087-0156, 1087-0156 KW - Biotechnology and Bioengineering Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1554953467?accountid=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=Nature+Biotechnology&rft.atitle=Expanding+rare+disease+drug+trials+based+on+shared+molecular+etiology&rft.au=Brooks%2C+Philip+J%3BTagle%2C+Danilo+A%3BGroft%2C+Steve&rft.aulast=Brooks&rft.aufirst=Philip&rft.date=2014-06-01&rft.volume=32&rft.issue=6&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=Nature+Biotechnology&rft.issn=10870156&rft_id=info:doi/10.1038%2Fnbt.2924 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-08-21 DO - http://dx.doi.org/10.1038/nbt.2924 ER - TY - JOUR T1 - Receiving and Adhering to Lifestyle Modification Counseling for Hypertension: Disparities Between Smokers and Nonsmokers AN - 1547864626; 20167163 AB - Hypertensive patients who smoke are in particular need of lifestyle modification counseling because they are at increased risk for poorer outcomes. The authors examined whether hypertensive smokers were more or less likely than nonsmokers to report receiving recommendations for diet, salt intake, exercise, alcohol use, and medication and whether receipt of recommendations was differentially associated with lifestyle changes among smokers vs nonsmokers. In an analysis of data from the 2011 Behavioral Risk Factor Surveillance System on a representative sample of hypertensive adults from 9 US states (N=23,093), smokers were less likely than nonsmokers to report being told by a provider to exercise (odds ratio [OR], 0.66; P<.001) and change their diet (OR, 0.83; P<.05). Receiving dietary recommendations was more strongly associated with self-reported dietary improvements among smokers (OR, 7.08; P<.001) compared with nonsmokers (OR, 4.17; P<.001) P<.01. Delivery of counseling may vary by smoking status. When provided, lifestyle counseling may be equally or more effective for smokers compared with nonsmokers. JF - Journal of Clinical Hypertension AU - Persoskie, Alexander AU - Kaufman, Annette R AU - Leyva, Bryan AD - Basic Biobehavioral and Psychological Sciences Branch. National Cancer Institute Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 429 EP - 436 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 16 IS - 6 SN - 1524-6175, 1524-6175 KW - Risk Abstracts KW - Diets KW - Salts KW - Smoking KW - Alcohol KW - Risk factors KW - Drugs KW - Hypertension KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547864626?accountid=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+Clinical+Hypertension&rft.atitle=Receiving+and+Adhering+to+Lifestyle+Modification+Counseling+for+Hypertension%3A+Disparities+Between+Smokers+and+Nonsmokers&rft.au=Persoskie%2C+Alexander%3BKaufman%2C+Annette+R%3BLeyva%2C+Bryan&rft.aulast=Persoskie&rft.aufirst=Alexander&rft.date=2014-06-01&rft.volume=16&rft.issue=6&rft.spage=429&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Hypertension&rft.issn=15246175&rft_id=info:doi/10.1111%2Fjch.12314 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-07-01 N1 - Last updated - 2014-08-07 N1 - SubjectsTermNotLitGenreText - Diets; Alcohol; Smoking; Salts; Risk factors; Drugs; Hypertension DO - http://dx.doi.org/10.1111/jch.12314 ER - TY - JOUR T1 - Class probability estimation for medical studies AN - 1547848057; 20215403 AB - I provide a commentary on two papers "Probability estimation with machine learning methods for dichotomous and multicategory outcome: Theory" by Jochen Kruppa, Yufeng Liu, Gerard Biau, Michael Kohler, Inke R. Konig, James D. Malley, and Andreas Ziegler; and "Probability estimation with machine learning methods for dichotomous and multicategory outcome: Applications" by Jochen Kruppa, Yufeng Liu, Hans-Christian Diener, Theresa Holste, Christian Weimar, Inke R. Konig, and Andreas Ziegler. Those papers provide an up-to-date review of some popular machine learning methods for class probability estimation and compare those methods to logistic regression modeling in real and simulated datasets. JF - Biometrical Journal AU - Simon, Richard AD - Biometric Research Branch, National Cancer Institute, 9609 Medical Park Drive, Rockville, MD, 20892-9735, USA. Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 597 EP - 600 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 56 IS - 4 SN - 0323-3847, 0323-3847 KW - Biotechnology and Bioengineering Abstracts KW - Statistics KW - Reviews KW - Learning algorithms KW - Biometrics KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1547848057?accountid=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=Class+probability+estimation+for+medical+studies&rft.au=Simon%2C+Richard&rft.aulast=Simon&rft.aufirst=Richard&rft.date=2014-06-01&rft.volume=56&rft.issue=4&rft.spage=597&rft.isbn=&rft.btitle=&rft.title=Biometrical+Journal&rft.issn=03233847&rft_id=info:doi/10.1002%2Fbimj.201300296 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-07-01 N1 - Last updated - 2014-08-21 N1 - SubjectsTermNotLitGenreText - Statistics; Reviews; Biometrics; Learning algorithms DO - http://dx.doi.org/10.1002/bimj.201300296 ER - TY - JOUR T1 - Discovery of mesothelin and exploiting it as a target for immunotherapy. AN - 1543995528; 24824231 AB - We have recently reported that an immunotoxin targeting mesothelin produced durable major tumor regressions in patients with extensive treatment-refractory mesothelioma. These unprecedented tumor responses have prompted us to review how mesothelin was discovered and the advances that led to these tumor responses. This review is not comprehensive but focuses on major developments over the past 20 years since mesothelin was first identified in our laboratory. Mesothelin is a cell-surface glycoprotein whose expression in normal human tissues is restricted to mesothelial cells. Because it is highly expressed by many solid tumors, it is an attractive immunotherapy target. Antibody-based therapies currently in clinical trials include an immunotoxin, a chimeric monoclonal antibody, and an antibody drug conjugate. In addition, a mesothelin tumor vaccine and a mesothelin- chimeric antigen receptor are being evaluated in the clinic. SS1P, an anti-mesothelin immunotoxin, was the first mesothelin-directed therapy to enter the clinic, and its use showed that mesothelin-targeted therapy was safe in patients. More importantly, our recent work has shown that SS1P in combination with pentostatin and cyclophosphamide can result in durable tumor regression in patients with advanced mesothelioma and opens up the possibility that such an approach can benefit patients with many common cancers. ©2014 American Association for Cancer Research. JF - Cancer research AU - Pastan, Ira AU - Hassan, Raffit AD - Authors' Affiliation: Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland pastani@mail.nih.gov hassanr@mail.nih.gov. Y1 - 2014/06/01/ PY - 2014 DA - 2014 Jun 01 SP - 2907 EP - 2912 VL - 74 IS - 11 KW - Antibodies, Monoclonal KW - 0 KW - Cancer Vaccines KW - GPI-Linked Proteins KW - Immunotoxins KW - Membrane Glycoproteins KW - mesothelin KW - Index Medicus KW - Animals KW - Humans KW - Molecular Targeted Therapy KW - Cancer Vaccines -- therapeutic use KW - Clinical Trials as Topic KW - Antibodies, Monoclonal -- immunology KW - Antibodies, Monoclonal -- therapeutic use KW - Immunotherapy -- methods KW - Cancer Vaccines -- immunology KW - Immunotoxins -- immunology KW - Immunotoxins -- therapeutic use KW - Drug Evaluation, Preclinical KW - Membrane Glycoproteins -- immunology KW - Membrane Glycoproteins -- metabolism KW - GPI-Linked Proteins -- metabolism KW - GPI-Linked Proteins -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1543995528?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Discovery+of+mesothelin+and+exploiting+it+as+a+target+for+immunotherapy.&rft.au=Pastan%2C+Ira%3BHassan%2C+Raffit&rft.aulast=Pastan&rft.aufirst=Ira&rft.date=2014-06-01&rft.volume=74&rft.issue=11&rft.spage=2907&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-0337 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-28 N1 - Date created - 2014-06-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cell Biol. 2000 Apr;20(8):2902-6 [10733593] Cancer Immunol Res. 2014 Feb;2(2):112-20 [24579088] Clin Cancer Res. 2001 Dec;7(12):3862-8 [11751476] Am J Surg Pathol. 2003 Nov;27(11):1418-28 [14576474] Lancet. 2003 Nov 15;362(9396):1612-6 [14630441] Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):16-8 [14734446] J Biol Chem. 2004 Mar 5;279(10):9190-8 [14676194] J Biol Response Mod. 1990 Aug;9(4):345-54 [2395000] Int J Cancer. 1992 Feb 1;50(3):373-81 [1735605] Am J Surg Pathol. 1992 Mar;16(3):259-68 [1599018] Int J Cancer. 1992 Jun 19;51(4):548-54 [1351045] J Immunother Emphasis Tumor Immunol. 1993 Apr;13(3):201-7 [8471594] J Biol Chem. 1994 Jan 14;269(2):805-8 [8288629] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):136-40 [8552591] Proc Natl Acad Sci U S A. 1998 Jan 20;95(2):669-74 [9435250] Int J Cancer. 1999 Feb 9;80(4):559-63 [9935157] Nat Biotechnol. 1999 Jun;17(6):568-72 [10385321] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11531-6 [10500211] Am J Clin Pathol. 2005 Dec;124(6):838-45 [16416732] Clin Cancer Res. 2006 Jan 15;12(2):447-53 [16428485] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638] Clin Cancer Res. 2006 Jul 15;12(14 Pt 1):4225-31 [16857795] Clin Cancer Res. 2006 Aug 1;12(15):4695-701 [16899620] Cancer Epidemiol Biomarkers Prev. 2006 Sep;15(9):1751 [16985043] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569] Cancer Immun. 2007;7:20 [18088084] Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873] Lung Cancer. 2010 Jun;68(3):455-9 [19744744] Int J Mol Med. 2010 Aug;26(2):185-91 [20596597] Clin Cancer Res. 2010 Dec 15;16(24):6132-8 [21037025] J Biol Chem. 2011 Apr 8;286(14):11960-9 [21288909] Clin Cancer Res. 2011 Jun 1;17(11):3697-705 [21521777] Cancer Res. 2011 Sep 1;71(17):5915-22 [21775520] Clin Cancer Res. 2012 Feb 1;18(3):858-68 [22147941] Clin Chem Lab Med. 2012 Apr;50(4):721-5 [22149739] Breast Cancer Res Treat. 2012 Jun;133(2):799-804 [22418702] Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11782-7 [22753489] Anticancer Res. 2012 Dec;32(12):5151-8 [23225411] Proc Natl Acad Sci U S A. 2012 Dec 18;109(51):E3597-603 [23213206] J Exp Clin Cancer Res. 2012;31:84 [23034174] Sci Transl Med. 2013 Oct 23;5(208):208ra147 [24154601] Clin Cancer Res. 2014 Feb 15;20(4):1020-8 [24334761] J Immunother. 2000 Jul-Aug;23(4):473-9 [10916757] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-0337 ER - TY - JOUR T1 - Fronto-limbic-striatal dysfunction in pediatric and adult patients with bipolar disorder: impact of face emotion and attentional demands AN - 1541979861; 201415508 AB - Research in bipolar disorder (BD) implicates fronto-limbic-striatal dysfunction during face emotion processing but it is unknown how such dysfunction varies by task demands, face emotion and patient age. During functional magnetic resonance imaging (fMRI), 181 participants, including 62 BD (36 children and 26 adults) and 119 healthy comparison (HC) subjects (57 children and 62 adults), engaged in constrained and unconstrained processing of emotional (angry, fearful, happy) and non-emotional (neutral) faces. During constrained processing, subjects answered questions focusing their attention on the face; this was processed either implicitly (nose width rating) or explicitly (hostility; subjective fear ratings). Unconstrained processing consisted of passive viewing. Pediatric BD rated neutral faces as more hostile than did other groups. In BD patients, family-wise error (FWE)-corrected region of interest (ROI) analyses revealed dysfunction in the amygdala, inferior frontal gyrus (IFG), anterior cingulate cortex (ACC) and putamen. Patients with BD showed amygdala hyperactivation during explicit processing (hostility ratings) of fearful faces and passive viewing of angry and neutral faces but IFG hypoactivation during implicit processing of neutral and happy faces. In the ACC and striatum, the direction of dysfunction varied by task demand: BD demonstrated hyperactivation during unconstrained processing of angry or neutral faces but hypoactivation during constrained processing (implicit or explicit) of angry, neutral or happy faces. Findings suggest amygdala hyperactivation in BD while processing negatively valenced and neutral faces, regardless of attentional condition, and BD IFG hypoactivation during implicit processing. In the cognitive control circuit involving the ACC and putamen, BD neural dysfunction was sensitive to task demands. Adapted from the source document. JF - Psychological Medicine AU - Brotman, M A AU - Tseng, W.-L. AU - Olsavsky, A K AU - Fromm, S J AU - Muhrer, E J AU - Rutenberg, J G AU - Deveney, C M AU - Adleman, N E AU - Zarate, C A AU - Pine, D S AU - Leibenluft, E AD - Emotion and Development Branch, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA brotmanm@mail.nih.gov Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1639 EP - 1651 PB - Cambridge University Press, UK VL - 44 IS - 8 SN - 0033-2917, 0033-2917 KW - Paediatrics KW - Emotions KW - Hostility KW - Facial expressions KW - Dysfunction KW - Anger KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541979861?accountid=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=Fronto-limbic-striatal+dysfunction+in+pediatric+and+adult+patients+with+bipolar+disorder%3A+impact+of+face+emotion+and+attentional+demands&rft.au=Brotman%2C+M+A%3BTseng%2C+W.-L.%3BOlsavsky%2C+A+K%3BFromm%2C+S+J%3BMuhrer%2C+E+J%3BRutenberg%2C+J+G%3BDeveney%2C+C+M%3BAdleman%2C+N+E%3BZarate%2C+C+A%3BPine%2C+D+S%3BLeibenluft%2C+E&rft.aulast=Brotman&rft.aufirst=M&rft.date=2014-06-01&rft.volume=44&rft.issue=8&rft.spage=1639&rft.isbn=&rft.btitle=&rft.title=Psychological+Medicine&rft.issn=00332917&rft_id=info:doi/10.1017%2FS003329171300202X LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-07-01 N1 - Number of references - 77 N1 - Last updated - 2016-09-27 N1 - CODEN - PSMDCO N1 - SubjectsTermNotLitGenreText - Dysfunction; Facial expressions; Anger; Emotions; Paediatrics; Hostility DO - http://dx.doi.org/10.1017/S003329171300202X ER - TY - JOUR T1 - Association Between Informal Caregiving and Cellular Aging in the Survey of the Health of Wisconsin: The Role of Caregiving Characteristics, Stress, and Strain AN - 1540232223; 20082649 AB - The pathophysiological consequences of caregiving have not been fully elucidated. We evaluated how caregiving, stress, and caregiver strain were associated with shorter relative telomere length (RTL), a marker of cellular aging. Caregivers (n = 240) and some noncaregivers (n = 98) in the 2008-2010 Survey of the Health of Wisconsin, comprising a representative sample of Wisconsin adults aged 21-74 years, reported their sociodemographic, health, and psychological characteristics. RTL was assayed from blood or saliva samples. Median T and S values were used to determine the telomere-to-single copy gene ratio (T/S) for each sample, and log(T/S) was used as the dependent variable in analyses. Multivariable generalized additive models showed that RTL did not differ between caregivers and noncaregivers (difference in log(T/S) = -0.03; P > 0.05), but moderate-to-high levels of stress versus low stress were associated with longer RTL (difference = 0.15; P = 0.04). Among caregivers, more hours per week of care, caring for a young person, and greater strain were associated with shorter RTL (P < 0.05). Caregivers with discordant levels of stress and strain (i.e., low perceived stress/high strain) compared with low stress/low strain had the shortest RTL (difference = -0.24; P = 0.02, P sub(interaction) = 0.13), corresponding to approximately 10-15 additional years of aging. Caregivers with these characteristics may be at increased risk for accelerated aging. Future work is necessary to better elucidate these relationships and develop interventions to improve the long-term health and well-being of caregivers. JF - American Journal of Epidemiology AU - Litzelman, Kristin AU - Witt, Whitney P AU - Gangnon, Ronald E AU - Nieto, F Javier AU - Engelman, Corinne D AU - Mailick, Marsha R AU - Skinner, Halcyon G AD - Correspondence to Dr. Kristin Litzelman, National Cancer Institute, 9609 Medical Center Drive, MSC 9761, Room 3E620, Bethesda, MD 20892-9761,; kristin.litzelman@gmail.com] kristin.litzelman@nih.gov Y1 - 2014/06/01/ PY - 2014 DA - 2014 Jun 01 SP - 1340 EP - 1352 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 179 IS - 11 SN - 0002-9262, 0002-9262 KW - Health & Safety Science Abstracts; Risk Abstracts KW - caregivers KW - caregiver strain KW - population-based studies KW - stress, psychological KW - Survey of the Health of Wisconsin KW - Psychology KW - Perception KW - Aging KW - Stress KW - Intervention KW - USA, Wisconsin 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/1540232223?accountid=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=Association+Between+Informal+Caregiving+and+Cellular+Aging+in+the+Survey+of+the+Health+of+Wisconsin%3A+The+Role+of+Caregiving+Characteristics%2C+Stress%2C+and+Strain&rft.au=Litzelman%2C+Kristin%3BWitt%2C+Whitney+P%3BGangnon%2C+Ronald+E%3BNieto%2C+F+Javier%3BEngelman%2C+Corinne+D%3BMailick%2C+Marsha+R%3BSkinner%2C+Halcyon+G&rft.aulast=Litzelman&rft.aufirst=Kristin&rft.date=2014-06-01&rft.volume=179&rft.issue=11&rft.spage=1340&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu066 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Perception; Psychology; Aging; Intervention; Stress; USA, Wisconsin DO - http://dx.doi.org/10.1093/aje/kwu066 ER - TY - JOUR T1 - The Francisella O-antigen mediates survival in the macrophage cytosol via autophagy avoidance AN - 1540221968; 19971649 AB - Autophagy is a key innate immune response to intracellular parasites that promotes their delivery to degradative lysosomes following detection in the cytosol or within damaged vacuoles. Like Listeria and Shigella, which use specific mechanisms to avoid autophagic detection and capture, the bacterial pathogen Francisella tularensis proliferates within the cytosol of macrophages without demonstrable control by autophagy. To examine how Francisella evades autophagy, we screened a library of F. tularensis subsp. tularensisSchu S4 HimarFT transposon mutants in GFP-LC3-expressing murine macrophages by microscopy for clones localized within autophagic vacuoles after phagosomal escape. Eleven clones showed autophagic capture at 6 h post-infection, whose HimarFT insertions clustered to fourgenetic loci involved in lipopolysaccharidic and capsular O-antigen biosynthesis. Consistent with the HimarFT mutants, in-frame deletion mutants of two representative loci, FTT1236 and FTT1448c (manC), lacking both LPS and capsular O-antigen, underwent phagosomal escape but were cleared from the host cytosol. Unlike wild-type Francisella, the O-antigen deletion mutants were ubiquitinated, and recruited the autophagy adaptor p62/SQSTM1 and LC3 prior to cytosolic clearance. Autophagy-deficient macrophages partially supported replication of both mutants, indicating that O-antigen-lacking Francisella are controlled by autophagy. These data demonstrate the intracellular protective role of this bacterial surface polysaccharide against autophagy. JF - Cellular Microbiology AU - Case, Elizabeth Di Russo AU - Chong, Audrey AU - Wehrly, Tara D AU - Hansen, Bryan AU - Child, Robert AU - Hwang, Seungmin AU - Virgin, Herbert W AU - Celli, Jean AD - Laboratory of Intracellular Parasites Rocky Mountain Laboratories. National Institute of Allergy and Infectious Diseases, National Institutes of Health Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 862 EP - 877 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 16 IS - 6 SN - 1462-5814, 1462-5814 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts B: Bacteriology KW - Cell survival KW - Macrophages KW - Parasites KW - Avoidance reactions KW - Survival KW - Polysaccharides KW - Defence mechanisms KW - Listeria KW - Transposons KW - Lipopolysaccharides KW - Phagocytosis KW - Clones KW - Data processing KW - Deletion mutant KW - Replication KW - Francisella tularensis KW - Shigella KW - Pathogens KW - Insertion KW - Microscopy KW - Vacuoles KW - Microbiology KW - Cytosol KW - Immune response KW - Lysosomes KW - Q1 08484:Species interactions: parasites and diseases KW - J 02350:Immunology KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1540221968?accountid=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=The+Francisella+O-antigen+mediates+survival+in+the+macrophage+cytosol+via+autophagy+avoidance&rft.au=Case%2C+Elizabeth+Di+Russo%3BChong%2C+Audrey%3BWehrly%2C+Tara+D%3BHansen%2C+Bryan%3BChild%2C+Robert%3BHwang%2C+Seungmin%3BVirgin%2C+Herbert+W%3BCelli%2C+Jean&rft.aulast=Case&rft.aufirst=Elizabeth+Di&rft.date=2014-06-01&rft.volume=16&rft.issue=6&rft.spage=862&rft.isbn=&rft.btitle=&rft.title=Cellular+Microbiology&rft.issn=14625814&rft_id=info:doi/10.1111%2Fcmi.12246 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2015-06-26 N1 - SubjectsTermNotLitGenreText - Clones; Macrophages; Replication; Microbiology; Survival; Avoidance reactions; Pathogens; Defence mechanisms; Lysosomes; Cell survival; Parasites; Deletion mutant; Data processing; Polysaccharides; Transposons; Insertion; Vacuoles; Microscopy; Cytosol; Lipopolysaccharides; Immune response; Phagocytosis; Shigella; Francisella tularensis; Listeria DO - http://dx.doi.org/10.1111/cmi.12246 ER - TY - JOUR T1 - Eosinophilic gastroenteritis and related eosinophilic disorders. AN - 1535622928; 24813518 AB - Eosinophilic gastroenteritis (EGE) represents one member within the spectrum of diseases collectively referred to as eosinophilic gastrointestinal disorders, which includes eosinophilic esophagitis (EoE), gastritis, enteritis, and colitis. EGE is less common than EoE and involves a different site of disease but otherwise shares many common features with EoE. The clinical manifestations of EGE are protean and can vary from nausea and vomiting to protein-losing enteropathy or even bowel obstruction requiring surgery. Although systemic corticosteroids are an effective treatment for EGE, their use results in substantial corticosteroid toxicity. Accordingly, there is a great need for improved therapies for these patients. Published by Elsevier Inc. JF - Gastroenterology clinics of North America AU - Prussin, Calman AD - Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive, MSC-1881, Bethesda, MD 20892-1881, USA. Electronic address: cprussin@niaid.nih.gov. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 317 EP - 327 VL - 43 IS - 2 KW - Index Medicus KW - Food allergy KW - Eosinophilic gastritis KW - Eosinophilic gastroenteritis KW - Eosinophilia KW - EGID KW - Humans KW - Enteritis -- etiology KW - Eosinophilia -- therapy KW - Enteritis -- complications KW - Enteritis -- therapy KW - Enteritis -- diagnosis KW - Gastritis -- diagnosis KW - Eosinophilia -- diagnosis KW - Gastritis -- therapy KW - Gastritis -- etiology KW - Gastritis -- complications KW - Eosinophilia -- etiology KW - Eosinophilia -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1535622928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology+clinics+of+North+America&rft.atitle=Eosinophilic+gastroenteritis+and+related+eosinophilic+disorders.&rft.au=Prussin%2C+Calman&rft.aulast=Prussin&rft.aufirst=Calman&rft.date=2014-06-01&rft.volume=43&rft.issue=2&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Gastroenterology+clinics+of+North+America&rft.issn=1558-1942&rft_id=info:doi/10.1016%2Fj.gtc.2014.02.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-15 N1 - Date created - 2014-05-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Scand J Gastroenterol. 2011 Sep;46(9):1074-80 [21623674] J Allergy Clin Immunol. 2011 Jul;128(1):3-20.e6; quiz 21-2 [21477849] Eur J Pediatr. 2011 Nov;170(11):1471-4 [21809010] Dig Dis Sci. 2011 Dec;56(12):3551-8 [21674173] Clin Exp Allergy. 2012 May;42(5):712-37 [22092535] J Okla State Med Assoc. 2012 Apr-May;105(4-5):134, 136 [22803505] J Pediatr Gastroenterol Nutr. 2000;30 Suppl:S28-35 [10634296] Eur J Gastroenterol Hepatol. 2001 Apr;13(4):425-7 [11338074] J Allergy Clin Immunol. 2001 May;107(5):924-5 [11344364] Br J Clin Pharmacol. 2001 May;51(5):400-9 [11421996] Dig Dis Sci. 2001 Aug;46(8):1787-90 [11508684] Ann Allergy Asthma Immunol. 2003 Jan;90(1):23-7 [12546333] J Pediatr Gastroenterol Nutr. 2003 Feb;36(2):293-4 [12548071] Am J Gastroenterol. 2003 Apr;98(4):777-82 [12738455] Asian Pac J Allergy Immunol. 2003 Sep;21(3):193-7 [15032404] Gut. 1990 Jan;31(1):54-8 [2318432] J Allergy Clin Immunol. 2012 Sep;130(3):563-71 [22935585] Am J Med. 1991 Mar;90(3):310-4 [2003512] Scott Med J. 1990 Dec;35(6):163-5 [2077646] Mayo Clin Proc. 1994 May;69(5):441-4 [8170195] J Clin Immunol. 1994 Sep;14(5):299-309 [7814459] Dig Dis Sci. 1995 Feb;40(2):308-14 [7851195] Dig Dis Sci. 1997 Feb;42(2):342-4 [9052516] Am J Gastroenterol. 1997 Jul;92(7):1205-8 [9219801] Aliment Pharmacol Ther. 1998 Jul;12(7):591-603 [9701522] J Allergy Clin Immunol. 1999 Aug;104(2 Pt 1):506 [10452782] J Allergy Clin Immunol. 2004 Dec;114(6):1449-55 [15577851] J Pediatr Gastroenterol Nutr. 2005 Jan;40(1):83-6 [15625432] Best Pract Res Clin Gastroenterol. 2005 Apr;19(2):177-98 [15833687] Immunol Allergy Clin North Am. 2005 Aug;25(3):469-88 [16054538] Clin Gastroenterol Hepatol. 2005 Dec;3(12):1198-206 [16361045] Dig Liver Dis. 2006 Jan;38(1):55-9 [16326154] JOP. 2006;7(2):211-7 [16525206] J Pediatr Gastroenterol Nutr. 2006 May;42(5):516-21 [16707973] Pediatr Dev Pathol. 2006 May-Jun;9(3):210-8 [16944979] Z Gastroenterol. 2007 Feb;45(2):187-9 [17304405] World J Gastroenterol. 2007 Mar 21;13(11):1758-60 [17461485] J Allergy Clin Immunol. 2007 Sep;120(3):594-601 [17765756] J Pediatr Gastroenterol Nutr. 2007 Sep;45(3):354-7 [17873749] Can J Gastroenterol. 2009 Sep;23(9):632-4 [19816628] J Allergy Clin Immunol. 2009 Dec;124(6):1319-25.e3 [19910029] J Allergy Clin Immunol. 2009 Dec;124(6):1326-32.e6 [20004787] Curr Opin Allergy Clin Immunol. 2010 Jun;10(3):231-7 [20410819] J Allergy Clin Immunol. 2010 Jul;126(1):45-9 [20639008] Clin Gastroenterol Hepatol. 2010 Aug;8(8):669-75; quiz e88 [20451664] HPB Surg. 2010;2010:906496 [21076681] J Pediatr Gastroenterol Nutr. 2010 Dec;51(6):723-6 [20601904] Dig Endosc. 2010 Oct;22(4):312-5 [21175485] J Pediatr Gastroenterol Nutr. 2011 Mar;52(3):300-6 [21057327] Eur Ann Allergy Clin Immunol. 2011 Feb;43(1):29-30 [21409859] Mod Pathol. 2011 Apr;24(4):556-63 [21169993] J Immunol. 2011 Sep 15;187(6):3111-20 [21849680] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.gtc.2014.02.013 ER - TY - JOUR T1 - Establishing a Bone Marrow Stromal Cell Transplant Program at the National Institutes of Health Clinical Center AN - 1534847262; 19986459 AB - A repository of cryopreserved bone marrow stromal cell (BMSC) products prepared from marrow aspirates of healthy subjects has been created and is being used to treat patients with inflammatory bowel disease, cardiovascular disease, and acute graft-versus-host disease following allogeneic hematopoietic stem cell transplantation. New methods of manufacturing BMSCs are being investigated including the use of an automated bioreactor for BMSC expansion and the replacement of fetal bovine serum with human platelet lysate as a media supplement. Efforts are also being made to identify markers that can be used to assess the potency of BMSCs. JF - Tissue Engineering, Part B: Reviews AU - Stroncek, David F AU - Sabatino, Marianna AU - Ren, Jiaqiang AU - England, Lee AU - Kuznetsov, Sergei A AU - Klein, Harvey G AU - Robey, Pamela G AD - Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 200 EP - 205 PB - Mary Ann Liebert, Inc., 140 Huguenot St 3rd Fl New Rochelle NY 10801 United States VL - 20 IS - 3 SN - 1937-3368, 1937-3368 KW - Biotechnology and Bioengineering Abstracts KW - stromal cells KW - Inflammatory bowel diseases KW - Reviews KW - stem cell transplantation KW - Bioreactors KW - Platelets KW - Graft-versus-host reaction KW - Cardiovascular diseases KW - Tissue engineering KW - Cryopreservation KW - Bone marrow transplantation KW - W 30920:Tissue Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534847262?accountid=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+B%3A+Reviews&rft.atitle=Establishing+a+Bone+Marrow+Stromal+Cell+Transplant+Program+at+the+National+Institutes+of+Health+Clinical+Center&rft.au=Stroncek%2C+David+F%3BSabatino%2C+Marianna%3BRen%2C+Jiaqiang%3BEngland%2C+Lee%3BKuznetsov%2C+Sergei+A%3BKlein%2C+Harvey+G%3BRobey%2C+Pamela+G&rft.aulast=Stroncek&rft.aufirst=David&rft.date=2014-06-01&rft.volume=20&rft.issue=3&rft.spage=200&rft.isbn=&rft.btitle=&rft.title=Tissue+Engineering%2C+Part+B%3A+Reviews&rft.issn=19373368&rft_id=info:doi/10.1089%2Ften.teb.2013.0529 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Number of references - 37 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Inflammatory bowel diseases; stromal cells; Bioreactors; stem cell transplantation; Reviews; Platelets; Graft-versus-host reaction; Cardiovascular diseases; Tissue engineering; Cryopreservation; Bone marrow transplantation DO - http://dx.doi.org/10.1089/ten.teb.2013.0529 ER - TY - JOUR T1 - Bone Marrow Mesenchymal Stromal Cells to Treat Complications Following Allogeneic Stem Cell Transplantation AN - 1534846644; 19986460 AB - Allogeneic hematopoietic stem cell transplantation (HSCT) is a technologically complicated procedure that represents the only cure for many hematologic malignancies. However, HSCT is often complicated by life-threatening toxicities related to the chemo-radiation conditioning regimen, poor engraftment of donor HSCs, the hyperinflammatory syndrome of graft-versus-host disease (GVHD), infection risks from immunosuppression, and end-organ damage. Bone marrow stromal cells (MSCs), also known as "mesenchymal stromal cells," not only play a nurturing role in the hematopoietic microenvironment but also can differentiate into other cell types of mesenchymal origin. MSCs are poorly immunogenic, and they can modulate immunological responses through interactions with a wide range of innate and adaptive immune cells to reduce inflammation. They are easily expanded ex vivo and after infusion, home to sites of injury and inflammation to promote tissue repair. Despite promising early trial results in HSCT with significant responses that have translated into survival benefits, there have been significant barriers to successful commercialization as an off-the-shelf therapy. Current efforts with MSCs in the HSCT setting are geared toward determining the factors determining potency, understanding the precise mechanisms of action in human HSCT, knowing their kinetics and fate, optimizing dose and schedule, incorporating biomarkers as response surrogates, addressing concerns about safety, optimizing clinical trial design, and negotiating the uncharted regulatory landscape for licensable cellular therapy. JF - Tissue Engineering, Part B: Reviews AU - Battiwalla, Minoo AU - Barrett, AJohn AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 211 EP - 217 PB - Mary Ann Liebert, Inc., 140 Huguenot St 3rd Fl New Rochelle NY 10801 United States VL - 20 IS - 3 SN - 1937-3368, 1937-3368 KW - Biotechnology and Bioengineering Abstracts KW - Donors KW - stromal cells KW - Injuries KW - stem cell transplantation KW - Bone marrow KW - Graft-versus-host reaction KW - Toxicity KW - Infection KW - Tissue engineering KW - biomarkers KW - Clinical trials KW - Inflammation KW - Malignancy KW - Immunogenicity KW - Kinetics KW - Microenvironments KW - Mesenchyme KW - Bone marrow transplantation KW - Immunosuppression KW - W 30920:Tissue Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534846644?accountid=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+B%3A+Reviews&rft.atitle=Bone+Marrow+Mesenchymal+Stromal+Cells+to+Treat+Complications+Following+Allogeneic+Stem+Cell+Transplantation&rft.au=Battiwalla%2C+Minoo%3BBarrett%2C+AJohn&rft.aulast=Battiwalla&rft.aufirst=Minoo&rft.date=2014-06-01&rft.volume=20&rft.issue=3&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Tissue+Engineering%2C+Part+B%3A+Reviews&rft.issn=19373368&rft_id=info:doi/10.1089%2Ften.teb.2013.0566 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Number of references - 55 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Donors; Injuries; stromal cells; stem cell transplantation; Bone marrow; Graft-versus-host reaction; Toxicity; Tissue engineering; Infection; Clinical trials; biomarkers; Inflammation; Malignancy; Immunogenicity; Kinetics; Microenvironments; Mesenchyme; Bone marrow transplantation; Immunosuppression DO - http://dx.doi.org/10.1089/ten.teb.2013.0566 ER - TY - JOUR T1 - Risk of second benign brain tumors among cancer survivors in the surveillance, epidemiology, and end results program AN - 1534830371; 19902424 AB - Purpose: To assess risk of developing a second benign brain tumor in a nationwide population of cancer survivors. Methods: We evaluated the risk of developing second benign brain tumors among 2,038,074 1-year minimum cancer survivors compared to expected risk in the general population between 1973 and 2007 in nine population-based cancer registries in the NCI's surveillance, epidemiology, and end results program. Excess risk was estimated using standardized incidence ratios (SIRs) for all second benign brain tumors and specifically for second meningiomas and acoustic neuromas diagnosed during 2004-2008. Results: 1,025 patients were diagnosed with a second primary benign brain tumor, of which second meningiomas composed the majority (n = 745). Statistically significant increases in risk of developing a second meningioma compared to the general population were observed following first cancers of the brain [SIR = 19.82; 95 % confidence interval (CI) 13.88-27.44], other central nervous system (CNS) (SIR = 9.54; CI 3.10-22.27), thyroid (SIR = 2.05; CI 1.47-2.79), prostate (SIR = 1.21; CI 1.02-1.43), and acute lymphocytic leukemia (ALL) (SIR = 42.4; CI 23.18-71.13). Statistically significant decreases in risk were observed following first cancers of the uterine corpus (SIR = 0.63; CI 0.42-0.91) and colon (SIR = 0.56; CI 0.37-0.82). Differences in risk between patients initially treated with radiotherapy versus non-irradiated patients were statistically significant for second meningioma after primary cancers of the brain (p sub(Het) < 0.001) and ALL (p sub(Het) = 0.02). No statistically significant increased risks were detected for second acoustic neuromas (n = 114) following any first primary tumor. Conclusions: Risk of second benign brain tumors, particularly meningioma, is increased following first primary cancers of the brain/CNS, thyroid, prostate, and ALL. Radiation exposure likely contributes to these excess risks. JF - Cancer Causes & Control AU - Kutsenko, Alina AU - Berrington de Gonzalez, Amy AU - Curtis, Rochelle E AU - Rajaraman, Preetha AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, NCI/NIH, 9609 Medical Center Drive, MSC 9778, Bethesda, MD, 20892, USA, alk2022@med.cornell.edu Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 659 EP - 668 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 25 IS - 6 SN - 0957-5243, 0957-5243 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Risk assessment KW - Central nervous system KW - Thyroid KW - Brain KW - Radiotherapy KW - Tumors KW - Cancer KW - Brain tumors KW - Leukemia KW - Health risks KW - Radiation KW - Epidemiology KW - Standards 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/1534830371?accountid=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=Risk+of+second+benign+brain+tumors+among+cancer+survivors+in+the+surveillance%2C+epidemiology%2C+and+end+results+program&rft.au=Kutsenko%2C+Alina%3BBerrington+de+Gonzalez%2C+Amy%3BCurtis%2C+Rochelle+E%3BRajaraman%2C+Preetha&rft.aulast=Kutsenko&rft.aufirst=Alina&rft.date=2014-06-01&rft.volume=25&rft.issue=6&rft.spage=659&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-014-0367-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Number of references - 36 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Risk assessment; Central nervous system; Brain; Thyroid; Radiotherapy; Tumors; Cancer; Brain tumors; Health risks; Leukemia; Epidemiology; Radiation; Standards DO - http://dx.doi.org/10.1007/s10552-014-0367-5 ER - TY - JOUR T1 - Brucella arteritis: clinical manifestations, treatment, and prognosis AN - 1534819831; 19918688 AB - Brucellosis is the most common bacterial zoonosis, and causes a considerable burden of disease in endemic countries. Cardiovascular involvement is the main cause of mortality due to infection with spp, and most commonly manifests as endocarditis, peripheral and cerebrovascular aneurysms, or arterial and venous thromboses. We report a case of brucellosis presenting as bacteraemia and aortic endarteritis 18 years after the last known exposure to risk factors for brucella infection. The patient was treated with doxycycline, rifampicin, and gentamicin, and underwent surgical repair of a penetrating aortic ulcer, with a good clinical recovery. We review the signs and symptoms, diagnostic approach, prognosis, and treatment of brucella arteritis. We draw attention to the absence of consensus about the optimum therapy for vascular brucellosis, and the urgent need for additional studies and renewed scientific interest in this major pathogen. JF - Lancet Infectious Diseases AU - Herrick, Jesica A AU - Lederman, Robert J AU - Sullivan, Brigit AU - Powers, John H AU - Palmore, Tara N AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 520 EP - 526 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 14 IS - 6 SN - 1473-3099, 1473-3099 KW - Microbiology Abstracts B: Bacteriology KW - Mortality KW - Aneurysm KW - Aorta KW - Prognosis KW - Bacteremia KW - Brucella KW - Pathogens KW - Infection KW - Endocarditis KW - Gentamicin KW - Rifampin KW - Case reports KW - Ulcers KW - Risk factors KW - Reviews KW - Arteritis KW - Brucellosis KW - Doxycycline KW - Endarteritis KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534819831?accountid=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=Lancet+Infectious+Diseases&rft.atitle=Brucella+arteritis%3A+clinical+manifestations%2C+treatment%2C+and+prognosis&rft.au=Herrick%2C+Jesica+A%3BLederman%2C+Robert+J%3BSullivan%2C+Brigit%3BPowers%2C+John+H%3BPalmore%2C+Tara+N&rft.aulast=Herrick&rft.aufirst=Jesica&rft.date=2014-06-01&rft.volume=14&rft.issue=6&rft.spage=520&rft.isbn=&rft.btitle=&rft.title=Lancet+Infectious+Diseases&rft.issn=14733099&rft_id=info:doi/10.1016%2FS1473-3099%2813%2970270-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Mortality; Aneurysm; Aorta; Prognosis; Bacteremia; Pathogens; Infection; Endocarditis; Gentamicin; Rifampin; Case reports; Ulcers; Reviews; Risk factors; Arteritis; Brucellosis; Endarteritis; Doxycycline; Brucella DO - http://dx.doi.org/10.1016/S1473-3099(13)70270-6 ER - TY - JOUR T1 - HIV-1 Vaginal Transmission: Cell-Free or Cell-Associated Virus? AN - 1534819384; 19972757 AB - The vast majority of new HIV infections in male-to-female transmission occurs through semen, where HIV-1 is present in two different forms: as free and as cell-associated virus. In the female lower genital tract, semen mixes with female genital secretions that contain various factors, some of which facilitate or inhibit HIV-1 transmission. Next, HIV-1 crosses the genital epithelia, reaches the regional lymph nodes, and disseminates through the female host. Cervico-vaginal mucosa contains multiple barriers, resulting in a low probability of vaginal transmission. However, in some cases, HIV-1 is able to break these barriers. Although the exact mechanisms of how these barriers function remain unclear, their levels of efficiency against cell-free and cell-associated HIV-1 are different, and both cell-free and cell-associated virions seem to use different strategies to overcome these barriers. Understanding the basic mechanisms of HIV-1 vaginal transmission is required for the development of new antiviral strategies to contain HIV-1 epidemics. JF - American Journal of Reproductive Immunology AU - Barreto-de-Souza, Victor AU - Arakelyan, Anush AU - Margolis, Leonid AU - Vanpouille, Christophe AD - Section of Intercellular Interactions Program in Physical Biology. Eunice Kennedy Shriver National Institute of Child Health and Human Development Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 589 EP - 599 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 71 IS - 6 SN - 1046-7408, 1046-7408 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts KW - Virions KW - Epidemics KW - Immunology KW - Secretions KW - Mucosa KW - Infection KW - Lymph nodes KW - Disease transmission KW - Human immunodeficiency virus KW - Human immunodeficiency virus 1 KW - Vagina KW - Semen KW - Genital tract KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma KW - F 06935:Development, Aging & Organ Systems UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534819384?accountid=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+Reproductive+Immunology&rft.atitle=HIV-1+Vaginal+Transmission%3A+Cell-Free+or+Cell-Associated+Virus%3F&rft.au=Barreto-de-Souza%2C+Victor%3BArakelyan%2C+Anush%3BMargolis%2C+Leonid%3BVanpouille%2C+Christophe&rft.aulast=Barreto-de-Souza&rft.aufirst=Victor&rft.date=2014-06-01&rft.volume=71&rft.issue=6&rft.spage=589&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Reproductive+Immunology&rft.issn=10467408&rft_id=info:doi/10.1111%2Faji.12240 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Virions; Epidemics; Mucosa; Secretions; Vagina; Semen; Genital tract; Infection; Lymph nodes; Disease transmission; Human immunodeficiency virus; Immunology; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1111/aji.12240 ER - TY - JOUR T1 - Maternal overweight and obesity and risk of congenital heart defects in offspring. AN - 1534792383; 24362506 AB - Obesity is a risk factor for congenital heart defects (CHDs), but whether risk is independent of abnormal glucose metabolism remains unknown. Data on whether overweight status increases the risk are also conflicting. We included 121 815 deliveries from a cohort study, the Consortium on Safe Labor (CSL), after excluding women with pregestational diabetes as recorded in the electronic medical record. CHD was identified via medical record discharge summaries. Adjusted odds ratios (ORs) for any CHD were calculated for prepregnancy body mass index (BMI) categories of overweight (25-<30 kg m(-2)), obese (30-<40 kg m(-2)) and morbidly obese (≥40 kg m(-2)) compared with normal weight (18.5-<25 kg m(-2)) women, and for specific CHD with obese groups combined (≥30 kg m(-2)). A subanalysis adjusting for oral glucose tolerance test (OGTT) results where available was performed as a proxy for potential abnormal glucose metabolism present at the time of organogenesis. There were 1388 (1%) infants with CHD. Overweight (OR=1.15, 95% confidence interval (95% CI): 1.01-1.32), obese (OR=1.26, 95% CI: 1.09-1.44) and morbidly obese (OR=1.34, 95% CI: 1.02-1.76) women had greater OR of having a neonate with CHD than normal weight women (P<0.001 for trend). Obese women (BMI≥30 kg m(-2)) had higher OR of having an infant with conotruncal defects (OR = 1.33, 95% CI: (1.03–1.72) [corrected], atrial septal defects (OR=1.22, 95% CI: 1.04-1.43) and ventricular septal defects (OR=1.38, 95% CI: 1.06-1.79). Being obese remained a significant predictor of CHD risk after adjusting for OGTT. Increasing maternal weight class was associated with an increased risk for CHD. In obese women, abnormal glucose metabolism did not completely explain the increased risk for CHD; the possibility that other obesity-related factors are teratogenic requires further investigation. JF - International journal of obesity (2005) AU - Brite, J AU - Laughon, S K AU - Troendle, J AU - Mills, J AD - 1] Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA [2] Epidemiology and Biostatistics, CUNY School of Public Health at Hunter College, New York, NY, USA [3] CUNY Institute for Demographic Research (CIDR), New York, NY, USA. ; Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA. ; Office of Biostatistics Research, Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD, USA. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 878 EP - 882 VL - 38 IS - 6 KW - Index Medicus KW - Odds Ratio KW - Prospective Studies KW - Logistic Models KW - Risk Factors KW - Humans KW - Cohort Studies KW - Adult KW - Infant, Newborn KW - Body Mass Index KW - Female KW - Risk Assessment KW - Pregnancy KW - Heart Defects, Congenital -- epidemiology KW - Pregnancy Complications -- etiology KW - Heart Defects, Congenital -- etiology KW - Mothers KW - Glucose Metabolism Disorders -- epidemiology KW - Obesity -- epidemiology KW - Glucose Metabolism Disorders -- etiology KW - Pregnancy Complications -- epidemiology KW - Obesity -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534792383?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+obesity+%282005%29&rft.atitle=Maternal+overweight+and+obesity+and+risk+of+congenital+heart+defects+in+offspring.&rft.au=Brite%2C+J%3BLaughon%2C+S+K%3BTroendle%2C+J%3BMills%2C+J&rft.aulast=Brite&rft.aufirst=J&rft.date=2014-06-01&rft.volume=38&rft.issue=6&rft.spage=878&rft.isbn=&rft.btitle=&rft.title=International+journal+of+obesity+%282005%29&rft.issn=1476-5497&rft_id=info:doi/10.1038%2Fijo.2013.244 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-30 N1 - Date created - 2014-06-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: JAMA. 2012 Feb 1;307(5):491-7 [22253363] Am J Obstet Gynecol. 2010 Oct;203(4):326.e1-326.e10 [20708166] Congenit Heart Dis. 2013 Mar-Apr;8(2):131-41 [22967199] Obes Res. 2003 Sep;11(9):1065-71 [12972676] Am J Obstet Gynecol. 2012 May;206(5):419.e1-9 [22542117] Paediatr Perinat Epidemiol. 2000 Jul;14(3):234-9 [10949215] Epidemiology. 2000 Nov;11(6):689-94 [11055631] Obstet Gynecol. 2001 Sep;98(3):525-38 [11547793] Scand J Work Environ Health. 2002 Feb;28(1):12-7 [11873776] Pediatrics. 2003 May;111(5 Pt 2):1152-8 [12728129] Am J Epidemiol. 1991 Aug 15;134(4):393-402 [1877600] Arch Pediatr Adolesc Med. 2007 Aug;161(8):745-50 [17679655] Birth Defects Res A Clin Mol Teratol. 2007 Oct;79(10):714-27 [17729292] N Engl J Med. 2008 May 8;358(19):1991-2002 [18463375] Epidemiology. 2008 Jul;19(4):616-20 [18552593] Am J Obstet Gynecol. 2008 Sep;199(3):237.e1-9 [18674752] Int J Obes (Lond). 2008 Sep;32(9):1431-7 [18607383] Cardiol Young. 2008 Dec;18 Suppl 2:92-100 [19063779] JAMA. 2009 Feb 11;301(6):636-50 [19211471] Diabetes Care. 2009 Sep;32(9):1639-43 [19549728] Birth Defects Res A Clin Mol Teratol. 2010 Jan;88(1):35-40 [19711433] Am J Obstet Gynecol. 2010 Jan;202(1):51.e1-51.e10 [19796755] Am J Clin Nutr. 2010 Jun;91(6):1543-9 [20375192] Erratum In: Int J Obes (Lond). 2014 Jun;38(6):886 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ijo.2013.244 ER - TY - JOUR T1 - Exploitation of Langerhans cells for in vivo DNA vaccine delivery into the lymph nodes. AN - 1534102037; 24694539 AB - There is no clinically available cancer immunotherapy that exploits Langerhans cells (LCs), the epidermal precursors of dendritic cells (DCs) that are the natural agent of antigen delivery. We developed a DNA formulation with a polymer and obtained synthetic 'pathogen-like' nanoparticles that preferentially targeted LCs in epidermal cultures. These nanoparticles applied topically under a patch-elicited robust immune responses in human subjects. To demonstrate the mechanism of action of this novel vaccination strategy in live animals, we assembled a high-resolution two-photon laser scanning-microscope. Nanoparticles applied on the native skin poorly penetrated and poorly induced LC motility. The combination of nanoparticle administration and skin treatment was essential both for efficient loading the vaccine into the epidermis and for potent activation of the LCs to migrate into the lymph nodes. LCs in the epidermis picked up nanoparticles and accumulated them in the nuclear region demonstrating an effective nuclear DNA delivery in vivo. Tissue distribution studies revealed that the majority of the DNA was targeted to the lymph nodes. Preclinical toxicity of the LC-targeting DNA vaccine was limited to mild and transient local erythema caused by the skin treatment. This novel, clinically proven LC-targeting DNA vaccine platform technology broadens the options on DC-targeting vaccines to generate therapeutic immunity against cancer. JF - Gene therapy AU - Tőke, E R AU - Lőrincz, O AU - Csiszovszki, Z AU - Somogyi, E AU - Felföldi, G AU - Molnár, L AU - Szipőcs, R AU - Kolonics, A AU - Malissen, B AU - Lori, F AU - Trocio, J AU - Bakare, N AU - Horkay, F AU - Romani, N AU - Tripp, C H AU - Stoitzner, P AU - Lisziewicz, J AD - Genetic Immunity Kft, H-1045 Budapest, Hungary. ; 1] Wigner RCP of HAS, H-1121 Budapest, Hungary [2] R&D Ultrafast Lasers Ltd, H-1539 Budapest, Hungary. ; Centre d'Immunologie de Marseille-Luminy, INSERM U1104, CNRS UMR7280, Aix Marseille Université, Marseille, France. ; Research Institute for Genetic and Human Therapy (RIGHT), Bethesda, MD, USA. ; Section on Tissue Biophysics and Biomimetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD, USA. ; Department of Dermatology and Venereology, Innsbruck Medical University, Innsbruck, Austria. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 566 EP - 574 VL - 21 IS - 6 KW - Vaccines, DNA KW - 0 KW - Index Medicus KW - Cell Movement KW - Drug Delivery Systems KW - Animals KW - Epidermis -- drug effects KW - Microscopy, Confocal -- instrumentation KW - Epidermis -- cytology KW - Rabbits KW - Tissue Distribution KW - Microscopy, Confocal -- methods KW - Mice, Transgenic KW - Nanoparticles -- administration & dosage KW - Administration, Topical KW - Immunotherapy -- methods KW - Langerhans Cells KW - Vaccines, DNA -- administration & dosage KW - Vaccines, DNA -- pharmacokinetics KW - Lymph Nodes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534102037?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene+therapy&rft.atitle=Exploitation+of+Langerhans+cells+for+in+vivo+DNA+vaccine+delivery+into+the+lymph+nodes.&rft.au=T%C5%91ke%2C+E+R%3BL%C5%91rincz%2C+O%3BCsiszovszki%2C+Z%3BSomogyi%2C+E%3BFelf%C3%B6ldi%2C+G%3BMoln%C3%A1r%2C+L%3BSzip%C5%91cs%2C+R%3BKolonics%2C+A%3BMalissen%2C+B%3BLori%2C+F%3BTrocio%2C+J%3BBakare%2C+N%3BHorkay%2C+F%3BRomani%2C+N%3BTripp%2C+C+H%3BStoitzner%2C+P%3BLisziewicz%2C+J&rft.aulast=T%C5%91ke&rft.aufirst=E&rft.date=2014-06-01&rft.volume=21&rft.issue=6&rft.spage=566&rft.isbn=&rft.btitle=&rft.title=Gene+therapy&rft.issn=1476-5462&rft_id=info:doi/10.1038%2Fgt.2014.29 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-12 N1 - Date created - 2014-06-06 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/gt.2014.29 ER - TY - JOUR T1 - Dietary flavonoid intake and thyroid cancer risk in the NIH-AARP diet and health study. AN - 1532951261; 24686895 AB - Experimental studies suggested that flavonoids may influence thyroid carcinogenesis, but epidemiologic evidence is sparse. No study has examined different classes of flavonoids in relation to thyroid cancer risk. Using data from the NIH-AARP Diet and Health Study, which enrolled 491,840 U.S. men and women, ages 50 to 71 years at baseline, we prospectively examined the risk of thyroid cancer in relation to dietary intakes of catechins, flavanones, flavonols, anthocyanidins, flavones, isoflavones, and total flavonoids. Dietary intakes were assessed using a food frequency questionnaire. Cancer cases were ascertained by linkage to state cancer registries. Multivariable-adjusted Cox proportional hazard models were used to estimate HRs and 95% confidence intervals (CI). During follow up (mean = 9 years), we identified 586 thyroid cancer cases. Thyroid cancer risk was inversely associated with dietary flavan-3-ols [HRQ5 vs. Q1 (95% CI): 0.70 (0.55, 0.91), PTrend = 0.03], but positively associated with flavanones [HRQ5 vs. Q1 (95% CI): 1.50 (1.14, 1.96), PTrend = 0.004]. Other classes of flavonoids and total flavonoids were not associated with thyroid cancer risk. Similar associations were found for papillary thyroid cancer. Our findings suggest that dietary intake of different classes of dietary flavonoids may have divergent effects on thyroid cancer risk. More studies are needed to clarify a role of flavonoids in thyroid cancer development. Results from our study suggest a potential nutritional etiology of thyroid cancer. Cancer Epidemiol Biomarkers Prev; 23(6); 1102-8. ©2014 AACR. ©2014 American Association for Cancer Research. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Xiao, Qian AU - Park, Yikyung AU - Hollenbeck, Albert R AU - Kitahara, Cari M AD - Authors' Affiliations: Nutritional Epidemiology Branch and Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland; and AARP, Washington, District of Columbia qian.xiao@nih.gov. ; Authors' Affiliations: Nutritional Epidemiology Branch and Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland; and AARP, Washington, District of Columbia. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1102 EP - 1108 VL - 23 IS - 6 KW - Flavonoids KW - 0 KW - Index Medicus KW - United States KW - Prospective Studies KW - Risk Factors KW - Humans KW - National Institutes of Health (U.S.) KW - Aged KW - Middle Aged KW - Diet KW - Male KW - Female KW - Thyroid Neoplasms -- diet therapy KW - Flavonoids -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1532951261?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dietary+flavonoid+intake+and+thyroid+cancer+risk+in+the+NIH-AARP+diet+and+health+study.&rft.au=Xiao%2C+Qian%3BPark%2C+Yikyung%3BHollenbeck%2C+Albert+R%3BKitahara%2C+Cari+M&rft.aulast=Xiao&rft.aufirst=Qian&rft.date=2014-06-01&rft.volume=23&rft.issue=6&rft.spage=1102&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-13-1150 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-15 N1 - Date created - 2014-06-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517] Am J Epidemiol. 2000 Aug 1;152(3):279-86 [10933275] Ann Epidemiol. 2002 Aug;12(6):395-401 [12160598] Chem Res Toxicol. 1996 Jan-Feb;9(1):16-23 [8924586] Cancer Epidemiol Biomarkers Prev. 1998 Jul;7(7):613-9 [9681530] Thyroid. 1999 Apr;9(4):369-76 [10319943] J Nutr. 1957 Jan 10;61(1):97-101 [13406611] Cancer Causes Control. 2009 Feb;20(1):75-86 [18766448] Cancer Causes Control. 2009 Jul;20(5):525-31 [19016336] Future Oncol. 2010 Nov;6(11):1771-9 [21142662] Cancer Epidemiol Biomarkers Prev. 2011 Mar;20(3):464-72 [21266520] Cancer Causes Control. 2011 Jul;22(7):985-93 [21562752] Food Chem Toxicol. 2011 Oct;49(10):2495-502 [21745527] J Nutr Gerontol Geriatr. 2012;31(3):206-38 [22888839] Cancer Causes Control. 2012 Oct;23(10):1615-24 [22843022] Br J Nutr. 2013 Jan 14;109(1):118-28 [22455656] Br J Cancer. 2013 Mar 19;108(5):1168-72 [23299536] J Clin Endocrinol Metab. 1989 Apr;68(4):707-14 [2921306] Cancer Epidemiol Biomarkers Prev. 2002 Jan;11(1):43-9 [11815400] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1055-9965.EPI-13-1150 ER - TY - JOUR T1 - Novel DNA motif binding activity observed in vivo with an estrogen receptor α mutant mouse. AN - 1532947160; 24713037 AB - Estrogen receptor α (ERα) interacts with DNA directly or indirectly via other transcription factors, referred to as "tethering." Evidence for tethering is based on in vitro studies and a widely used "KIKO" mouse model containing mutations that prevent direct estrogen response element DNA- binding. KIKO mice are infertile, due in part to the inability of estradiol (E2) to induce uterine epithelial proliferation. To elucidate the molecular events that prevent KIKO uterine growth, regulation of the pro-proliferative E2 target gene Klf4 and of Klf15, a progesterone (P4) target gene that opposes the pro-proliferative activity of KLF4, was evaluated. Klf4 induction was impaired in KIKO uteri; however, Klf15 was induced by E2 rather than by P4. Whole uterine chromatin immunoprecipitation-sequencing revealed enrichment of KIKO ERα binding to hormone response elements (HREs) motifs. KIKO binding to HRE motifs was verified using reporter gene and DNA-binding assays. Because the KIKO ERα has HRE DNA-binding activity, we evaluated the "EAAE" ERα, which has more severe DNA-binding domain mutations, and demonstrated a lack of estrogen response element or HRE reporter gene induction or DNA-binding. The EAAE mouse has an ERα null-like phenotype, with impaired uterine growth and transcriptional activity. Our findings demonstrate that the KIKO mouse model, which has been used by numerous investigators, cannot be used to establish biological functions for ERα tethering, because KIKO ERα effectively stimulates transcription using HRE motifs. The EAAE-ERα DNA-binding domain mutant mouse demonstrates that ERα DNA-binding is crucial for biological and transcriptional processes in reproductive tissues and that ERα tethering may not contribute to estrogen responsiveness in vivo. JF - Molecular endocrinology (Baltimore, Md.) AU - Hewitt, Sylvia C AU - Li, Leping AU - Grimm, Sara A AU - Winuthayanon, Wipawee AU - Hamilton, Katherine J AU - Pockette, Brianna AU - Rubel, Cory A AU - Pedersen, Lars C AU - Fargo, David AU - Lanz, Rainer B AU - DeMayo, Francesco J AU - Schütz, Günther AU - Korach, Kenneth S AD - Receptor Biology (S.C.H., W.W., K.J.H., B.P., K.S.K.), Laboratory of Reproductive and Developmental Toxicology, Biostatistics Branch (L.L.), Integrative Bioinformatics (S.A.G., D.F.), Laboratory of Structural Biology (L.C.P.), National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709; Department of Molecular and Cellular Biology (C.A.R., R.B.L., F.J.D.), Baylor College of Medicine, Houston, Texas 77030; and Department of Molecular Biology of the Cell (G.S.), German Cancer Research Center, 69121 Heidelberg, Germany. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 899 EP - 911 VL - 28 IS - 6 KW - Estrogen Receptor alpha KW - 0 KW - GKLF protein KW - KLF15 protein, human KW - Kruppel-Like Transcription Factors KW - Nuclear Proteins KW - Estradiol KW - 4TI98Z838E KW - Index Medicus KW - Animals KW - Nuclear Proteins -- genetics KW - Estradiol -- physiology KW - Protein Binding KW - Mutation, Missense KW - Mice, Knockout KW - Uterus -- metabolism KW - Phenotype KW - Mice, 129 Strain KW - Base Sequence KW - Mice, Inbred C57BL KW - Kruppel-Like Transcription Factors -- metabolism KW - Consensus Sequence KW - Response Elements KW - Nuclear Proteins -- metabolism KW - Female KW - Kruppel-Like Transcription Factors -- genetics KW - Estrogen Receptor alpha -- genetics KW - Estrogen Receptor alpha -- metabolism KW - Transcriptional Activation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1532947160?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Novel+DNA+motif+binding+activity+observed+in+vivo+with+an+estrogen+receptor+%CE%B1+mutant+mouse.&rft.au=Hewitt%2C+Sylvia+C%3BLi%2C+Leping%3BGrimm%2C+Sara+A%3BWinuthayanon%2C+Wipawee%3BHamilton%2C+Katherine+J%3BPockette%2C+Brianna%3BRubel%2C+Cory+A%3BPedersen%2C+Lars+C%3BFargo%2C+David%3BLanz%2C+Rainer+B%3BDeMayo%2C+Francesco+J%3BSch%C3%BCtz%2C+G%C3%BCnther%3BKorach%2C+Kenneth+S&rft.aulast=Hewitt&rft.aufirst=Sylvia&rft.date=2014-06-01&rft.volume=28&rft.issue=6&rft.spage=899&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=1944-9917&rft_id=info:doi/10.1210%2Fme.2014-1051 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-20 N1 - Date created - 2014-06-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Trends Biochem Sci. 2001 Jun;26(6):384-90 [11406412] Recent Prog Horm Res. 2002;57:339-55 [12017551] Mol Endocrinol. 2002 Oct;16(10):2188-201 [12351685] Nature. 1987 Oct 22-28;329(6141):734-6 [3670376] Nature. 1989 Mar 16;338(6212):271-4 [2922054] Cell. 1989 Jun 30;57(7):1131-8 [2500250] Mol Endocrinol. 1990 Feb;4(2):276-86 [2330006] Annu Rev Biochem. 1994;63:451-86 [7979245] Cell Stress Chaperones. 2004 Autumn;9(3):243-52 [15544162] J Bone Miner Res. 2005 Nov;20(11):1992-2001 [16234973] Mol Cell Endocrinol. 2005 Dec 21;245(1-2):53-9 [16298037] J Biol Chem. 2006 Sep 8;281(36):26683-92 [16847062] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15847-51 [17895382] Endocrinology. 2008 Aug;149(8):4168-76 [18467444] Mol Cell Endocrinol. 2008 Aug 13;290(1-2):24-30 [18534740] Endocrinology. 2008 Nov;149(11):5328-34 [18635656] J Comput Biol. 2009 Feb;16(2):317-29 [19193149] Proc Natl Acad Sci U S A. 2009 Apr 28;106(17):7221-6 [19359483] J Neurosci. 2009 Jul 22;29(29):9390-5 [19625529] Environ Health Perspect. 2009 Jul;117(7):1155-61 [19654927] Mol Endocrinol. 2009 Oct;23(10):1544-55 [19574448] Diabetes. 2009 Oct;58(10):2292-302 [19587358] Mol Endocrinol. 2009 Dec;23(12):2111-6 [19812388] J Biol Chem. 2010 Jan 22;285(4):2676-85 [19920132] Mol Endocrinol. 2010 Feb;24(2):323-34 [20053716] Biol Reprod. 2010 Apr;82(4):783-90 [20056671] Biol Reprod. 2010 May;82(5):991-9 [20130264] Endocrinology. 2010 Jun;151(6):2811-8 [20308531] J Bone Miner Res. 2010 Apr;25(4):769-81 [19821774] Nucleic Acids Res. 2007;35(10):3465-77 [17478511] Mol Cell Biol. 2010 Aug;30(16):3943-55 [20547749] FASEB J. 2010 Dec;24(12):4660-7 [20667977] J Clin Invest. 2011 Feb;121(2):604-12 [21245576] Bone. 2011 Aug;49(2):208-16 [21458604] FASEB J. 2012 Mar;26(3):1218-27 [22155565] Mol Cell Endocrinol. 2012 Jun 24;357(1-2):108-18 [22115959] Mol Endocrinol. 2012 May;26(5):887-98 [22446102] J Cell Biochem. 2012 Jul;113(7):2248-55 [22573547] Proc Natl Acad Sci U S A. 2012 May 22;109(21):E1334-43 [22538816] Mol Endocrinol. 2012 Aug;26(8):1428-42 [22638070] Genes Brain Behav. 2012 Oct;11(7):828-36 [22883149] Endocrinology. 2012 Nov;153(11):5325-33 [23015293] Cancer Res. 2013 Aug 15;73(16):5130-9 [23803465] Proc Natl Acad Sci U S A. 2014 Jan 14;111(2):E283-90 [24371309] Steroids. 2014 Mar;81:88-98 [24252383] Endocrinology. 2007 Nov;148(11):5288-94 [17673514] Mol Cell Biol. 2007 Feb;27(4):1516-30 [17158928] Endocrinology. 2007 Apr;148(4):1902-10 [17204553] Proc Natl Acad Sci U S A. 2007 May 8;104(19):8173-7 [17470805] Proc Natl Acad Sci U S A. 2010 Jul 20;107(29):13057-62 [20616010] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/me.2014-1051 ER - TY - JOUR T1 - Breast cancer risk after occupational solvent exposure: the influence of timing and setting. AN - 1531956773; 24879566 AB - Organic solvents are ubiquitous in occupational settings where they may contribute to risks for carcinogenesis. However, there is limited information on organic solvents as human breast carcinogens. We examined the relationship between occupational exposure to solvents and breast cancer in a prospective study of 47,661 women with an occupational history in the Sister Study cohort. Occupational solvent exposure was categorized using self-reported job-specific solvent use collected at baseline. Multivariable Cox regression analyses were used to assess breast cancer risk, adjusting for established breast cancer risk factors. A total of 1,798 women were diagnosed with breast cancer during follow-up, including 1,255 invasive cases. Overall the risk of invasive breast cancer was not associated with lifetime exposure to solvents [HR, 1.04; 95% confidence interval (CI), 0.88-1.24]. Parous women who worked with solvents before their first full-term birth had an increased risk of estrogen receptor-positive invasive breast cancer compared with women who never worked with solvents (HR, 1.39; 95% CI, 1.03-1.86). A significantly elevated risk for estrogen receptor-positive invasive breast cancer was associated with solvent exposure among clinical laboratory technologists and technicians (HR, 2.00; 95% CI, 1.07-3.73). Occupational exposure to solvents before first birth, a critical period of breast tissue differentiation, may result in increased vulnerability for breast cancer. Our findings suggest a need for future studies in this area to focus on exposure time windows and solvent types in different occupational settings. ©2014 American Association for Cancer Research. JF - Cancer research AU - Ekenga, Christine C AU - Parks, Christine G AU - D'Aloisio, Aimee A AU - DeRoo, Lisa A AU - Sandler, Dale P AD - Authors' Affiliations: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, North Carolina; and Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway christine.ekenga@nih.gov. ; Authors' Affiliations: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, North Carolina; and Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway. ; Authors' Affiliations: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, North Carolina; and Department of Global Public Health and Primary Care, University of Bergen, Bergen, NorwayAuthors' Affiliations: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Department of Health and Human Services, Research Triangle Park, North Carolina; and Department of Global Public Health and Primary Care, University of Bergen, Bergen, Norway. Y1 - 2014/06/01/ PY - 2014 DA - 2014 Jun 01 SP - 3076 EP - 3083 VL - 74 IS - 11 KW - Receptors, Estrogen KW - 0 KW - Solvents KW - Index Medicus KW - Self Report KW - Prospective Studies KW - Risk Factors KW - Humans KW - Cohort Studies KW - Middle Aged KW - Receptors, Estrogen -- metabolism KW - United States -- epidemiology KW - Puerto Rico -- epidemiology KW - Female KW - Occupational Exposure -- statistics & numerical data KW - Occupational Diseases -- metabolism KW - Solvents -- poisoning KW - Occupational Exposure -- adverse effects KW - Breast Neoplasms -- metabolism KW - Occupational Diseases -- epidemiology KW - Breast Neoplasms -- epidemiology KW - Breast Neoplasms -- chemically induced KW - Occupational Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1531956773?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Breast+cancer+risk+after+occupational+solvent+exposure%3A+the+influence+of+timing+and+setting.&rft.au=Ekenga%2C+Christine+C%3BParks%2C+Christine+G%3BD%27Aloisio%2C+Aimee+A%3BDeRoo%2C+Lisa+A%3BSandler%2C+Dale+P&rft.aulast=Ekenga&rft.aufirst=Christine&rft.date=2014-06-01&rft.volume=74&rft.issue=11&rft.spage=3076&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-13-2430 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-28 N1 - Date created - 2014-06-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Ind Med. 2000 Apr;37(4):349-52 [10706746] J Natl Cancer Inst. 2013 Apr 17;105(8):515-25 [23449445] Environ Health Perspect. 2002 Aug;110(8):805-11 [12153763] Environ Health Perspect. 2003 Jun;111(8):1007-19 [12826474] Radiat Res. 2003 Dec;160(6):707-17 [14640793] Carcinogenesis. 1995 Feb;16(2):173-9 [7859345] Cancer Epidemiol Biomarkers Prev. 1995 Jul-Aug;4(5):567-71 [7549816] Am J Ind Med. 1997 Jul;32(1):1-14 [9131206] IARC Monogr Eval Carcinog Risks Hum. 1995;63:33-477 [9139128] Occup Environ Med. 1998 Mar;55(3):161-71 [9624267] Am J Ind Med. 1998 Nov;34(5):477-83 [9787852] Epidemiology. 1999 Jan;10(1):37-48 [9888278] Am J Ind Med. 1999 Jul;36(1):43-7 [10361585] Am J Ind Med. 1999 Jul;36(1):48-53 [10361586] Scand J Work Environ Health. 1999 Jun;25(3):215-21 [10450771] Cancer Epidemiol Biomarkers Prev. 2005 Jan;14(1):61-6 [15668477] Am J Ind Med. 2005 Sep;48(3):157-67 [16094615] Int J Cancer. 2007 Jul 15;121(2):386-94 [17372900] Cancer Causes Control. 2007 Nov;18(9):947-55 [17632764] Environ Health Perspect. 2007 Oct;115(10):1406-14 [17938728] BMC Med Res Methodol. 2008;8:70 [18973665] Endocr Rev. 2009 Jun;30(4):293-342 [19502515] Environ Health Perspect. 2010 Mar;118(3):375-81 [20194067] Occup Environ Med. 2010 Apr;67(4):263-9 [20360196] Environ Health. 2010;9:40 [20646273] Occup Environ Med. 2010 Nov;67(11):722-9 [19819862] Arch Intern Med. 2011 Jan 24;171(2):125-33 [21263102] Am J Ind Med. 2011 Jul;54(7):499-509 [21472744] Environ Health. 2012;11:87 [23164221] J Mammary Gland Biol Neoplasia. 2013 Mar;18(1):43-61 [23417729] Environ Health Perspect. 2001 Jul;109(7):699-703 [11485868] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/0008-5472.CAN-13-2430 ER - TY - JOUR T1 - Predictive value of a proteomic signature in patients with non-small-cell lung cancer treated with second-line erlotinib or chemotherapy (PROSE): a biomarker-stratified, randomised phase 3 trial. AN - 1530958099; 24831979 AB - An established multivariate serum protein test can be used to classify patients according to whether they are likely to have a good or poor outcome after treatment with EGFR tyrosine-kinase inhibitors. We assessed the predictive power of this test in the comparison of erlotinib and chemotherapy in patients with non-small-cell lung cancer. From Feb 26, 2008, to April 11, 2012, patients (aged ≥18 years) with histologically or cytologically confirmed, second-line, stage IIIB or IV non-small-cell lung cancer were enrolled in 14 centres in Italy. Patients were stratified according to a minimisation algorithm by Eastern Cooperative Oncology Group performance status, smoking history, centre, and masked pretreatment serum protein test classification, and randomly assigned centrally in a 1:1 ratio to receive erlotinib (150 mg/day, orally) or chemotherapy (pemetrexed 500 mg/m(2), intravenously, every 21 days, or docetaxel 75 mg/m(2), intravenously, every 21 days). The proteomic test classification was masked for patients and investigators who gave treatments, and treatment allocation was masked for investigators who generated the proteomic classification. The primary endpoint was overall survival and the primary hypothesis was the existence of a significant interaction between the serum protein test classification and treatment. Analyses were done on the per-protocol population. This trial is registered with ClinicalTrials.gov, number NCT00989690. 142 patients were randomly assigned to chemotherapy and 143 to erlotinib, and 129 (91%) and 134 (94%), respectively, were included in the per-protocol analysis. 88 (68%) patients in the chemotherapy group and 96 (72%) in the erlotinib group had a proteomic test classification of good. Median overall survival was 9·0 months (95% CI 6·8-10·9) in the chemotherapy group and 7·7 months (5·9-10·4) in the erlotinib group. We noted a significant interaction between treatment and proteomic classification (pinteraction=0·017 when adjusted for stratification factors; pinteraction=0·031 when unadjusted for stratification factors). Patients with a proteomic test classification of poor had worse survival on erlotinib than on chemotherapy (hazard ratio 1·72 [95% CI 1·08-2·74], p=0·022). There was no significant difference in overall survival between treatments for patients with a proteomic test classification of good (adjusted HR 1·06 [0·77-1·46], p=0·714). In the group of patients who received chemotherapy, the most common grade 3 or 4 toxic effect was neutropenia (19 [15%] vs one [<1%] in the erlotinib group), whereas skin toxicity (one [<1%] vs 22 [16%]) was the most frequent in the erlotinib group. Our findings indicate that serum protein test status is predictive of differential benefit in overall survival for erlotinib versus chemotherapy in the second-line setting. Patients classified as likely to have a poor outcome have better outcomes on chemotherapy than on erlotinib. Italian Ministry of Health, Italian Association of Cancer Research, and Biodesix. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - The Lancet. Oncology AU - Gregorc, Vanesa AU - Novello, Silvia AU - Lazzari, Chiara AU - Barni, Sandro AU - Aieta, Michele AU - Mencoboni, Manlio AU - Grossi, Francesco AU - De Pas, Tommaso AU - de Marinis, Filippo AU - Bearz, Alessandra AU - Floriani, Irene AU - Torri, Valter AU - Bulotta, Alessandra AU - Cattaneo, Angela AU - Grigorieva, Julia AU - Tsypin, Maxim AU - Roder, Joanna AU - Doglioni, Claudio AU - Levra, Matteo Giaj AU - Petrelli, Fausto AU - Foti, Silvia AU - Viganò, Mariagrazia AU - Bachi, Angela AU - Roder, Heinrich AD - Department of Medical Oncology, Istituto di Ricovero e Cura a Carattere Scientifico, Ospedale San Raffaele, Milan, Italy. Electronic address: vanesa.gregorc@hsr.it. ; Department of Oncology, University of Turin, Azienda Ospedaliera Universitaria San Luigi Orbassano, Turin, Italy. ; Department of Medical Oncology, Istituto di Ricovero e Cura a Carattere Scientifico, Ospedale San Raffaele, Milan, Italy. ; Division of Medical Oncology, Department of Medical Oncology, Azienda Ospedaliera Treviglio, Treviglio, Italy. ; Division of Medical Oncology, Centro di Riferimento Oncologico di Basilicata, Istituto di Ricovero e Cura a Carattere Scientifico, Rionero in Vulture, Italy. ; Oncology Unit, Villa Scassi Hospital, Azienda Sanitaria Locale 3, Genoa, Italy. ; Lung Cancer Unit, Istituto di Ricovero e Cura a Carattere Scientifico, Azienda Ospedaliera Universitaria San Martino, Istituto Nazionale per la Ricerca sul Cancro, Genoa, Italy. ; Division of Thoracic Oncology, European Institute of Oncology, Milan, Italy. ; Division of Thoracic Oncology, European Institute of Oncology, Milan, Italy; 1st Oncological Pulmonary Unit, San Camillo, High Specialization Hospital, Rome, Italy. ; Department of Medical Oncology, National Cancer Institute of Aviano, Aviano, Italy. ; Department of Oncology, Istituto di Ricovero e Cura a Carattere Scientifico-Istituto di Richerche Farmacologiche Mario Negri, Milan, Italy. ; Biodesix, Boulder, CO, USA. ; Università Vita-Salute San Raffaele, School of Medicine, Department of Pathology, Istituto di Ricovero e Cura a Carattere Scientifico, Ospedale San Raffaele, Milan, Italy. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 713 EP - 721 VL - 15 IS - 7 KW - Biomarkers, Tumor KW - 0 KW - Blood Proteins KW - Protein Kinase Inhibitors KW - Quinazolines KW - Erlotinib Hydrochloride KW - DA87705X9K KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Disease-Free Survival KW - Receptor, Epidermal Growth Factor -- genetics KW - Humans KW - Male KW - Female KW - Carcinoma, Non-Small-Cell Lung -- blood KW - Protein Kinase Inhibitors -- therapeutic use KW - Carcinoma, Non-Small-Cell Lung -- mortality KW - Lung Neoplasms -- blood KW - Proteomics KW - Lung Neoplasms -- drug therapy KW - Quinazolines -- therapeutic use KW - Lung Neoplasms -- mortality KW - Carcinoma, Non-Small-Cell Lung -- drug therapy KW - Blood Proteins -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1530958099?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Oncology&rft.atitle=Predictive+value+of+a+proteomic+signature+in+patients+with+non-small-cell+lung+cancer+treated+with+second-line+erlotinib+or+chemotherapy+%28PROSE%29%3A+a+biomarker-stratified%2C+randomised+phase+3+trial.&rft.au=Gregorc%2C+Vanesa%3BNovello%2C+Silvia%3BLazzari%2C+Chiara%3BBarni%2C+Sandro%3BAieta%2C+Michele%3BMencoboni%2C+Manlio%3BGrossi%2C+Francesco%3BDe+Pas%2C+Tommaso%3Bde+Marinis%2C+Filippo%3BBearz%2C+Alessandra%3BFloriani%2C+Irene%3BTorri%2C+Valter%3BBulotta%2C+Alessandra%3BCattaneo%2C+Angela%3BGrigorieva%2C+Julia%3BTsypin%2C+Maxim%3BRoder%2C+Joanna%3BDoglioni%2C+Claudio%3BLevra%2C+Matteo+Giaj%3BPetrelli%2C+Fausto%3BFoti%2C+Silvia%3BVigan%C3%B2%2C+Mariagrazia%3BBachi%2C+Angela%3BRoder%2C+Heinrich&rft.aulast=Gregorc&rft.aufirst=Vanesa&rft.date=2014-06-01&rft.volume=15&rft.issue=7&rft.spage=713&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Oncology&rft.issn=1474-5488&rft_id=info:doi/10.1016%2FS1470-2045%2814%2970162-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-30 N1 - Date created - 2014-05-29 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00989690; ClinicalTrials.gov N1 - SuppNotes - Comment In: Lancet Oncol. 2014 Jun;15(7):671-2 [24831978] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/S1470-2045(14)70162-7 ER - TY - JOUR T1 - Lenalidomide plus R-CHOP21 in elderly patients with untreated diffuse large B-cell lymphoma: results of the REAL07 open-label, multicentre, phase 2 trial. AN - 1530957903; 24831981 AB - Up to 40% of elderly patients with untreated diffuse large B-cell lymphoma (DLBCL) given a regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone every 21 days (R-CHOP21) relapse or develop refractory disease. Lenalidomide has high activity in relapsed or refractory aggressive B-cell lymphomas. In phase 2 of the REAL07 trial, we aimed to establish the safety and efficacy of the combination of lenalidomide and R-CHOP21 in elderly patients with untreated DLBCL. REAL07 was an open-label, multicentre trial that was done in 13 centres in Italy and one in Germany. Eligible patients were aged 60-80 years; had newly diagnosed, untreated, CD20-positive, Ann Arbor stage II-IV DLBCL or grade 3b follicular lymphoma; had an Eastern Cooperative Oncology Group performance status of 0-2; had an International Prognostic Index (IPI) risk of low-intermediate, intermediate-high, or high; and were fit according to comprehensive geriatric assessment. Participants were to receive 15 mg oral lenalidomide on days 1-14 of six 21-day cycles, and standard doses of R-CHOP21 chemotherapy (375 mg/m(2) intravenous rituximab, 750 mg/m(2) intravenous cyclophosphamide, 50 mg/m(2) intravenous doxorubicin, and 1·4 mg/m(2) intravenous vincristine on day 1, and 40 mg/m(2) oral prednisone on days 1-5). The primary endpoint was frequency of overall response (complete response [CR] and partial response [PR]), which was assessed by (18)F-fluorodeoxyglucose ((18)F-FDG) PET at the end of the treatment. Analyses were by intention to treat. This trial is registered with ClinicalTrials.gov, number NCT00907348. 49 patients were included in phase 2: nine had been enrolled into phase 1 between Oct 23, 2008, and June 4, 2009, and had received the maximum tolerated dose of 15 mg lenalidomide; and 40 were enrolled into phase 2 between April 28, 2010, and June 3, 2011. 45 patients (92%, 95% CI 81-97) achieved a response (42 [86%] CR; three [6%] PR). Three patients (6%) did not respond and one (2%) died for reasons unrelated to treatment or disease. 277 (94%) of 294 planned cycles of lenalidomide and R-CHOP21 were completed. Grade 3-4 neutropenia was reported in 87 cycles (31%), grade 3-4 leukopenia in 77 (28%), and grade 3-4 thrombocytopenia in 35 (13%). No grade 4 non-haematological adverse events were reported. No patients died during the study as a result of toxic effects. Lenalidomide with R-CHOP21 is effective and safe in elderly patients with untreated DLBCL. Fondazione Italiana Linfomi and Celgene. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - The Lancet. Oncology AU - Vitolo, Umberto AU - Chiappella, Annalisa AU - Franceschetti, Silvia AU - Carella, Angelo Michele AU - Baldi, Ileana AU - Inghirami, Giorgio AU - Spina, Michele AU - Pavone, Vincenzo AU - Ladetto, Marco AU - Liberati, Anna Marina AU - Molinari, Anna Lia AU - Zinzani, Pierluigi AU - Salvi, Flavia AU - Fattori, Pier Paolo AU - Zaccaria, Alfonso AU - Dreyling, Martin AU - Botto, Barbara AU - Castellino, Alessia AU - Congiu, Angela AU - Gaudiano, Marcello AU - Zanni, Manuela AU - Ciccone, Giovannino AU - Gaidano, Gianluca AU - Rossi, Giuseppe AU - Fondazione Italiana Linfomi AD - Hematology, Azienda Ospedaliero Universitaria Città della Salute e della Scienza di Torino, Turin, Italy. Electronic address: uvitolo@cittadellasalute.to.it. ; Hematology, Azienda Ospedaliero Universitaria Città della Salute e della Scienza di Torino, Turin, Italy. ; Division of Hematology, Department of Translational Medicine, Amedeo Avogadro University of Eastern Piedmont, Azienda Ospedaliero-Universitaria Maggiore della Carità, Novara, Italy. ; Unit of Hematology 1, Istituto di Ricovero e Cura a Carattere Scientifico Hospital and University, Istituto dei Tumori San Martino, Genoa, Italy. ; Unit of Biostatistics, Epidemiology and Public Health, Department of Cardiac, Thoracic and Vascular Sciences, University of Padua, Padua, Italy. ; Department of Molecular Biotechnology and Health Science and Center for Experimental Research and Medical Studies, University of Turin, Turin, Italy; Department of Pathology and Laboratory Medicine, Weill Cornell Medical College, New York, NY, USA. ; Division of Medical Oncology A, Centro di Riferimento Oncologico Aviano National Cancer Institute, Aviano, Italy. ; Unit of Hematology and Hemopoietic Stem Cell Transplantation, Ospedale Cardinale G Panico, Tricase, Italy. ; Department of Molecular Biotechnologies and Health Sciences, University of Turin, Turin, Italy. ; Università degli studi di Perugia, Azienda Ospedaliera Santa Maria, Terni, Italy. ; Department of Oncology and Hematology, Infermi Hospital, Rimini, Italy. ; Institute of Hematology Lorenzo ed Ariosto Seràgnoli, University of Bologna, Bologna, Italy. ; Hematology Unit, S S Antonio e Biagio e Cesare Arrigo Hospital, Alessandria, Italy. ; Istituto Scientifico Romagnolo per lo studio e la Cura dei Tumori, Istituti di Ricovero e Cura a Carattere Scientifico, Meldola, Italy. ; Hematology Unit, Department of Oncology and Hematology, Santa Maria delle Croci Hospital, Ravenna, Italy. ; Medizinische Klinik und Poliklinik III, Klinikum der Universität München, Munich, Germany. ; Unit of Clinical Epidemiology, Azienda Ospedaliero Universitaria Città della Salute e della Scienza di Torino and Centro di Riferimento per l'Epidemiologia e la Prevenzione Oncologica in Piemonte, Turin, Italy. ; Struttura Complessa Ematologia e Dipartimento Oncologia Medica, Spedali Civili, Brescia, Italy. ; Fondazione Italiana Linfomi Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 730 EP - 737 VL - 15 IS - 7 KW - Antibodies, Monoclonal, Murine-Derived KW - 0 KW - R-CHOP protocol KW - Thalidomide KW - 4Z8R6ORS6L KW - Vincristine KW - 5J49Q6B70F KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - lenalidomide KW - F0P408N6V4 KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Doxorubicin -- adverse effects KW - Vincristine -- adverse effects KW - Thalidomide -- adverse effects KW - Humans KW - Vincristine -- administration & dosage KW - Aged KW - Antibodies, Monoclonal, Murine-Derived -- adverse effects KW - Doxorubicin -- administration & dosage KW - Cyclophosphamide -- adverse effects KW - Prednisone -- adverse effects KW - Aged, 80 and over KW - Antibodies, Monoclonal, Murine-Derived -- administration & dosage KW - Thalidomide -- administration & dosage KW - Middle Aged KW - Prednisone -- administration & dosage KW - Female KW - Male KW - Thalidomide -- analogs & derivatives KW - Lymphoma, Large B-Cell, Diffuse -- mortality KW - Lymphoma, Large B-Cell, Diffuse -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1530957903?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Oncology&rft.atitle=Lenalidomide+plus+R-CHOP21+in+elderly+patients+with+untreated+diffuse+large+B-cell+lymphoma%3A+results+of+the+REAL07+open-label%2C+multicentre%2C+phase+2+trial.&rft.au=Vitolo%2C+Umberto%3BChiappella%2C+Annalisa%3BFranceschetti%2C+Silvia%3BCarella%2C+Angelo+Michele%3BBaldi%2C+Ileana%3BInghirami%2C+Giorgio%3BSpina%2C+Michele%3BPavone%2C+Vincenzo%3BLadetto%2C+Marco%3BLiberati%2C+Anna+Marina%3BMolinari%2C+Anna+Lia%3BZinzani%2C+Pierluigi%3BSalvi%2C+Flavia%3BFattori%2C+Pier+Paolo%3BZaccaria%2C+Alfonso%3BDreyling%2C+Martin%3BBotto%2C+Barbara%3BCastellino%2C+Alessia%3BCongiu%2C+Angela%3BGaudiano%2C+Marcello%3BZanni%2C+Manuela%3BCiccone%2C+Giovannino%3BGaidano%2C+Gianluca%3BRossi%2C+Giuseppe%3BFondazione+Italiana+Linfomi&rft.aulast=Vitolo&rft.aufirst=Umberto&rft.date=2014-06-01&rft.volume=15&rft.issue=7&rft.spage=730&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Oncology&rft.issn=1474-5488&rft_id=info:doi/10.1016%2FS1470-2045%2814%2970191-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-30 N1 - Date created - 2014-05-29 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00907348; ClinicalTrials.gov N1 - SuppNotes - Comment In: Lancet Oncol. 2014 Jun;15(7):674-5 [24872095] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/S1470-2045(14)70191-3 ER - TY - JOUR T1 - A recurrent neomorphic mutation in MYOD1 defines a clinically aggressive subset of embryonal rhabdomyosarcoma associated with PI3K-AKT pathway mutations. AN - 1530319319; 24793135 AB - Rhabdomyosarcoma, a cancer of skeletal muscle lineage, is the most common soft-tissue sarcoma in children. Major subtypes of rhabdomyosarcoma include alveolar (ARMS) and embryonal (ERMS) tumors. Whereas ARMS tumors typically contain translocations generating PAX3-FOXO1 or PAX7-FOXO1 fusions that block terminal myogenic differentiation, no functionally comparable genetic event has been found in ERMS tumors. Here we report the discovery, through whole-exome sequencing, of a recurrent somatic mutation encoding p.Leu122Arg in the myogenic transcription factor MYOD1 in a distinct subset of ERMS tumors with poor outcomes that also often contain mutations altering PI3K-AKT pathway components. Previous mutagenesis studies had shown that MYOD1 with a p.Leu122Arg substitution can block wild-type MYOD1 function and bind to MYC consensus sequences, suggesting a possible switch from differentiation to proliferation. Our functional data now confirm this prediction. Thus, MYOD1 p.Leu122Arg defines a subset of rhabdomyosarcomas eligible for high-risk protocols and the development of targeted therapeutics. JF - Nature genetics AU - Kohsaka, Shinji AU - Shukla, Neerav AU - Ameur, Nabahet AU - Ito, Tatsuo AU - Ng, Charlotte K Y AU - Wang, Lu AU - Lim, Diana AU - Marchetti, Angela AU - Viale, Agnes AU - Pirun, Mono AU - Socci, Nicholas D AU - Qin, Li-Xuan AU - Sciot, Raf AU - Bridge, Julia AU - Singer, Samuel AU - Meyers, Paul AU - Wexler, Leonard H AU - Barr, Frederic G AU - Dogan, Snjezana AU - Fletcher, Jonathan A AU - Reis-Filho, Jorge S AU - Ladanyi, Marc AD - 1] Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA. [2] Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA. [3]. ; 1] Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York, USA. [2]. ; Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Genomics Core Laboratory, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Bioinformatics Core Facility, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Department of Pathology, University Hospital Gasthuisberg and University of Leuven, Leuven, Belgium. ; Department of Pathology, University of Nebraska Medical Center, Omaha, Nebraska, USA. ; Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York, USA. ; Laboratory of Pathology, National Cancer Institute, Bethesda, Maryland, USA. ; Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, USA. ; 1] Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA. [2] Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, USA. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 595 EP - 600 VL - 46 IS - 6 KW - MyoD Protein KW - 0 KW - MyoD1 myogenic differentiation protein KW - Phosphatidylinositol 3-Kinases KW - EC 2.7.1.- KW - AKT1 protein, human KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins c-akt KW - Index Medicus KW - Young Adult KW - Animals KW - DNA Mutational Analysis KW - Humans KW - Mice KW - Amino Acid Sequence KW - Child KW - Cell Proliferation KW - Mutagenesis KW - Genotype KW - Exome KW - Adult KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Adolescent KW - Transcriptome KW - Male KW - Female KW - High-Throughput Nucleotide Sequencing KW - Proto-Oncogene Proteins c-akt -- genetics KW - Phosphatidylinositol 3-Kinases -- genetics KW - Rhabdomyosarcoma, Embryonal -- genetics KW - MyoD Protein -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1530319319?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+genetics&rft.atitle=A+recurrent+neomorphic+mutation+in+MYOD1+defines+a+clinically+aggressive+subset+of+embryonal+rhabdomyosarcoma+associated+with+PI3K-AKT+pathway+mutations.&rft.au=Kohsaka%2C+Shinji%3BShukla%2C+Neerav%3BAmeur%2C+Nabahet%3BIto%2C+Tatsuo%3BNg%2C+Charlotte+K+Y%3BWang%2C+Lu%3BLim%2C+Diana%3BMarchetti%2C+Angela%3BViale%2C+Agnes%3BPirun%2C+Mono%3BSocci%2C+Nicholas+D%3BQin%2C+Li-Xuan%3BSciot%2C+Raf%3BBridge%2C+Julia%3BSinger%2C+Samuel%3BMeyers%2C+Paul%3BWexler%2C+Leonard+H%3BBarr%2C+Frederic+G%3BDogan%2C+Snjezana%3BFletcher%2C+Jonathan+A%3BReis-Filho%2C+Jorge+S%3BLadanyi%2C+Marc&rft.aulast=Kohsaka&rft.aufirst=Shinji&rft.date=2014-06-01&rft.volume=46&rft.issue=6&rft.spage=595&rft.isbn=&rft.btitle=&rft.title=Nature+genetics&rft.issn=1546-1718&rft_id=info:doi/10.1038%2Fng.2969 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-08 N1 - Date created - 2014-05-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Genet. 1993 Feb;3(2):113-7 [8098985] Nat Genet. 1993 Nov;5(3):230-5 [8275086] J Clin Invest. 1994 Jan;93(1):5-9 [8282820] Cancer Res. 1994 Jun 1;54(11):2869-72 [8187070] Genome Biol. 2002;3(6):RESEARCH0030 [12093377] Cancer Biol Ther. 2002 Mar-Apr;1(2):97-104 [12170781] J Clin Oncol. 2003 Jan 1;21(1):78-84 [12506174] Biostatistics. 2003 Apr;4(2):249-64 [12925520] Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13567-72 [14597713] Genome Biol. 2004;5(10):R80 [15461798] Cell. 1987 Dec 24;51(6):987-1000 [3690668] Cancer Res. 1989 Nov 15;49(22):6324-7 [2680062] Proc Natl Acad Sci U S A. 1990 Mar;87(6):2182-6 [2315312] Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9010-4 [1329087] J Cell Biol. 1994 Jun;125(5):1137-45 [8195295] Am J Surg Pathol. 2005 Aug;29(8):1106-13 [16006807] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517] Cell. 2008 Jun 13;133(6):1106-17 [18555785] Genome Biol. 2008;9(9):R137 [18798982] Am J Pathol. 2009 Feb;174(2):550-64 [19147825] J Clin Invest. 2009 Nov;119(11):3395-407 [19809159] Bioinformatics. 2010 Mar 1;26(5):589-95 [20080505] Cancer Res. 2010 Aug 15;70(16):6497-508 [20663909] Proc Natl Acad Sci U S A. 2011 May 31;108(22):E149-58 [21551099] Nature. 2012 Jan 19;481(7381):389-93 [22217937] Clin Cancer Res. 2012 Feb 1;18(3):748-57 [22142829] Cancer Cell. 2012 Mar 20;21(3):362-73 [22439933] Pediatr Blood Cancer. 2012 Jul 15;59(1):5-10 [22378628] Cancer Cell. 2012 Jul 10;22(1):117-30 [22789543] Genes Dev. 2012 Dec 15;26(24):2763-79 [23249738] Oncogene. 2013 Jan 31;32(5):651-62 [22710712] Oncol Rep. 2013 Aug;30(2):968-78 [23733015] Arch Pathol Lab Med. 2013 Aug;137(8):1155-8 [23899074] Comment In: Bull Cancer. 2014 Sep;101(9):776-7 [25295632] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ng.2969 ER - TY - JOUR T1 - Essential Role for the Response Regulator PmrA in Coxiella burnetii Type 4B Secretion and Colonization of Mammalian Host Cells AN - 1529932114; 19846360 AB - Successful host cell colonization by the Q fever pathogen, Coxiella burnetii, requires translocation of effector proteins into the host cytosol by a Dot/Icm type 4B secretion system (T4BSS). In Legionella pneumophila, the two-component system (TCS) PmrAB regulates the Dot/Icm T4BSS and several additional physiological processes associated with pathogenesis. Because PmrA consensus regulatory elements are associated with some dot/icm and substrate genes, a similar role for PmrA in regulation of the C. burnetii T4BSS has been proposed. Here, we constructed a C. burnetii pmrA deletion mutant to directly probe PmrA-mediated gene regulation. Compared to wild-type bacteria, C. burnetii Delta pmrA exhibited severe intracellular growth defects that coincided with failed secretion of effector proteins. Luciferase gene reporter assays demonstrated PmrA-dependent expression of 5 of 7 dot/icm operons and 9 of 11 effector-encoding genes with a predicted upstream PmrA regulatory element. Mutational analysis verified consensus sequence nucleotides required for PmrA-directed transcription. RNA sequencing and whole bacterial cell mass spectrometry of wild-type C. burnetii and the Delta pmrA mutant uncovered new components of the PmrA regulon, including several genes lacking PmrA motifs that encoded Dot/Icm substrates. Collectively, our results indicate that the PmrAB TCS is a critical virulence factor that regulates C. burnetii Dot/Icm secretion. The presence of PmrA-responsive genes lacking PmrA regulatory elements also suggests that the PmrAB TCS controls expression of regulatory systems associated with the production of additional C. burnetii proteins involved in host cell parasitism. JF - Journal of Bacteriology AU - Beare, Paul A AU - Sandoz, Kelsi M AU - Larson, Charles L AU - Howe, Dale AU - Kronmiller, Brent 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 - 2014/06// PY - 2014 DA - June 2014 SP - 1925 EP - 1940 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 196 IS - 11 SN - 0021-9193, 0021-9193 KW - Microbiology Abstracts B: Bacteriology KW - Legionella pneumophila KW - Deletion mutant KW - virulence factors KW - Nucleotide sequence KW - Regulatory sequences KW - Secretion KW - DNA probes KW - Transcription KW - Pathogens KW - Parasitism KW - Mass spectroscopy KW - Coxiella burnetii KW - Colonization KW - RNA KW - Gene regulation KW - Cytosol KW - Conserved sequence KW - Operons KW - Q fever KW - Translocation KW - J 02310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1529932114?accountid=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=Essential+Role+for+the+Response+Regulator+PmrA+in+Coxiella+burnetii+Type+4B+Secretion+and+Colonization+of+Mammalian+Host+Cells&rft.au=Beare%2C+Paul+A%3BSandoz%2C+Kelsi+M%3BLarson%2C+Charles+L%3BHowe%2C+Dale%3BKronmiller%2C+Brent%3BHeinzen%2C+Robert+A&rft.aulast=Beare&rft.aufirst=Paul&rft.date=2014-06-01&rft.volume=196&rft.issue=11&rft.spage=1925&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.01532-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Number of references - 76 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Deletion mutant; virulence factors; DNA probes; Secretion; Regulatory sequences; Nucleotide sequence; Transcription; Pathogens; Parasitism; Mass spectroscopy; Colonization; RNA; Gene regulation; Cytosol; Conserved sequence; Operons; Translocation; Q fever; Legionella pneumophila; Coxiella burnetii DO - http://dx.doi.org/10.1128/JB.01532-14 ER - TY - JOUR T1 - Evaluation of intracellular and extracellular trehalose as a cryoprotectant of stem cells obtained from umbilical cord blood. AN - 1529843315; 24769312 AB - Cord blood is a source of hematopoietic stem cells used in transplantation in which hematopoietic reconstitution is necessary. This transplant modality requires the cryopreservation of hematopoietic stem cells (HSCs). Dimethyl sulfoxide has been used as a cryoprotectant (CPA) in the cryopreservation of HSCs; however, it has been demonstrated that Me2SO exhibits toxic side effects to the human body. Due to its stability upon freezing, disaccharides such as trehalose have been investigated as a cryoprotectant. This study investigated the hypothesis that a cryopreservation solution containing intracellular and extracellular trehalose improves the recovery of stem cells after cryopreservation. After thawing, the cells were tested for their viability using the 7AAD stain, CD45+/CD34+ cells were assessed using flow cytometry and the MTT viability assay, and the proportion of hematopoietic progenitor cells was measured using the CFU assay. Our results showed the effectiveness of the solution containing intracellular and extracellular trehalose in the cryopreservation of cord blood cells, demonstrating that trehalose may be an optimal cryoprotectant when present both inside and outside of cells. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Cryobiology AU - Motta, Juliana Pessanha Rodrigues AU - Paraguassú-Braga, Flávio Henrique AU - Bouzas, Luis Fernando AU - Porto, Luís Cristóvão AD - Histocompatibility and Cryopreservation Laboratory, Department of Histology and Embryology, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Pav. Jose Roberto Feresin Moraes, Av Marechal Rondon 381, São Francisco Xavier, 20950-003 Rio de Janeiro, Brazil. ; Umbilical Cord Blood Bank, Bone Marrow Transplantation Unit, National Cancer Institute, Rio de Janeiro, Brazil. ; Histocompatibility and Cryopreservation Laboratory, Department of Histology and Embryology, Institute of Biology Roberto Alcantara Gomes, Rio de Janeiro State University, Pav. Jose Roberto Feresin Moraes, Av Marechal Rondon 381, São Francisco Xavier, 20950-003 Rio de Janeiro, Brazil. Electronic address: lcporto@uerj.br. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 343 EP - 348 VL - 68 IS - 3 KW - Cryoprotective Agents KW - 0 KW - Liposomes KW - Trehalose KW - B8WCK70T7I KW - Index Medicus KW - Cord blood KW - Liposome KW - Me(2)SO KW - Cryopreservation KW - Cells, Cultured KW - Humans KW - Female KW - Cell Survival KW - Fetal Blood -- cytology KW - Cryoprotective Agents -- analysis KW - Cryoprotective Agents -- metabolism KW - Trehalose -- analysis KW - Hematopoietic Stem Cells -- cytology KW - Trehalose -- administration & dosage KW - Cryopreservation -- methods KW - Hematopoietic Stem Cells -- metabolism KW - Trehalose -- metabolism KW - Cryoprotective Agents -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1529843315?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cryobiology&rft.atitle=Evaluation+of+intracellular+and+extracellular+trehalose+as+a+cryoprotectant+of+stem+cells+obtained+from+umbilical+cord+blood.&rft.au=Motta%2C+Juliana+Pessanha+Rodrigues%3BParaguass%C3%BA-Braga%2C+Fl%C3%A1vio+Henrique%3BBouzas%2C+Luis+Fernando%3BPorto%2C+Lu%C3%ADs+Crist%C3%B3v%C3%A3o&rft.aulast=Motta&rft.aufirst=Juliana+Pessanha&rft.date=2014-06-01&rft.volume=68&rft.issue=3&rft.spage=343&rft.isbn=&rft.btitle=&rft.title=Cryobiology&rft.issn=1090-2392&rft_id=info:doi/10.1016%2Fj.cryobiol.2014.04.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-05 N1 - Date created - 2014-05-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.cryobiol.2014.04.007 ER - TY - JOUR T1 - Sputum neutrophil counts are associated with more severe asthma phenotypes using cluster analysis AN - 1529150333; 24332216 AB - Background Clinical cluster analysis from the Severe Asthma Research Program (SARP) identified 5 asthma subphenotypes that represent the severity spectrum of early-onset allergic asthma, late-onset severe asthma, and severe asthma with chronic obstructive pulmonary disease characteristics. Analysis of induced sputum from a subset of SARP subjects showed 4 sputum inflammatory cellular patterns. Subjects with concurrent increases in eosinophil (>=2%) and neutrophil (>=40%) percentages had characteristics of very severe asthma. Objective To better understand interactions between inflammation and clinical subphenotypes, we integrated inflammatory cellular measures and clinical variables in a new cluster analysis. Methods Participants in SARP who underwent sputum induction at 3 clinical sites were included in this analysis (n = 423). Fifteen variables, including clinical characteristics and blood and sputum inflammatory cell assessments, were selected using factor analysis for unsupervised cluster analysis. Results Four phenotypic clusters were identified. Cluster A (n = 132) and B (n = 127) subjects had mild-to-moderate early-onset allergic asthma with paucigranulocytic or eosinophilic sputum inflammatory cell patterns. In contrast, these inflammatory patterns were present in only 7% of cluster C (n = 117) and D (n = 47) subjects who had moderate-to-severe asthma with frequent health care use despite treatment with high doses of inhaled or oral corticosteroids and, in cluster D, reduced lung function. The majority of these subjects (>83%) had sputum neutrophilia either alone or with concurrent sputum eosinophilia. Baseline lung function and sputum neutrophil percentages were the most important variables determining cluster assignment. Conclusion This multivariate approach identified 4 asthma subphenotypes representing the severity spectrum from mild-to-moderate allergic asthma with minimal or eosinophil-predominant sputum inflammation to moderate-to-severe asthma with neutrophil-predominant or mixed granulocytic inflammation. JF - Journal of Allergy and Clinical Immunology AU - Moore, Wendy C AU - Hastie, Annette T AU - Li, Xingnan AU - Li, Huashi AU - Busse, William W AU - Jarjour, Nizar N AU - Wenzel, Sally E AU - Peters, Stephen P AU - Meyers, Deborah A AU - Bleecker, Eugene R Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 1557 EP - 63.e5 CY - St. Louis PB - Elsevier Science Ltd. VL - 133 IS - 6 SN - 00916749 KW - Abstracting And Indexing Services KW - Cluster analysis KW - Asthma KW - Colleges & universities KW - Statistical methods KW - Age KW - Body mass index KW - Multivariate analysis KW - Family medical history KW - Discriminant analysis KW - Respiratory Function Tests KW - Granulocytes KW - Young Adult KW - Age Factors KW - Asthma -- blood KW - Risk Factors KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Asthma -- physiopathology KW - Severity of Illness Index KW - Phenotype KW - Sputum -- cytology KW - Neutrophils KW - Asthma -- diagnosis KW - Cluster Analysis KW - Leukocyte Count UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1529150333?accountid=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=Journal+of+Allergy+and+Clinical+Immunology&rft.atitle=Sputum+neutrophil+counts+are+associated+with+more+severe+asthma+phenotypes+using+cluster+analysis&rft.au=Moore%2C+Wendy+C%3BHastie%2C+Annette+T%3BLi%2C+Xingnan%3BLi%2C+Huashi%3BBusse%2C+William+W%3BJarjour%2C+Nizar+N%3BWenzel%2C+Sally+E%3BPeters%2C+Stephen+P%3BMeyers%2C+Deborah+A%3BBleecker%2C+Eugene+R&rft.aulast=Moore&rft.aufirst=Wendy&rft.date=2014-06-01&rft.volume=133&rft.issue=6&rft.spage=1557&rft.isbn=&rft.btitle=&rft.title=Journal+of+Allergy+and+Clinical+Immunology&rft.issn=00916749&rft_id=info:doi/10.1016%2Fj.jaci.2013.10.011 LA - English DB - ProQuest Central N1 - Copyright - Copyright Elsevier Limited Jun 2014 N1 - Last updated - 2014-07-19 DO - http://dx.doi.org/10.1016/j.jaci.2013.10.011 ER - TY - JOUR T1 - Effects of prenatal methamphetamine exposure on behavioral and cognitive findings at 7.5 years of age. AN - 1528884286; 24630350 AB - To examine child behavioral and cognitive outcomes after prenatal exposure to methamphetamine. We enrolled 412 mother-infant pairs (204 methamphetamine-exposed and 208 unexposed matched comparisons) in the Infant Development, Environment, and Lifestyle study. The 151 children exposed to methamphetamine and 147 comparisons who attended the 7.5-year visit were included. Exposure was determined by maternal self-report and/or positive meconium toxicology. Maternal interviews assessed behavioral and cognitive outcomes using the Conners' Parent Rating Scale-Revised: Short Form. After adjusting for covariates, children exposed to methamphetamine had significantly higher cognitive problems subscale scores than comparisons and were 2.8 times more likely to have cognitive problems scores that were above average on the Conners' Parent Rating Scale-Revised: Short Form. No association between prenatal methamphetamine exposure and behavioral problems, measured by the oppositional, hyperactivity, and attention-deficit/hyperactivity disorder index subscales, were found. Prenatal methamphetamine exposure was associated with increased cognitive problems, which may affect academic achievement and lead to increased negative behavioral outcomes. Copyright © 2014 Elsevier Inc. All rights reserved. JF - The Journal of pediatrics AU - Diaz, Sabrina D AU - Smith, Lynne M AU - LaGasse, Linda L AU - Derauf, Chris AU - Newman, Elana AU - Shah, Rizwan AU - Arria, Amelia AU - Huestis, Marilyn A AU - Della Grotta, Sheri AU - Dansereau, Lynne M AU - Neal, Charles AU - Lester, Barry M AD - LA Biomed Institute at Harbor-UCLA Medical Center and David Geffen School of Medicine at UCLA, Los Angeles, CA. ; LA Biomed Institute at Harbor-UCLA Medical Center and David Geffen School of Medicine at UCLA, Los Angeles, CA. Electronic address: smith@labiomed.org. ; Brown Center for the Study of Children at Risk, Warren Alpert Medical School of Brown University, Women and Infants Hospital, Providence, RI. ; Mayo Clinic, Rochester, MN. ; Department of Psychology, The University of Tulsa, Tulsa, OK. ; Blank Hospital Regional Child Protection Center-Iowa Health, Des Moines, IA. ; Center on Young Adult Health and Development, University of Maryland, School of Public Health, College Park, MD. ; Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD. ; John A. Burns School of Medicine, University of Hawaii, Honolulu, HI. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1333 EP - 1338 VL - 164 IS - 6 KW - Methamphetamine KW - 44RAL3456C KW - Abridged Index Medicus KW - Index Medicus KW - Severity of Illness Index KW - Amphetamine-Related Disorders -- epidemiology KW - Age Factors KW - Methamphetamine -- adverse effects KW - Humans KW - Retrospective Studies KW - Prognosis KW - Infant, Newborn KW - Child KW - Risk Assessment KW - Pregnancy KW - Child, Preschool KW - Infant KW - Case-Control Studies KW - Incidence KW - Amphetamine-Related Disorders -- diagnosis KW - Time Factors KW - Female KW - Male KW - Maternal Exposure -- adverse effects KW - Attention Deficit Disorder with Hyperactivity -- diagnosis KW - Attention Deficit Disorder with Hyperactivity -- epidemiology KW - Child Behavior KW - Prenatal Exposure Delayed Effects -- psychology KW - Cognition Disorders -- epidemiology KW - Prenatal Exposure Delayed Effects -- epidemiology KW - Prenatal Exposure Delayed Effects -- diagnosis KW - Cognition Disorders -- chemically induced KW - Cognition Disorders -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1528884286?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pediatrics&rft.atitle=Effects+of+prenatal+methamphetamine+exposure+on+behavioral+and+cognitive+findings+at+7.5+years+of+age.&rft.au=Diaz%2C+Sabrina+D%3BSmith%2C+Lynne+M%3BLaGasse%2C+Linda+L%3BDerauf%2C+Chris%3BNewman%2C+Elana%3BShah%2C+Rizwan%3BArria%2C+Amelia%3BHuestis%2C+Marilyn+A%3BDella+Grotta%2C+Sheri%3BDansereau%2C+Lynne+M%3BNeal%2C+Charles%3BLester%2C+Barry+M&rft.aulast=Diaz&rft.aufirst=Sabrina&rft.date=2014-06-01&rft.volume=164&rft.issue=6&rft.spage=1333&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pediatrics&rft.issn=1097-6833&rft_id=info:doi/10.1016%2Fj.jpeds.2014.01.053 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-18 N1 - Date created - 2014-05-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Obstet Gynecol. 2002 Mar;186(3):487-95 [11904612] Pediatrics. 2002 Dec;110(6):1182-92 [12456917] J Pers Assess. 2003 Jun;80(3):252-9 [12763699] JAMA. 2004 May 26;291(20):2448-56 [15161895] Child Abuse Negl. 1988;12(4):503-7 [3233516] Psychol Bull. 1992 Jan;111(1):127-55 [1539086] Child Abuse Negl. 1994 Jan;18(1):3-9 [7510211] Acta Paediatr. 1996 Feb;85(2):204-8 [8640051] Neurotoxicol Teratol. 1996 Nov-Dec;18(6):627-34 [8947939] J Am Acad Child Adolesc Psychiatry. 1997 Jan;36(1):123-31 [9000790] Integr Physiol Behav Sci. 1997 Jan-Mar;32(1):62-74 [9105915] Obstet Gynecol Clin North Am. 1998 Mar;25(1):119-38 [9547763] J Abnorm Child Psychol. 1998 Aug;26(4):257-68 [9700518] Psychiatry Res. 2004 Dec 15;132(2):95-106 [15598544] Pediatrics. 2006 Sep;118(3):1149-56 [16951010] Dev Psychol. 2006 Sep;42(5):913-28 [16953696] Addiction. 2007 Apr;102 Suppl 1:16-32 [17493050] Am J Drug Alcohol Abuse. 2007;33(2):281-9 [17497551] Curr Opin Obstet Gynecol. 2007 Dec;19(6):578-85 [18007137] Neurotoxicol Teratol. 2008 Jan-Feb;30(1):20-8 [18031987] Br J Clin Pharmacol. 2009 Apr;67(4):455-9 [19371319] J Pediatr. 2010 Aug;157(2):337-9 [20570284] Neurotoxicol Teratol. 2011 Jan-Feb;33(1):176-84 [21256431] Am J Perinatol. 2012 Mar;29(3):203-10 [21818727] Pediatrics. 2012 Apr;129(4):681-8 [22430455] Am J Perinatol. 2012 May;29(5):391-400 [22399214] J Pediatr. 2012 Sep;161(3):452-9 [22424953] Child Psychiatry Hum Dev. 2012 Dec;43(6):943-57 [22552952] Dev Neurosci. 2012;34(4):327-41 [22907274] J Dev Behav Pediatr. 2013 Jan;34(1):31-7 [23275056] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jpeds.2014.01.053 ER - TY - JOUR T1 - A novel trafficking-defective HCN4 mutation is associated with early-onset atrial fibrillation. AN - 1528873564; 24607718 AB - Atrial fibrillation (AF) is the most common arrhythmia, and a recent genome-wide association study identified the hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) as a novel AF susceptibility locus. HCN4 encodes for the cardiac pacemaker channel, and HCN4 mutations are associated with familial sinus bradycardia and AF. The purpose of this study was to determine whether novel variants in the coding region of HCN4 contribute to the susceptibility for AF. We sequenced the coding region of HCN4 for novel variants from 527 cases with early-onset AF from the Massachusetts General Hospital AF Study and 443 referents from the Framingham Heart Study. We used site-directed mutagenesis, cellular electrophysiology, immunocytochemistry, and confocal microscopy to functionally characterize novel variants. We found the frequency of novel coding HCN4 variants was 2-fold greater for individuals with AF (7 variants) compared to the referents (3 variants). We determined that of the 7 novel HCN4 variants in our AF cases, 1 (p.Pro257Ser, located in the amino-terminus adjacent to the first transmembrane spanning domain) did not traffic to cell membrane, whereas the remaining 6 were not functionally different from wild type. In addition, the 3 novel variants in our referents did not alter function compared to wild-type. Coexpression studies showed that the p.Pro257Ser mutant channel failed to colocalize with the wild-type HCN4 channel on the cell membrane. Our findings are consistent with HCN4 haploinsufficiency as the likely mechanism for early-onset AF in the p.Pro257Ser carrier. Copyright © 2014 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved. JF - Heart rhythm AU - Macri, Vincenzo AU - Mahida, Saagar N AU - Zhang, Michael L AU - Sinner, Moritz F AU - Dolmatova, Elena V AU - Tucker, Nathan R AU - McLellan, Micheal AU - Shea, Marisa A AU - Milan, David J AU - Lunetta, Kathryn L AU - Benjamin, Emelia J AU - Ellinor, Patrick T AD - Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts; Harvard Medical School, Boston, Massachusetts. ; Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts. ; Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts; Department of Medicine I, University Hospital Grosshadern, Ludwig-Maximilians University, Munich, Germany; National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts. ; Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, Massachusetts. ; National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts; Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts; Department of Biostatistics, Boston University School of Public Health, Boston, Massachusetts. ; National Heart, Lung, and Blood Institute's and Boston University's Framingham Heart Study, Framingham, Massachusetts; Department of Epidemiology, Boston University School of Public Health, Boston, Massachusetts; Preventive Medicine Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts; Cardiology Section, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts. ; Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts; Harvard Medical School, Boston, Massachusetts; Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, Massachusetts. Electronic address: ellinor@mgh.harvard.edu. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1055 EP - 1062 VL - 11 IS - 6 KW - HCN4 protein, human KW - 0 KW - Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels KW - Muscle Proteins KW - Potassium Channels KW - Index Medicus KW - Electrophysiology KW - Atrial fibrillation KW - HCN4 KW - Mutation KW - Mutagenesis, Site-Directed KW - Microscopy, Confocal KW - Animals KW - Cricetulus KW - Age of Onset KW - Electrophysiologic Techniques, Cardiac KW - Humans KW - CHO Cells KW - Middle Aged KW - Haploinsufficiency KW - Male KW - Female KW - Protein Transport KW - Muscle Proteins -- metabolism KW - Muscle Proteins -- genetics KW - Potassium Channels -- metabolism KW - Atrial Fibrillation -- genetics KW - Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels -- metabolism KW - Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels -- genetics KW - Potassium Channels -- genetics KW - Atrial Fibrillation -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1528873564?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Heart+rhythm&rft.atitle=A+novel+trafficking-defective+HCN4+mutation+is+associated+with+early-onset+atrial+fibrillation.&rft.au=Macri%2C+Vincenzo%3BMahida%2C+Saagar+N%3BZhang%2C+Michael+L%3BSinner%2C+Moritz+F%3BDolmatova%2C+Elena+V%3BTucker%2C+Nathan+R%3BMcLellan%2C+Micheal%3BShea%2C+Marisa+A%3BMilan%2C+David+J%3BLunetta%2C+Kathryn+L%3BBenjamin%2C+Emelia+J%3BEllinor%2C+Patrick+T&rft.aulast=Macri&rft.aufirst=Vincenzo&rft.date=2014-06-01&rft.volume=11&rft.issue=6&rft.spage=1055&rft.isbn=&rft.btitle=&rft.title=Heart+rhythm&rft.issn=1556-3871&rft_id=info:doi/10.1016%2Fj.hrthm.2014.03.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-12 N1 - Date created - 2014-05-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am Heart J. 2000 Oct;140(4):541-51 [11011325] J Biol Chem. 2002 Aug 16;277(33):29634-42 [12034718] J Biol Chem. 2002 Nov 15;277(46):43588-92 [12193608] J Biol Chem. 2002 Dec 13;277(50):48610-6 [12354768] J Clin Invest. 2003 May;111(10):1537-45 [12750403] Cardiovasc Res. 2004 Jul 1;63(1):60-8 [15194462] JAMA. 2004 Jun 16;291(23):2851-5 [15199036] J Biol Chem. 2004 Jun 25;279(26):27194-8 [15123648] N Engl J Med. 1982 Apr 29;306(17):1018-22 [7062992] Circulation. 1996 Dec 1;94(11):2953-60 [8941126] Genome Res. 2005 Jul;15(7):901-13 [15965027] N Engl J Med. 2006 Jan 12;354(2):151-7 [16407510] Br J Pharmacol. 2007 Jan;150(1):37-46 [17128289] J Physiol. 2007 Jul 15;582(Pt 2):675-93 [17478540] Circulation. 2007 Jul 31;116(5):463-70 [17646576] Nat Protoc. 2009;4(7):1073-81 [19561590] Physiol Rev. 2009 Jul;89(3):847-85 [19584315] Circulation. 2009 Nov 3;120(18):1752-60 [19841300] J Am Coll Cardiol. 2011 Jun 7;57(23):2317-27 [21636032] Epilepsia. 2012 Jan;53(1):87-100 [22150645] Circulation. 2012 May 1;125(17):2059-70 [22456474] Nat Genet. 2012 Jun;44(6):670-5 [22544366] Eur Heart J. 2013 Sep;34(35):2768-75 [23178648] J Physiol. 2013 Sep 1;591(Pt 17):4117-24 [23507880] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.hrthm.2014.03.002 ER - TY - JOUR T1 - Deleted in liver cancer-1 (DLC1): an emerging metastasis suppressor gene. AN - 1528341063; 24519699 AB - While significant progress continues to be made in the early detection and therapeutic management of primary tumors, the incidence of metastatic disease remains the major cause of mortality. Accordingly, the development of novel effective therapies that can ameliorate dissemination and secondary tumor growth are a clinical priority. The identification of genetic and functional alterations in cancer cells that affect factors implicated in the metastatic process is critical for designing preventive and therapeutic strategies. Evidence implicating the protein deleted in liver cancer-1 (DLC1), a Rho GTPase activator, in metastasis has accumulated to a point where DLC1 may be considered as a metastasis suppressor gene. This review presents evidence supporting an anti-metastatic role for DLC1 in several human cancers and discusses the mechanisms contributing to its inhibitory effects. In addition, promising opportunities for therapeutic interventions based on DLC1 function and downstream pathways involved in the metastatic process are considered. JF - Molecular diagnosis & therapy AU - Popescu, Nicholas C AU - Goodison, Steve AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Building 37, Room 4140, 37 Convent Dr., MSC 4262, Bethesda, MD, 20892-4262, USA, popescun@dc37a.nci.nih.gov. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 293 EP - 302 VL - 18 IS - 3 KW - Antineoplastic Agents KW - 0 KW - DLC1 protein, human KW - GTPase-Activating Proteins KW - Tumor Suppressor Proteins KW - Index Medicus KW - Gene Expression Regulation, Neoplastic KW - Genes, Tumor Suppressor KW - Humans KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - GTPase-Activating Proteins -- genetics KW - Neoplasms -- pathology KW - Neoplasm Metastasis -- genetics KW - GTPase-Activating Proteins -- metabolism KW - Tumor Suppressor Proteins -- metabolism KW - Tumor Suppressor Proteins -- genetics KW - Neoplasm Metastasis -- pathology KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1528341063?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+diagnosis+%26+therapy&rft.atitle=Deleted+in+liver+cancer-1+%28DLC1%29%3A+an+emerging+metastasis+suppressor+gene.&rft.au=Popescu%2C+Nicholas+C%3BGoodison%2C+Steve&rft.aulast=Popescu&rft.aufirst=Nicholas&rft.date=2014-06-01&rft.volume=18&rft.issue=3&rft.spage=293&rft.isbn=&rft.btitle=&rft.title=Molecular+diagnosis+%26+therapy&rft.issn=1179-2000&rft_id=info:doi/10.1007%2Fs40291-014-0086-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-12 N1 - Date created - 2014-05-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 1999 Nov 15;59(22):5662-5 [10582679] Cancer Res. 2000 Dec 1;60(23):6581-4 [11118037] Adv Cancer Res. 2002;84:57-80 [11883532] Oncogene. 2003 Jan 23;22(3):445-50 [12545165] J Biol Chem. 2003 Mar 21;278(12):10824-30 [12531887] Cancer Genet Cytogenet. 2003 Jan 15;140(2):113-7 [12645648] Cancer Cell. 2003 Jun;3(6):537-49 [12842083] Cancer Res. 2003 Jul 15;63(14):4232-8 [12874031] Oncogene. 2004 Nov 25;23(55):8971-8 [15467750] Zhonghua Gan Zang Bing Za Zhi. 2005 Jun;13(6):428-31 [15975276] Cancer Res. 2005 Jul 15;65(14):6042-53 [16024604] Cancer Res. 2005 Oct 1;65(19):8861-8 [16204057] Am J Clin Pathol. 2005 Dec;124 Suppl:S16-28 [16468415] Cancer Res. 2006 Sep 1;66(17):8367-72 [16951145] Int J Oncol. 2006 Nov;29(5):1127-32 [17016643] Biochem Biophys Res Commun. 2007 Mar 30;355(1):72-7 [17292327] Transplantation. 2007 Apr 15;83(7):973-81 [17460570] Cancer Detect Prev. 2007;31(2):110-8 [17418982] Proc Natl Acad Sci U S A. 2007 May 22;104(21):9012-7 [17517630] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3808-14 [14506175] Oncogene. 2004 Feb 12;23(6):1308-13 [14647417] Oncogene. 2004 Feb 19;23(7):1405-11 [14661059] Cancer Res. 1994 May 15;54(10):2577-81 [8168083] EMBO J. 1995 Jan 16;14(2):286-91 [7835339] Cancer Res. 1998 May 15;58(10):2196-9 [9605766] J Cell Biol. 1998 Jul 27;142(2):573-86 [9679153] J Biol Chem. 1999 Jun 18;274(25):17757-62 [10364218] 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] Int J Biochem Cell Biol. 2008;40(5):874-91 [18280770] Mol Carcinog. 2008 May;47(5):326-37 [17932950] Cancer Gene Ther. 2008 Jun;15(6):371-81 [18369381] Cancer Res. 2010 Nov 1;70(21):8270-5 [20861185] Mol Cancer Ther. 2009 May;8(5):1218-26 [19417142] Int J Oncol. 2008 Jun;32(6):1285-91 [18497990] Genes Dev. 2008 Jun 1;22(11):1439-44 [18519636] Genes Dev. 2008 Jul 1;22(13):1724-30 [18593873] APMIS. 2008 Jul-Aug;116(7-8):586-601 [18834404] Mutat Res. 2008 Dec 1;647(1-2):21-9 [18723033] 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] Oncogene. 2009 Mar 19;28(11):1401-9 [19151751] Nat Rev Cancer. 2009 Apr;9(4):253-64 [19242414] Urol Int. 2009;82(4):380-7 [19506402] Oncogene. 2009 Jul 23;28(29):2634-42 [19483726] Exp Cell Res. 2009 Sep 10;315(15):2505-14 [19482022] PLoS One. 2010;5(8):e12222 [20808922] Gastroenterology. 2010 Oct;139(4):1397-407 [20600027] J Transl Med. 2010;8:86 [20849603] Sci Transl Med. 2010 Oct 20;2(54):54ra77 [20962331] Semin Cancer Biol. 2011 Apr;21(2):89-98 [21147228] Semin Cancer Biol. 2011 Apr;21(2):113-22 [21168504] Cancer Res. 2011 Apr 15;71(8):2916-25 [21372205] Cell. 2011 Oct 14;147(2):275-92 [22000009] Int J Mol Sci. 2011;12(12):8489-501 [22272086] Proc Natl Acad Sci U S A. 2012 Jan 31;109(5):1455-60 [22307599] Biochem Biophys Res Commun. 2012 Apr 6;420(2):325-30 [22425986] Mol Cell Biol. 2012 Jun;32(11):2145-59 [22473989] Int J Oncol. 2012 Aug;41(2):393-406 [22580498] Asian Pac J Cancer Prev. 2012;13(4):1231-3 [22799310] Cancer Res. 2012 Sep 1;72(17):4405-16 [22693251] PLoS One. 2012;7(10):e46814 [23056464] Cancer Res. 2012 Oct 15;72(20):5338-47 [22942252] Cancer Res. 2012 Nov 15;72(22):5900-11 [23010077] Cancer Lett. 2013 Jan 28;328(2):207-11 [23059758] PLoS One. 2012;7(12):e52626 [23285118] J Recept Signal Transduct Res. 2013;33(1):10-3 [23316797] Trends Mol Med. 2013 Feb;19(2):74-82 [23219172] Oncotarget. 2013 Jan;4(1):166-76 [23371049] Nat Commun. 2013;4:1618 [23511482] BMC Cancer. 2013;13:198 [23607551] Int J Oncol. 2013 Aug;43(2):548-60 [23708087] Cancer Res. 2013 Jul 1;73(13):3821-32 [23639940] EMBO Mol Med. 2013 Sep;5(9):1367-82 [23853104] Tumour Biol. 2013 Oct;34(5):2857-61 [23681804] J Exp Clin Cancer Res. 2013;32:60 [23988121] Oncogene. 2014 Feb 6;33(6):724-33 [23376848] Int J Cancer. 2014 Jul 15;135(2):264-9 [24114040] APMIS. 2013 Dec;121(12):1131-8 [23510351] Mol Carcinog. 2014 Nov;53(11):858-70 [23908159] Oncogene. 2014 Oct 30;33(44):5163-72 [24213569] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s40291-014-0086-3 ER - TY - JOUR T1 - Learning phenotype densities conditional on many interacting predictors. AN - 1528337791; 24501099 AB - Estimating a phenotype distribution conditional on a set of discrete-valued predictors is a commonly encountered task. For example, interest may be in how the density of a quantitative trait varies with single nucleotide polymorphisms and patient characteristics. The subset of important predictors is not usually known in advance. This becomes more challenging with a high-dimensional predictor set when there is the possibility of interaction. We demonstrate a novel non-parametric Bayes method based on a tensor factorization of predictor-dependent weights for Gaussian kernels. The method uses multistage predictor selection for dimension reduction, providing succinct models for the phenotype distribution. The resulting conditional density morphs flexibly with the selected predictors. In a simulation study and an application to molecular epidemiology data, we demonstrate advantages over commonly used methods. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - Bioinformatics (Oxford, England) AU - Kessler, David C AU - Taylor, Jack A AU - Dunson, David B AD - Advanced Analytics Division, SAS Institute Inc., Cary, NC 27513, Molecular and Genetic Epidemiology Section, Epidemiology Branch and Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709 and Department of Statistical Science, Duke University, Durham, NC 27708. Y1 - 2014/06/01/ PY - 2014 DA - 2014 Jun 01 SP - 1562 EP - 1568 VL - 30 IS - 11 KW - Index Medicus KW - Polymorphism, Single Nucleotide KW - Humans KW - Bayes Theorem KW - Algorithms KW - Phenotype UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1528337791?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics+%28Oxford%2C+England%29&rft.atitle=Learning+phenotype+densities+conditional+on+many+interacting+predictors.&rft.au=Kessler%2C+David+C%3BTaylor%2C+Jack+A%3BDunson%2C+David+B&rft.aulast=Kessler&rft.aufirst=David&rft.date=2014-06-01&rft.volume=30&rft.issue=11&rft.spage=1562&rft.isbn=&rft.btitle=&rft.title=Bioinformatics+%28Oxford%2C+England%29&rft.issn=1367-4811&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtu040 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-28 N1 - Date created - 2014-05-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Psychometrika. 1966 Sep;31(3):279-311 [5221127] Biometrics. 2011 Sep;67(3):886-95 [21039398] Biostatistics. 2009 Jan;10(1):155-71 [18708650] Cancer Res. 1991 Sep 1;51(17):4671-6 [1873812] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/bioinformatics/btu040 ER - TY - JOUR T1 - Phase I/Ib study of olaparib and carboplatin in BRCA1 or BRCA2 mutation-associated breast or ovarian cancer with biomarker analyses. AN - 1526731510; 24842883 AB - Olaparib has single-agent activity against breast/ovarian cancer (BrCa/OvCa) in germline BRCA1 or BRCA2 mutation carriers (gBRCAm). We hypothesized addition of olaparib to carboplatin can be administered safely and yield preliminary clinical activity. Eligible patients had measurable or evaluable disease, gBRCAm, and good end-organ function. A 3 + 3 dose escalation tested daily oral capsule olaparib (100 or 200mg every 12 hours; dose level1 or 2) with carboplatin area under the curve (AUC) on day 8 (AUC3 day 8), then every 21 days. For dose levels 3 to 6, patients were given olaparib days 1 to 7 at 200 and 400 mg every 12 hours, with carboplatin AUC3 to 5 on day 1 or 2 every 21 days; a maximum of eight combination cycles were permitted, after which daily maintenance of olaparib 400mg every12 hours continued until progression. Dose-limiting toxicity was defined in the first two cycles. Peripheral blood mononuclear cells were collected for polymorphism analysis and polyADP-ribose incorporation. Paired tumor biopsies (before/after cycle 1) were obtained for biomarker proteomics and apoptosis endpoints. Forty-five women (37 OvCa/8 BrCa) were treated. Dose-limiting toxicity was not reached on the intermittent schedule. Expansion proceeded with olaparib 400mg every 12 hours on days 1 to 7/carboplatin AUC5. Grade 3/4 adverse events included neutropenia (42.2%), thrombocytopenia (20.0%), and anemia (15.6%). Responses included 1 complete response (1 BrCa; 23 months) and 21 partial responses (50.0%; 15 OvCa; 6 BrCa; median = 16 [4 to >45] in OvCa and 10 [6 to >40] months in BrCa). Proteomic analysis suggests high pretreatment pS209-eIF4E and FOXO3a correlated with duration of response (two-sided P < .001; Pearson's R (2) = 0.94). Olaparib capsules 400mg every 12 hours on days 1 to 7/carboplatin AUC5 is safe and has activity in gBRCAm BrCa/OvCa patients. Exploratory translational studies indicate pretreatment tissue FOXO3a expression may be predictive for response to therapy, requiring prospective validation. Published by Oxford University Press 2014. JF - Journal of the National Cancer Institute AU - Lee, Jung-Min AU - Hays, John L AU - Annunziata, Christina M AU - Noonan, Anne M AU - Minasian, Lori AU - Zujewski, Jo Anne AU - Yu, Minshu AU - Gordon, Nicolas AU - Ji, Jiuping AU - Sissung, Tristan M AU - Figg, William D AU - Azad, Nilofer AU - Wood, Bradford J AU - Doroshow, James AU - Kohn, Elise C AD - Affiliations of authors: Medical Oncology Branch, Center for Cancer Research (J-ML, JLH, CMA, AMN, LM, JAZ, MY, NG, TMS, WDF, NA, ECK), National Clinical Target Validation Laboratory, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research (JJ), Center for Interventional Oncology, Radiology, and Imaging Sciences, Clinical Center and National Cancer Institute (BJW), and Division of Cancer Treatment and Diagnosis, National Cancer Institute (JD), National Institutes of Health, Bethesda, MD. leej6@mail.nih.gov. ; Affiliations of authors: Medical Oncology Branch, Center for Cancer Research (J-ML, JLH, CMA, AMN, LM, JAZ, MY, NG, TMS, WDF, NA, ECK), National Clinical Target Validation Laboratory, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research (JJ), Center for Interventional Oncology, Radiology, and Imaging Sciences, Clinical Center and National Cancer Institute (BJW), and Division of Cancer Treatment and Diagnosis, National Cancer Institute (JD), National Institutes of Health, Bethesda, MD. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1 VL - 106 IS - 6 KW - BRCA1 Protein KW - 0 KW - BRCA1 protein, human KW - BRCA2 Protein KW - BRCA2 protein, human KW - FOXO3 protein, human KW - Forkhead Box Protein O3 KW - Forkhead Transcription Factors KW - Phthalazines KW - Piperazines KW - Poly Adenosine Diphosphate Ribose KW - 26656-46-2 KW - Carboplatin KW - BG3F62OND5 KW - olaparib KW - WOH1JD9AR8 KW - Index Medicus KW - Administration, Oral KW - Phthalazines -- adverse effects KW - Drug Administration Schedule KW - Humans KW - Aged KW - Predictive Value of Tests KW - Piperazines -- adverse effects KW - Piperazines -- administration & dosage KW - Carboplatin -- administration & dosage KW - Carboplatin -- adverse effects KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Phthalazines -- administration & dosage KW - Monocytes -- metabolism KW - Adult KW - Monocytes -- drug effects KW - Middle Aged KW - Genetic Predisposition to Disease KW - Poly Adenosine Diphosphate Ribose -- metabolism KW - Female KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- drug therapy KW - Ovarian Neoplasms -- genetics KW - BRCA1 Protein -- genetics KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Forkhead Transcription Factors -- drug effects KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Forkhead Transcription Factors -- metabolism KW - Mutation KW - Ovarian Neoplasms -- drug therapy KW - BRCA2 Protein -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1526731510?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+I%2FIb+study+of+olaparib+and+carboplatin+in+BRCA1+or+BRCA2+mutation-associated+breast+or+ovarian+cancer+with+biomarker+analyses.&rft.au=Lee%2C+Jung-Min%3BHays%2C+John+L%3BAnnunziata%2C+Christina+M%3BNoonan%2C+Anne+M%3BMinasian%2C+Lori%3BZujewski%2C+Jo+Anne%3BYu%2C+Minshu%3BGordon%2C+Nicolas%3BJi%2C+Jiuping%3BSissung%2C+Tristan+M%3BFigg%2C+William+D%3BAzad%2C+Nilofer%3BWood%2C+Bradford+J%3BDoroshow%2C+James%3BKohn%2C+Elise+C&rft.aulast=Lee&rft.aufirst=Jung-Min&rft.date=2014-06-01&rft.volume=106&rft.issue=6&rft.spage=dju089&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju089 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-07 N1 - Date created - 2014-05-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Science. 1997 Nov 7;278(5340):1064-8 [9353181] Clin Cancer Res. 2013 Nov 15;19(22):6322-8 [24077350] Maturitas. 2001 Feb 28;38(1):17-22; discussion 22-3 [11311581] Br J Cancer. 2002 Jul 29;87(3):319-23 [12177802] Am J Hematol. 1991 Aug;37(4):223-7 [1907096] Clin Cancer Res. 1996 Jul;2(7):1163-7 [9816283] Nature. 2005 Apr 14;434(7035):913-7 [15829966] Nature. 2005 Apr 14;434(7035):917-21 [15829967] Med Chem. 2006 Jan;2(1):47-53 [16787355] Gynecol Oncol. 2007 Feb;104(2):296-303 [17034838] Cancer. 2007 Apr 1;109(7):1323-30 [17330838] Cancer. 2007 Jul 15;110(2):309-17 [17559139] Proteomics. 2007 Nov;7(22):4066-8 [17952872] J Clin Oncol. 2008 Jan 1;26(1):20-5 [18165636] Nat Rev Cancer. 2008 Mar;8(3):193-204 [18256616] Nat Cell Biol. 2008 Apr;10(4):460-7 [18344987] Mol Cancer Ther. 2008 May;7(5):1246-50 [18483312] Clin Cancer Res. 2008 Nov 1;14(21):6877-85 [18980982] Expert Opin Investig Drugs. 2009 Jan;18(1):31-43 [19053880] Br J Cancer. 2009 May 5;100(9):1393-9 [19367274] J Clin Oncol. 2009 Jun 1;27(16):2705-11 [19364967] N Engl J Med. 2009 Jul 9;361(2):189-91 [19553640] N Engl J Med. 2009 Jul 9;361(2):123-34 [19553641] Obstet Gynecol. 2010 Jan;115(1):49-54 [20027033] Clin Cancer Res. 2010 Jan 15;16(2):600-9 [20068074] J Clin Oncol. 2010 May 20;28(15):2512-9 [20406929] Lancet. 2010 Jul 24;376(9737):235-44 [20609467] Lancet. 2010 Jul 24;376(9737):245-51 [20609468] J Clin Oncol. 2010 Aug 1;28(22):3555-61 [20547991] Clin Cancer Res. 2010 Sep 15;16(18):4517-26 [20823142] J Clin Oncol. 2010 Oct 10;28(29):e563-4; author reply e565-6 [20679605] Clin Cancer Res. 2010 Dec 15;16(24):6159-68 [20802015] Clin Cancer Res. 2011 Feb 15;17(4):783-91 [21097693] Proc Natl Acad Sci U S A. 2011 Feb 22;108(8):3406-11 [21300883] Clin Cancer Res. 2011 May 1;17(9):2874-84 [21415224] Cell Cycle. 2010 Mar 15;9(6):1091-6 [20190568] Ann Oncol. 2011 Jun;22(6):1346-52 [21228333] Lancet Oncol. 2011 Sep;12(9):852-61 [21862407] Mol Cancer Ther. 2011 Oct;10(10):2000-7 [21835933] Proc Natl Acad Sci U S A. 2011 Nov 1;108(44):18032-7 [22006311] J Clin Oncol. 2012 Feb 1;30(4):372-9 [22203755] Clin Cancer Res. 2012 Mar 15;18(6):1726-34 [22307137] N Engl J Med. 2012 Apr 12;366(15):1382-92 [22452356] Clin Cancer Res. 2012 Apr 15;18(8):2344-51 [22371451] Cancer Discov. 2012 Apr;2(4):366-75 [22576213] J Clin Oncol. 2012 Jul 20;30(21):2654-63 [22711857] Nat Commun. 2012;3:1000 [22893124] Cancer. 2013 Apr 1;119(7):1357-64 [23280317] Mol Cell Proteomics. 2013 Jun;12(6):1621-31 [23449826] Lancet Oncol. 2013 Aug;14(9):882-92 [23810788] Gynecol Oncol. 2013 Sep;130(3):554-9 [23791828] Br J Cancer. 2013 Aug 20;109(4):1072-8 [23867999] J Clin Invest. 2013 Sep;123(9):3740-50 [23945238] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/dju089 ER - TY - JOUR T1 - Treatment outcomes of female germ cell tumors: the Egyptian National Cancer Institute experience. AN - 1526731459; 24841162 AB - Female germ cell tumors (GCTS) are rare tumors that carry a good prognosis. To report the experience of the Egyptian National Cancer Institute (ENCI) in managing female GCTs. This retrospective study included 19 females with ovarian GCTs presenting to the ENCI between 2006 and 2010. The median age was 23years. Ovaries were the primary site in all patients. Dysgerminoma and teratoma were the predominant pathologies followed by mixed GCT in females. Unilateral ovariectomy or ovarian tumorectomy were the classic surgical procedures with R0 resection being feasible in most cases. Surveillance was adopted in six patients with stage I disease. Chemotherapy was administered in 63% of ovarian GCTs with BEP being the commonest regimen with reasonable tolerability and good response rates. The median OS and EFS were not reached. The projected 5-year OS rate was 93.8%. Both OS and EFS were better in patients responding to chemotherapy than non-responders (p<0.002). Stage of disease did not significantly affect OS or EFS. Female GCTs rarely affect Egyptian females. They have good prognosis. Copyright © 2014. Production and hosting by Elsevier B.V. JF - Journal of the Egyptian National Cancer Institute AU - Saber, Magdy M AU - Zeeneldin, Ahmed A AU - El Gammal, Mosaad M AU - Salem, Salem E AU - Darweesh, Amira D AU - Abdelaziz, Alshaymaa A AU - Monir, Manar AD - Medical Oncology Department, NCI, Cairo University, Egypt. ; Medical Oncology Department, NCI, Cairo University, Egypt. Electronic address: elgammalmosaad@yahoo.com. ; Department of Medical Statics, NCI, Cairo University, Egypt. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 103 EP - 108 VL - 26 IS - 2 SN - 1110-0362, 1110-0362 KW - Etoposide KW - 6PLQ3CP4P3 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Chemotherapy KW - Survival KW - Female germ-cell tumors KW - Treatment KW - Side effects KW - Disease-Free Survival KW - Neoplasm Staging KW - Etoposide -- administration & dosage KW - Humans KW - Adult KW - Retrospective Studies KW - Prognosis KW - Aged KW - Middle Aged KW - Adolescent KW - Female KW - Cisplatin -- administration & dosage KW - Genital Neoplasms, Female -- surgery KW - Genital Neoplasms, Female -- pathology KW - Treatment Outcome KW - Neoplasms, Germ Cell and Embryonal -- pathology KW - Neoplasms, Germ Cell and Embryonal -- drug therapy KW - Neoplasms, Germ Cell and Embryonal -- surgery KW - Genital Neoplasms, Female -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1526731459?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Egyptian+National+Cancer+Institute&rft.atitle=Treatment+outcomes+of+female+germ+cell+tumors%3A+the+Egyptian+National+Cancer+Institute+experience.&rft.au=Saber%2C+Magdy+M%3BZeeneldin%2C+Ahmed+A%3BEl+Gammal%2C+Mosaad+M%3BSalem%2C+Salem+E%3BDarweesh%2C+Amira+D%3BAbdelaziz%2C+Alshaymaa+A%3BMonir%2C+Manar&rft.aulast=Saber&rft.aufirst=Magdy&rft.date=2014-06-01&rft.volume=26&rft.issue=2&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Egyptian+National+Cancer+Institute&rft.issn=11100362&rft_id=info:doi/10.1016%2Fj.jnci.2014.03.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-30 N1 - Date created - 2014-05-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jnci.2014.03.001 ER - TY - JOUR T1 - The origin of cancer stem cells. AN - 1526133491; 24631602 JF - Journal of hepatology AU - Dang, Hien T AU - Budhu, Anuradha AU - Wang, Xin W AD - Liver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Liver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: xw3u@nih.gov. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1304 EP - 1305 VL - 60 IS - 6 KW - Interleukin-6 KW - 0 KW - Index Medicus KW - IL-6 KW - HCC progenitor cells KW - Foci altered hepatocytes KW - Cancer stem cells KW - Hepatocellular carcinoma KW - Hepatocarcinogenesis KW - Animals KW - Gene Expression Regulation, Neoplastic KW - Liver Neoplasms -- pathology KW - Interleukin-6 -- metabolism KW - Autocrine Communication KW - Neoplastic Stem Cells -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1526133491?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+origin+of+cancer+stem+cells.&rft.au=Dang%2C+Hien+T%3BBudhu%2C+Anuradha%3BWang%2C+Xin+W&rft.aulast=Dang&rft.aufirst=Hien&rft.date=2014-06-01&rft.volume=60&rft.issue=6&rft.spage=1304&rft.isbn=&rft.btitle=&rft.title=Journal+of+hepatology&rft.issn=1600-0641&rft_id=info:doi/10.1016%2Fj.jhep.2014.03.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-06 N1 - Date created - 2014-05-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment On: Cell. 2013 Oct 10;155(2):384-96 [24120137] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jhep.2014.03.001 ER - TY - JOUR T1 - Immunomodulatory activity of orphan drug Elmiron® in female B6C3F1/N mice. AN - 1526129724; 24657363 AB - Interstitial cystitis (IC) is a chronic disorder characterized by bladder discomfort and urinary urgency in the absence of identifiable infection. Despite the expanding use in IC treatment and other chronic conditions, the effects of Elmiron® treatment on immune system remain unknown. Therefore, female B6C3F1/N mice were orally administered Elmiron® daily for 28-days at doses of 63, 125, 250, 500 or 1000mg/kg to evaluate its immunomodulatory effects. Mice treated with Elmiron® had a significant increase in absolute numbers of splenic macrophages (63, 500 and 1000mg/kg) and natural killer (NK) cells (250 and 1000mg/kg). Elmiron® treatment did not affect the humoral immune response or T cell proliferative response. However, innate immune responses such as phagocytosis by liver macrophages (1000mg/kg) and NK cell activity were enhanced (500 and 1000mg/kg). Further analysis using a disease resistance model showed that Elmiron®-treated mice demonstrated significantly increased anti-tumor activity against B16F10 melanoma cells at the 500 and 1000mg/kg doses. Collectively, we conclude that Elmiron® administration stimulates the immune system, increasing numbers of specific cell populations and enhancing macrophage phagocytosis and NK cell activity in female B6C3F1/N mice. This augmentation may have largely contributed to the reduced number of B16F10 melanoma tumors. Published by Elsevier Ltd. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Thakur, Sheetal A AU - Nyska, Abraham AU - White, Kimber L AU - Smith, Matthew J AU - Auttachoat, Wimolnut AU - Germolec, Dori R AD - Toxicology Branch, Division of National Toxicology Program, National Institute of Environmental Health Sciences, NIH, RTP, NC, United States. Electronic address: thakursa@niehs.nih.gov. ; Integrated Laboratory Systems, RTP, NC, United States. ; Virginia Commonwealth University, Richmond, VA, United States. ; Toxicology Branch, Division of National Toxicology Program, National Institute of Environmental Health Sciences, NIH, RTP, NC, United States. Electronic address: germolec@niehs.nih.gov. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 196 EP - 203 VL - 68 KW - Antineoplastic Agents KW - 0 KW - Immunoglobulin M KW - Pentosan Sulfuric Polyester KW - 37300-21-3 KW - Index Medicus KW - Interstitial cystitis KW - Immunotoxicity KW - Sodium pentosan polysulfate KW - Orphan drug KW - Cell Proliferation -- drug effects KW - Animals KW - Immunity, Innate -- drug effects KW - Spleen -- metabolism KW - Spleen -- cytology KW - Dose-Response Relationship, Drug KW - Immunoglobulin M -- metabolism KW - Liver -- metabolism KW - Mice KW - Cell Line, Tumor KW - Macrophages -- drug effects KW - Killer Cells, Natural -- drug effects KW - Mice, Inbred Strains KW - T-Lymphocytes -- metabolism KW - Liver -- drug effects KW - Body Weight -- drug effects KW - T-Lymphocytes -- drug effects KW - Phagocytosis -- drug effects KW - Spleen -- drug effects KW - Antineoplastic Agents -- pharmacology KW - Female KW - Organ Size -- drug effects KW - Macrophages -- metabolism KW - Pentosan Sulfuric Polyester -- pharmacology KW - Immunomodulation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1526129724?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.atitle=Immunomodulatory+activity+of+orphan+drug+Elmiron%C2%AE+in+female+B6C3F1%2FN+mice.&rft.au=Thakur%2C+Sheetal+A%3BNyska%2C+Abraham%3BWhite%2C+Kimber+L%3BSmith%2C+Matthew+J%3BAuttachoat%2C+Wimolnut%3BGermolec%2C+Dori+R&rft.aulast=Thakur&rft.aufirst=Sheetal&rft.date=2014-06-01&rft.volume=68&rft.issue=&rft.spage=196&rft.isbn=&rft.btitle=&rft.title=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.issn=1873-6351&rft_id=info:doi/10.1016%2Fj.fct.2014.03.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-05 N1 - Date created - 2014-05-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Drug Chem Toxicol. 1985;8(5):299-331 [4064946] Drug Chem Toxicol. 2000 Aug;23(3):433-57 [10959546] Fundam Appl Toxicol. 1993 Nov;21(4):412-9 [8253294] Am J Hematol. 1994 Mar;45(3):252-7 [7507640] Arthritis Rheum. 1994 Jan;37(1):125-36 [7510481] Fundam Appl Toxicol. 1995 Feb;24(2):238-46 [7737435] Invest New Drugs. 1995;13(1):55-62 [7499109] Ann Hematol. 1996 Jul;73(1):51-2 [8695727] Kidney Int Suppl. 1997 Dec;63:S120-3 [9407438] Clin Cancer Res. 1997 Dec;3(12 Pt 1):2347-54 [9815633] Science. 1963 Apr 26;140(3565):405 [13957684] Psychol Bull. 1956 Jan;53(1):96-101 [13289969] Clin Cancer Res. 2005 Aug 15;11(16):5984-92 [16115943] Blood. 2005 Oct 1;106(7):2252-8 [15933055] Am J Physiol Heart Circ Physiol. 2007 Feb;292(2):H743-50 [17071728] Immunity. 2007 Apr;26(4):385-7 [17459805] Acta Neuropathol. 2008 Feb;115(2):159-74 [17924126] Drug Chem Toxicol. 2009;32(1):77-87 [19514942] Methods Mol Biol. 2010;598:173-84 [19967513] BMC Clin Pharmacol. 2010;10:7 [20346179] J Immunotoxicol. 2010 Oct-Dec;7(4):289-97 [20560775] J Immunotoxicol. 2010 Oct-Dec;7(4):333-43 [20958156] Am Fam Physician. 2011 May 15;83(10):1175-81 [21568251] Blood. 2011 Sep 22;118(12):3347-9 [21768303] Lab Invest. 2011 Oct;91(10):1459-71 [21808238] Lab Invest. 2012 Feb;92(2):236-45 [22042083] Eur J Obstet Gynecol Reprod Biol. 2012 Mar;161(1):1-7 [22310942] Curr Urol Rep. 2012 Oct;13(5):319-26 [22965225] Explore (NY). 2013 Jan-Feb;9(1):48-52 [23294821] PLoS One. 2013;8(1):e54459 [23365668] Natl Toxicol Program Tech Rep Ser. 2004 May;(512):7-289 [15213766] Arch Toxicol. 2003 Dec;77(12):702-11 [14508637] IDrugs. 2003 May;6(5):470-8 [12789602] Arch Intern Med. 2002 Jul 22;162(14):1644-5 [12123410] Toxicol Pathol. 2002 Mar-Apr;30(2):178-87 [11950161] Ann Fr Anesth Reanim. 1986;5(5):539-41 [2433974] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.fct.2014.03.015 ER - TY - JOUR T1 - Probing the molecular mechanism of action of the HIV-1 reverse transcriptase inhibitor 4'-ethynyl-2-fluoro-2'-deoxyadenosine (EFdA) using pre-steady-state kinetics. AN - 1524822356; 24632447 AB - The novel antiretroviral 4'-ethynyl-2-fluoro-2'-deoxyadenosine (EFdA) is a potent nucleoside HIV-1 reverse transcriptase (RT) inhibitor (NRTI). Unlike other FDA-approved NRTIs, EFdA contains a 3'-hydroxyl. Pre-steady-state kinetics showed RT preferred incorporating EFdA-TP over native dATP. Moreover, RT slowly inserted nucleotides past an EFdA-terminated primer, resulting in delayed chain termination with unaffected fidelity. This is distinct from KP1212, another 3'-hydroxyl-containing RT inhibitor considered to promote viral lethal mutagenesis. New mechanistic features of RT inhibition by EFdA are revealed. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Antiviral research AU - Muftuoglu, Yagmur AU - Sohl, Christal D AU - Mislak, Andrea C AU - Mitsuya, Hiroaki AU - Sarafianos, Stefan G AU - Anderson, Karen S AD - Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, United States. ; Department of Infectious Diseases, Kumamoto University Graduate School of Medical Sciences, Kumamoto 860-8556, Japan; Department of Hematology, Kumamoto University Graduate School of Medical Sciences, Kumamoto 860-8556, Japan; Experimental Retrovirology Section, HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States. ; CS Bond Life Sciences Center and Department of Molecular Microbiology and Immunology, University of Missouri, School of Medicine, Columbia, MO 65211, United States; Department of Biochemistry, University of Missouri, School of Medicine, Columbia, MO 65211, United States. ; Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06520, United States. Electronic address: karen.anderson@yale.edu. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1 EP - 4 VL - 106 KW - 4'-ethynyl-2-fluoro-2'-deoxyadenosine KW - 0 KW - Anti-HIV Agents KW - Deoxyadenosines KW - Reverse Transcriptase Inhibitors KW - reverse transcriptase, Human immunodeficiency virus 1 KW - EC 2.7.7.- KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - Index Medicus KW - Polymerase KW - Reverse transcriptase KW - EFdA KW - Enzyme kinetics KW - HIV KW - Kinetics KW - Reverse Transcriptase Inhibitors -- pharmacology KW - Anti-HIV Agents -- pharmacology KW - HIV Reverse Transcriptase -- antagonists & inhibitors KW - Deoxyadenosines -- pharmacology KW - HIV-1 -- enzymology KW - HIV-1 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524822356?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antiviral+research&rft.atitle=Probing+the+molecular+mechanism+of+action+of+the+HIV-1+reverse+transcriptase+inhibitor+4%27-ethynyl-2-fluoro-2%27-deoxyadenosine+%28EFdA%29+using+pre-steady-state+kinetics.&rft.au=Muftuoglu%2C+Yagmur%3BSohl%2C+Christal+D%3BMislak%2C+Andrea+C%3BMitsuya%2C+Hiroaki%3BSarafianos%2C+Stefan+G%3BAnderson%2C+Karen+S&rft.aulast=Muftuoglu&rft.aufirst=Yagmur&rft.date=2014-06-01&rft.volume=106&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Antiviral+research&rft.issn=1872-9096&rft_id=info:doi/10.1016%2Fj.antiviral.2014.03.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-19 N1 - Date created - 2014-05-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Antimicrob Agents Chemother. 2000 Jan;44(1):217-21 [10602755] Drug Dev Ind Pharm. 2014 Aug;40(8):1101-11 [23841536] J Biol Chem. 2002 Oct 25;277(43):40479-90 [12176989] Biochemistry. 1997 Nov 18;36(46):14056-63 [9369477] Biochemistry. 1999 Jan 5;38(1):55-63 [9890882] Antiviral Res. 2005 Jul;67(1):1-9 [15890415] Antiviral Res. 2005 Jul;67(1):10-7 [15950748] Antimicrob Agents Chemother. 2007 Aug;51(8):2701-8 [17548498] Nucleosides Nucleotides Nucleic Acids. 2007;26(10-12):1543-6 [18066823] J Biol Chem. 2008 Feb 29;283(9):5452-9 [17962184] J Biol Chem. 2008 Dec 5;283(49):34218-28 [18940786] J Biol Chem. 2009 Dec 18;284(51):35681-91 [19837673] PLoS One. 2011;6(1):e15135 [21264288] Cell Mol Biol (Noisy-le-grand). 2011;57(1):40-6 [21366961] Biochemistry. 2011 Jun 7;50(22):5008-15 [21548586] Trends Pharmacol Sci. 2011 Dec;32(12):715-25 [21899897] J Mol Biol. 2012 Feb 3;415(5):866-80 [22210155] Antimicrob Agents Chemother. 2012 Mar;56(3):1630-4 [22155823] Mol Pharmacol. 2012 Jul;82(1):125-33 [22513406] Antiviral Res. 2012 Aug;95(2):93-103 [22664235] Hum Mol Genet. 2013 Mar 15;22(6):1074-85 [23208208] Retrovirology. 2013;10:65 [23800377] Antimicrob Agents Chemother. 2013 Dec;57(12):6254-64 [24100493] J Biol Chem. 2001 Nov 2;276(44):40847-57 [11526116] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.antiviral.2014.03.001 ER - TY - JOUR T1 - Vitamin D-binding protein, circulating vitamin D and risk of renal cell carcinoma AN - 1524426150; 19553242 AB - Cell culture experiments suggest that vitamin D may inhibit renal carcinogenesis, but human studies of circulating 25-hydroxyvitamin D [25(OH)D], the accepted measure of vitamin D status, and kidney cancer have been null. Limited research has examined the role of circulating vitamin D-binding protein (DBP) in the association between 25(OH)D and disease risk, and it is unclear whether free 25(OH)D in circulation is a better measure of effective exposure, or if DBP may independently impact outcomes. We conducted a nested case-control analysis within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study to examine whether circulating DBP concentration was prospectively associated with risk of renal cell carcinoma, and whether it modified the association with 25(OH)D. Renal cell carcinoma cases (n = 262) were matched 1:1 to controls on age ( plus or minus 1 year) and date of blood collection ( plus or minus 30 days). We estimated odds ratios (ORs) and 95% confidence intervals (CIs) of renal cell carcinoma risk by quartiles of 25(OH)D, DBP and the molar ratio of 25(OH)D:DBP, a proxy for free circulating 25(OH)D. Men with higher DBP concentrations were at significantly decreased risk of kidney cancer (Q4 vs. Q1: OR = 0.17, 95% CI = 0.08-0.33; p-trend < 0.0001), a finding unchanged by adjustment for 25(OH)D. Although we observed no association with total 25(OH)D, we found slightly increased risk with higher levels of estimated free 25(OH)D [Q4 vs. Q1 of the 25(OH)D:DBP ratio, OR = 1.61, 95% CI = 0.95-2.73; p-trend = 0.09]. The strong protective association observed between higher circulating DBP concentration and kidney cancer risk requires replication but suggests a vitamin D-independent influence of DBP. What's new? Circulating vitamin D binding protein (DBP) has been implicated in the etiology of certain cancers, where it may act directly or by modifying circulating vitamin D concentrations and disease risk. In this examination of the association between DBP and renal cell carcinoma (RCC) specifically, a strong protective association was found between elevated circulating DBP concentrations and kidney cancer. The association was unchanged after adjustment for circulating vitamin D. The results suggest that DBP may influence risk of RCC through a biologic mechanism unrelated to vitamin D status. JF - International Journal of Cancer AU - Mondul, Alison M AU - Weinstein, Stephanie J AU - Moy, Kristin A AU - Maennisto, Satu AU - Albanes, Demetrius AD - Nutritional Epidemiology Branch Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, MD. Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 2699 EP - 2706 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 134 IS - 11 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Risk Abstracts KW - renal cell carcinoma KW - vitamin D-binding protein KW - 25-hydroxyvitamin D KW - prospective studies KW - Renal KW - Health risks KW - Prevention KW - Age KW - Etiology KW - Vitamin D KW - Vitamins KW - Carcinogenesis KW - Kidney KW - Proteins KW - Cancer KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524426150?accountid=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=Vitamin+D-binding+protein%2C+circulating+vitamin+D+and+risk+of+renal+cell+carcinoma&rft.au=Mondul%2C+Alison+M%3BWeinstein%2C+Stephanie+J%3BMoy%2C+Kristin+A%3BMaennisto%2C+Satu%3BAlbanes%2C+Demetrius&rft.aulast=Mondul&rft.aufirst=Alison&rft.date=2014-06-01&rft.volume=134&rft.issue=11&rft.spage=2699&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28596 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Renal; Health risks; Etiology; Age; Prevention; Vitamin D; Vitamins; Carcinogenesis; Kidney; Proteins; Cancer DO - http://dx.doi.org/10.1002/ijc.28596 ER - TY - JOUR T1 - Dietary nitrate and nitrite intake and risk of colorectal cancer in the Shanghai Women's Health Study AN - 1524397976; 19625526 AB - Nitrate and nitrite are precursors of endogenously formed N-nitroso compounds (NOC), known animal carcinogens. Nitrosation reactions forming NOCs can be inhibited by vitamin C and other antioxidants. We prospectively investigated the association between dietary nitrate and nitrite intake and risk of colorectal cancer in the Shanghai Women's Health Study, a cohort of 73,118 women ages 40-70 residing in Shanghai. We evaluated effect modification by factors that affect endogenous formation of NOCs: vitamin C (at or above/below median) and red meat intake (at or above/below median). Nitrate, nitrite and other dietary intakes were estimated from a 77-item food frequency questionnaire administered at baseline. Over a mean of 11 years of follow-up, we identified 619 colorectal cancer cases (n=383, colon; n=236, rectum). Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox proportional hazard regression. Overall, nitrate intake was not associated with colorectal cancer risk (HR=1.08; 95% CI: 0.73-1.59). However, among women with vitamin C intake below the median (83.9 mg day super(-1)) and hence higher potential exposure to NOCs, risk of colorectal cancer increased with increasing quintiles of nitrate intake (highest vs. lowest quintile HR=2.45; 95% CI: 1.15-5.18; p trend=0.02). There was no association among women with higher vitamin C intake. We found no association between nitrite intake and risk of colorectal cancer overall or by intake level of vitamin C. Our findings suggest that high dietary nitrate intake among subgroups expected to have higher exposure to endogenously formed NOCs increases risk of colorectal cancer. What's new? Nitrate and nitrite are precursors in the endogenous formation of potentially carcinogenic N-nitroso compounds (NOC). These nitrosation reactions are linked to the consumption of red meat and can be inhibited by vitamin C and other antioxidants. Here, a potential association of dietary nitrate, nitrite and vitamin C intake with the risk of colorectal cancer was investigated in Chinese women. The authors find an increased risk of colorectal cancer in women with high nitrate intake and low vitamin C consumption linking high endogenous NOC exposure to colorectal carcinogenesis. JF - International Journal of Cancer AU - DellaValle, Curt T AU - Xiao, Qian AU - Yang, Gong AU - Shu, Xiao-Ou AU - Aschebrook-Kilfoy, Briseis AU - Zheng, Wei AU - Lan Li, Hong AU - Ji, Bu-Tian AU - Rothman, Nathaniel AU - Chow, Wong-Ho AU - Gao, Yu-Tang 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, Bethesda, MD. Y1 - 2014/06// PY - 2014 DA - Jun 2014 SP - 2917 EP - 2926 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 134 IS - 12 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Diets KW - Antioxidants KW - Nitrates KW - Ingestion KW - Cancer KW - Meat KW - Health risks KW - Nitrites KW - Carcinogenicity KW - Risk factors KW - Vitamins KW - Carcinogenesis KW - Colorectal carcinoma KW - China, People's Rep., Shanghai KW - Females 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/1524397976?accountid=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+nitrate+and+nitrite+intake+and+risk+of+colorectal+cancer+in+the+Shanghai+Women%27s+Health+Study&rft.au=DellaValle%2C+Curt+T%3BXiao%2C+Qian%3BYang%2C+Gong%3BShu%2C+Xiao-Ou%3BAschebrook-Kilfoy%2C+Briseis%3BZheng%2C+Wei%3BLan+Li%2C+Hong%3BJi%2C+Bu-Tian%3BRothman%2C+Nathaniel%3BChow%2C+Wong-Ho%3BGao%2C+Yu-Tang%3BWard%2C+Mary+H&rft.aulast=DellaValle&rft.aufirst=Curt&rft.date=2014-06-01&rft.volume=134&rft.issue=12&rft.spage=2917&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28612 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Diets; Antioxidants; Nitrates; Ingestion; Cancer; Meat; Health risks; Nitrites; Carcinogenicity; Vitamins; Risk factors; Carcinogenesis; Colorectal carcinoma; Females; China, People's Rep., Shanghai DO - http://dx.doi.org/10.1002/ijc.28612 ER - TY - JOUR T1 - Ribonucleotide incorporation by yeast DNA polymerase ζ. AN - 1524176962; 24674899 AB - During replication in yeast, the three B family DNA replicases frequently incorporate ribonucleotides (rNMPs) into DNA, and their presence in the nuclear genome can affect genome stability. This prompted us to examine ribonucleotide incorporation by the fourth B family member, Pol ζ, the enzyme responsible for the majority of damage-induced mutagenesis in eukaryotes. We first show that Pol ζ inserts rNMPs into DNA and can extend primer termini containing 3'-ribonucleotides. We then measure rNMP incorporation by Pol ζ in the presence of its cofactors, RPA, RFC and PCNA and at normal cellular dNTP and rNTP concentrations that exist under unstressed conditions. Under these conditions, Pol ζ stably incorporates one rNMP for every 200-300 dNMPs incorporated, a frequency that is slightly higher than for the high fidelity replicative DNA polymerases. Under damage-induced conditions wherein cellular dNTP concentrations are elevated 5-fold, Pol ζ only incorporates one rNMP per 1300 dNMPs. Functional interaction of Pol ζ with the mutasome assembly factor Rev1 gives comparable rNMP incorporation frequencies. These results suggest that ribonucleotide incorporation into DNA during Pol ζ-mediated mutagenesis in vivo may be rare. Copyright © 2014 Elsevier B.V. All rights reserved. JF - DNA repair AU - Makarova, Alena V AU - Nick McElhinny, Stephanie A AU - Watts, Brian E AU - Kunkel, Thomas A AU - Burgers, Peter M AD - Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Laboratory of Molecular Genetics and Laboratory of Structural Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA. ; Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: burgers@biochem.wustl.edu. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 63 EP - 67 VL - 18 KW - DNA, Fungal KW - 0 KW - Deoxyribonucleotides KW - REV7 protein, S cerevisiae KW - RFA1 protein, S cerevisiae KW - Replication Protein A KW - Ribonucleotides KW - Saccharomyces cerevisiae Proteins KW - DNA polymerase zeta KW - EC 2.7.7.- KW - Nucleotidyltransferases KW - REV1 protein, S cerevisiae KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - REV3 protein, S cerevisiae KW - Index Medicus KW - DNA polymerase KW - Translesion synthesis KW - Mutagenesis KW - Nucleotidyltransferases -- metabolism KW - Nucleotidyltransferases -- genetics KW - DNA Damage KW - Deoxyribonucleotides -- metabolism KW - Replication Protein A -- metabolism KW - Mutation KW - DNA Replication KW - Saccharomyces cerevisiae Proteins -- metabolism KW - Saccharomyces cerevisiae Proteins -- genetics KW - Ribonucleotides -- metabolism KW - Saccharomyces cerevisiae -- enzymology KW - DNA, Fungal -- metabolism KW - DNA-Directed DNA Polymerase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524176962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ribonucleotide+incorporation+by+yeast+DNA+polymerase+%CE%B6.&rft.au=Makarova%2C+Alena+V%3BNick+McElhinny%2C+Stephanie+A%3BWatts%2C+Brian+E%3BKunkel%2C+Thomas+A%3BBurgers%2C+Peter+M&rft.aulast=Makarova&rft.aufirst=Alena&rft.date=2014-06-01&rft.volume=18&rft.issue=&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=DNA+repair&rft.issn=1568-7856&rft_id=info:doi/10.1016%2Fj.dnarep.2014.02.017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-06 N1 - Date created - 2014-05-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2000 May 12;275(19):14541-9 [10799539] Science. 2014 Jan 17;343(6168):260-1 [24436412] Biochem Soc Trans. 2001 May;29(Pt 2):187-91 [11356151] Cell. 2003 Feb 7;112(3):391-401 [12581528] EMBO J. 2003 Dec 15;22(24):6621-30 [14657033] J Biol Chem. 1988 Jan 15;263(2):917-24 [3275661] J Biol Chem. 1994 Apr 15;269(15):11121-32 [8157639] Nature. 1996 Aug 22;382(6593):729-31 [8751446] Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1619-22 [9050827] Genetics. 1997 Nov;147(3):1017-24 [9383049] Curr Biol. 2006 Mar 21;16(6):586-90 [16546083] EMBO J. 2006 Sep 20;25(18):4316-25 [16957771] Nucleic Acids Res. 2006;34(17):4731-42 [16971464] Proc Natl Acad Sci U S A. 2010 Mar 16;107(11):4949-54 [20194773] Biochemistry. 2010 Jul 6;49(26):5504-10 [20518555] Genetics. 2011 Jan;187(1):21-35 [20980236] DNA Repair (Amst). 2012 Aug 1;11(8):649-56 [22682724] Mol Cell. 2012 Sep 28;47(6):980-6 [22864116] PLoS Genet. 2012;8(11):e1003030 [23144626] Nucleic Acids Res. 2012 Dec;40(22):11618-26 [23066099] DNA Repair (Amst). 2013 Feb 1;12(2):121-7 [23245697] Mol Cell. 2013 May 9;50(3):323-32 [23603115] Mol Cell. 2013 May 9;50(3):437-43 [23603118] Proc Natl Acad Sci U S A. 2013 Aug 6;110(32):12942-7 [23882084] Genes Dev. 2001 Apr 15;15(8):945-54 [11316789] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.dnarep.2014.02.017 ER - TY - JOUR T1 - Randomized, double-blind, placebo-controlled trial of soluble tumor necrosis factor receptor: enbrel (etanercept) for the treatment of idiopathic pneumonia syndrome after allogeneic stem cell transplantation: blood and marrow transplant clinical trials network protocol. AN - 1524174464; 24607553 AB - Idiopathic pneumonia syndrome (IPS) is a diffuse, noninfectious lung injury that occurs acutely after allogeneic hematopoietic cell transplantation (HCT). IPS-related mortality has been historically high (>50%) despite treatment with systemic corticosteroids and supportive care measures. We have now examined the role of tumor necrosis factor inhibition in a randomized, double-blind, placebo-controlled trial of corticosteroids with etanercept or placebo. Thirty-four subjects (≥18 years) with IPS after HCT were randomized to receive methylprednisolone (2 mg/kg/day) plus etanercept (0.4 mg/kg twice weekly × 4 weeks; n = 16) or placebo (n = 18). No active infections and a pathogen-negative bronchoscopy were required at study entry. Response (alive, with complete discontinuation of supplemental oxygen support) and overall survival were examined. This study, originally planned to accrue 120 patients, was terminated prematurely due to slow accrual. In the limited number of patients examined, there were no differences in response rates at day 28 of study. Ten of 16 patients (62.5% [95% confidence interval {CI}, 35.4% to 84.8%]) receiving etanercept and 12 of 18 patients (66.7% [95% CI, 41.0% to 86.7%]) receiving placebo met the day 28 response definition (P = 1.00). The median survival was 170 days (95% CI, 11 to 362) with etanercept versus 64 days (95% CI, 26 to 209) with placebo (P = .51). Among responders, the median time to discontinuation of supplemental oxygen was 9 days (etanercept) versus 7 days (placebo). Therapy was well tolerated, with 1 toxicity-related death from infectious pneumonia in the placebo arm. The treatment of IPS with corticosteroids in adult HCT recipients was associated with high early response rates (>60%) compared with historical reports, with poor overall survival. The addition of etanercept did not lead to further increases in response, although the sample size of this truncated trial preclude a definitive conclusion. Copyright © 2014. Published by Elsevier Inc. JF - Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation AU - Yanik, Gregory A AU - Horowitz, Mary M AU - Weisdorf, Daniel J AU - Logan, Brent R AU - Ho, Vincent T AU - Soiffer, Robert J AU - Carter, Shelly L AU - Wu, Juan AU - Wingard, John R AU - Difronzo, Nancy L AU - Ferrara, James L AU - Giralt, Sergio AU - Madtes, David K AU - Drexler, Rebecca AU - White, Eric S AU - Cooke, Kenneth R AD - Department of Pediatrics and Internal Medicine, Blood and Marrow Transplant Program, University of Michigan Medical Center, Ann Arbor, Michigan. Electronic address: gyanik@umich.edu. ; Center for International Blood and Marrow Transplant Research, Medical College of Wisconsin, Milwaukee, Wisconsin. ; Department of Internal Medicine, University of Minnesota Blood and Marrow Transplantation Program, Minneapolis, Minnesota. ; Department of Hematologic Malignancies, Dana Farber Cancer Institute, Boston, Massachusetts. ; The EMMES Corporation, Rockville, Maryland. ; Department of Medicine, University of Florida, Gainesville, Florida. ; Division of Blood Diseases and Resources, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. ; Department of Pediatrics and Internal Medicine, Blood and Marrow Transplant Program, University of Michigan Medical Center, Ann Arbor, Michigan. ; Department of Stem Cell Transplantation, Memorial Sloan Kettering Cancer Center, New York, New York. ; Clinical Research Division, Fred Hutchinson Cancer Research Center and Division of Pulmonary and Critical Care Medicine, University of Washington, Seattle, Washington. ; National Marrow Donor Program, Minneapolis, Minnesota; Center for International Blood and Marrow Transplant Research, Minneapolis, Minnesota. ; Department of Internal Medicine, Pulmonary and Critical Care Medicine, University of Michigan Medical Center, Ann Arbor, Michigan. ; Department of Oncology, Sidney Kimmel Cancer Center, Johns Hopkins University, School of Medicine, Baltimore, Maryland. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 858 EP - 864 VL - 20 IS - 6 KW - Adrenal Cortex Hormones KW - 0 KW - Immunoglobulin G KW - Receptors, Tumor Necrosis Factor KW - Etanercept KW - OP401G7OJC KW - Index Medicus KW - TNF KW - Pulmonary KW - IPS KW - Pneumonia KW - Bone marrow transplantation KW - Young Adult KW - Double-Blind Method KW - Humans KW - Adult KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Transplantation, Homologous KW - Male KW - Female KW - Adrenal Cortex Hormones -- therapeutic use KW - Idiopathic Interstitial Pneumonias -- etiology KW - Receptors, Tumor Necrosis Factor -- therapeutic use KW - Idiopathic Interstitial Pneumonias -- drug therapy KW - Immunoglobulin G -- therapeutic use KW - Hematopoietic Stem Cell Transplantation -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524174464?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Randomized%2C+double-blind%2C+placebo-controlled+trial+of+soluble+tumor+necrosis+factor+receptor%3A+enbrel+%28etanercept%29+for+the+treatment+of+idiopathic+pneumonia+syndrome+after+allogeneic+stem+cell+transplantation%3A+blood+and+marrow+transplant+clinical+trials+network+protocol.&rft.au=Yanik%2C+Gregory+A%3BHorowitz%2C+Mary+M%3BWeisdorf%2C+Daniel+J%3BLogan%2C+Brent+R%3BHo%2C+Vincent+T%3BSoiffer%2C+Robert+J%3BCarter%2C+Shelly+L%3BWu%2C+Juan%3BWingard%2C+John+R%3BDifronzo%2C+Nancy+L%3BFerrara%2C+James+L%3BGiralt%2C+Sergio%3BMadtes%2C+David+K%3BDrexler%2C+Rebecca%3BWhite%2C+Eric+S%3BCooke%2C+Kenneth+R&rft.aulast=Yanik&rft.aufirst=Gregory&rft.date=2014-06-01&rft.volume=20&rft.issue=6&rft.spage=858&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.2014.02.026 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-09 N1 - Date created - 2014-05-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Transplantation. 2000 Jul 27;70(2):272-9 [10933148] J Immunol. 2000 Dec 1;165(11):6612-9 [11086106] Biol Blood Marrow Transplant. 2002;8(7):395-400 [12171486] Blood. 2003 Oct 15;102(8):2777-85 [12855568] Am Rev Respir Dis. 1993 Jun;147(6 Pt 1):1393-400 [8503550] Am Rev Respir Dis. 1993 Jun;147(6 Pt 1):1601-6 [8503576] Blood. 1996 Oct 15;88(8):3230-9 [8963063] Transplantation. 1997 Apr 27;63(8):1079-86 [9133468] Crit Care Med. 1999 Sep;27(9):1800-6 [10507601] Blood. 2008 Oct 15;112(8):3073-81 [18664626] Biol Blood Marrow Transplant. 2010 Jan;16(1 Suppl):S106-14 [19896545] Bone Marrow Transplant. 2010 Apr;45(4):647-55 [19684637] Am J Respir Crit Care Med. 2011 May 1;183(9):1262-79 [21531955] Pediatr Blood Cancer. 2012 May;58(5):780-4 [21922645] Mol Cell Proteomics. 2012 Jun;11(6):M111.015479 [22337588] Bone Marrow Transplant. 2012 Oct;47(10):1332-7 [22307018] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbmt.2014.02.026 ER - TY - JOUR T1 - Relative potency for altered humoral immunity induced by polybrominated and polychlorinated dioxins/furans in female B6C3F1/N mice. AN - 1524168409; 24713691 AB - The use of brominated flame retardants and incineration of bromine-containing materials has lead to an increase in polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) in the environment. Measurable amounts of PBDD/Fs have been detected in soil, seafood, and human breast milk and serum. Studies indicate that the relative potencies of some PBDD/Fs based on enzyme induction are equivalent to those of some polychlorinated dibenzo-p-dioxins and dibenzofurans. To assess the humoral immunity relative potencies of PBDD/Fs and compare them to their chlorinated analogs, female B6C3F1/N mice received a single oral exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,7,8-tetrabromodibenzofuran (TBDF), 2,3,7,8-tetrachlorodibenzofuran (TCDF), 1,2,3,7,8-pentabromodibenzofuran (1PeBDF), 1,2,3,7,8-pentachlorodibenzofuran (1PeCDF), 2,3,4,7,8-pentabromodibenzofuran (4PeBDF), 2,3,4,7,8-pentachlorodibenzofuran (4PeCDF), 2,3-dibromo-7,8-dichlorodibenzo-p-dioxin (DBDCDD), or 2,3,7-tribromodibenzo-p-dioxin (TriBDD). Inhibition of the immunoglobulin M (IgM) antibody forming cell response was measured 4 days following immunization with sheep red blood cells. The data were fit to a Hill model to estimate the ED50 for inhibition. Expression of xenobiotic metabolizing enzyme (XME) and thyroxine transport protein (Ttr) genes in liver was measured by PCR to assess aryl hydrocarbon-mediated responses. TCDD, TBDF, TCDF, 1PeBDF, 4PeBDF, 4PeCDF, and DBDCDD suppressed the IgM antibody response and Ttr gene expression, and upregulated phase I XME genes. 1PeCDF suppressed the IgM antibody response but only upregulated phase I XME genes; TriBDD had no effect on antibody response. The rank order of potency (ED50) for these chemicals was TCDD>TBDF>4PeBDF>TCDF/4PeCDF/1PeBDF>1PeCDF. Whereas TCDD was the most potent compound tested, the brominated analogs were more potent than their chlorinated analogs, suggesting that these compounds should be considered in toxic equivalency factor evaluation and risk assessment. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Frawley, Rachel AU - DeVito, Michael AU - Walker, Nigel J AU - Birnbaum, Linda AU - White, Kimber AU - Smith, Matthew AU - Maynor, Timothy AU - Recio, Leslie AU - Germolec, Dori AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 488 EP - 500 VL - 139 IS - 2 KW - Benzofurans KW - 0 KW - Dioxins KW - Hydrocarbons, Brominated KW - Hydrocarbons, Chlorinated KW - Immunoglobulin M KW - Index Medicus KW - 3 KW - 2 KW - brominated furans KW - IgM antibody forming cell KW - 7 KW - toxic equivalency factor KW - 8-tetrachlorodibenzo-p-dioxin KW - relative potency KW - chlorinated furans KW - TEF KW - brominated dioxins KW - Molecular Structure KW - Animals KW - Liver -- enzymology KW - Dose-Response Relationship, Drug KW - Immunoglobulin M -- immunology KW - Liver -- metabolism KW - Gene Expression Profiling KW - Mice, Inbred Strains KW - Liver -- drug effects KW - Spleen -- immunology KW - Spleen -- drug effects KW - Transcriptome KW - Erythrocytes -- immunology KW - Female KW - Immunity, Humoral -- drug effects KW - Hydrocarbons, Chlorinated -- toxicity KW - Dioxins -- chemistry KW - Hydrocarbons, Chlorinated -- chemistry KW - Dioxins -- toxicity KW - Hydrocarbons, Brominated -- chemistry KW - Hydrocarbons, Brominated -- toxicity KW - Benzofurans -- toxicity KW - Benzofurans -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524168409?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Relative+potency+for+altered+humoral+immunity+induced+by+polybrominated+and+polychlorinated+dioxins%2Ffurans+in+female+B6C3F1%2FN+mice.&rft.au=Frawley%2C+Rachel%3BDeVito%2C+Michael%3BWalker%2C+Nigel+J%3BBirnbaum%2C+Linda%3BWhite%2C+Kimber%3BSmith%2C+Matthew%3BMaynor%2C+Timothy%3BRecio%2C+Leslie%3BGermolec%2C+Dori&rft.aulast=Frawley&rft.aufirst=Rachel&rft.date=2014-06-01&rft.volume=139&rft.issue=2&rft.spage=488&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfu041 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-29 N1 - Date created - 2014-05-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicology. 2000 Dec 7;156(1):1-11 [11162871] Toxicol Lett. 2013 Jul 18;220(3):294-302 [23680695] Environ Int. 2001 Nov;27(5):413-39 [11757855] Toxicol Sci. 2002 Aug;68(2):372-80 [12151633] Environ Sci Technol. 2003 Mar 1;37(5):817-21 [12666907] Environ Int. 2003 Sep;29(6):855-60 [12850101] Environ Int. 2003 Sep;29(6):861-77 [12850102] Food Cosmet Toxicol. 1980 Aug;18(4):387-92 [7461518] Toxicol Lett. 1983 Feb;15(2-3):259-64 [6829049] Annu Rev Pharmacol Toxicol. 1986;26:371-99 [3013079] Toxicology. 1987 Jun;44(3):245-55 [3033849] Toxicol Appl Pharmacol. 1988 Jun 15;94(1):141-9 [2836965] Fundam Appl Toxicol. 1992 Feb;18(2):200-10 [1534777] Fundam Appl Toxicol. 1993 Nov;21(4):412-9 [8253294] Fundam Appl Toxicol. 1995 Jan;24(1):145-8 [7713338] Environ Health Perspect. 1998 Dec;106(12):775-92 [9831538] Science. 1963 Apr 26;140(3565):405 [13957684] Toxicol Sci. 2006 Oct;93(2):223-41 [16829543] Toxicol Sci. 2008 Sep;105(1):33-43 [18566023] Toxicol Sci. 2009 Jan;107(1):27-39 [18978342] Environ Int. 2009 Apr;35(3):588-93 [19121869] J Nutr Biochem. 2009 Jun;20(6):469-76 [18789671] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2009 Jun;26(6):918-27 [19680967] Environ Sci Technol. 2009 Oct 1;43(19):7350-6 [19848145] Chemosphere. 2010 Jan;78(2):113-20 [19897226] Methods Mol Biol. 2010;598:173-84 [19967513] Biol Chem. 2009 Dec;390(12):1225-35 [19747074] Biol Chem. 2010 Oct;391(10):1205-19 [20707612] Environ Health Perspect. 2011 Mar;119(3):371-6 [21041162] J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):96-101 [21168493] J Chromatogr A. 2011 Dec 23;1218(51):9279-87 [22098927] Drug Metab Dispos. 2012 Mar;40(3):588-95 [22187485] Chemosphere. 2012 May;87(9):1063-9 [22405723] J Biopharm Stat. 2013 May;23(3):648-61 [23611201] Toxicol Sci. 2013 Jun;133(2):197-208 [23492812] Curr Drug Metab. 2001 Jun;2(2):149-64 [11469723] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kfu041 ER - TY - JOUR T1 - The effects of add-on low-dose memantine on cytokine levels in bipolar II depression: a 12-week double-blind, randomized controlled trial. AN - 1521329320; 24717258 AB - Memantine, a noncompetitive N-methyl-d-aspartate receptor antagonist with a mood-stabilizing effect, and an association between bipolar disorder and proinflammatory cytokine levels have been reported. Whether adding-on memantine would reduce cytokine levels and is more effective than valproic acid (VPA) alone in bipolar II disorder was investigated. A randomized, double-blind, controlled, 12-week study was conducted. Patients undergoing regular VPA treatments were randomly assigned to a group: VPA + memantine (5 mg/d) (n = 106) or VPA + placebo (n = 108). The Hamilton Depression Rating Scale (HDRS) and Young Mania Rating Scale (YMRS) were used to evaluate clinical response. Symptom severity, plasma tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-8, and IL-1 levels were examined during weeks 0, 1, 2, 4, 8, and 12. To adjust within-subject dependence over repeated assessments, multiple linear regressions with generalized estimating equation methods were used to examine the therapeutic effect. Tumor necrosis factor α levels were significantly lower in the VPA + memantine group than in the VPA + placebo group (P = 0.013). Posttreatment HDRS and YMRS scores decreased significantly in both groups, but not significant, nor was the other between-group cytokine level difference pretreatment and posttreatment. The HDRS score changes were significantly associated with IL-6 (P = 0.012) and IL-1 (P = 0.005) level changes and changes in YMRS score changes with TNF-α (P = 0.005) level changes. Treating bipolar II depression with VPA + memantine may improve the plasma TNF-α level. However, adding-on memantine may not improve clinical symptoms or cytokine levels other than TNF-α. Clinical symptoms may be correlated with certain cytokines. JF - Journal of clinical psychopharmacology AU - Lee, Sheng-Yu AU - Chen, Shiou-Lan AU - Chang, Yun-Hsuan AU - Chen, Po See AU - Huang, San-Yuan AU - Tzeng, Nian-Sheng AU - Wang, Yu-Shan AU - Wang, Liang-Jen AU - Lee, I Hui AU - Wang, Tzu-Yun AU - Yeh, Tzung Lieh AU - Yang, Yen Kuang AU - Hong, Jau-Shyong AU - Lu, Ru-Band AD - From the *Department of Psychiatry, †Institute of Behavioral Medicine, and ‡Institute of Allied Health Sciences, College of Medicine and Hospital, National Cheng Kung University, Tainan; §Department of Psychiatry, Tri-Service General Hospital, National Defense Medical Center, Taipei; ∥Department of Child and Adolescent Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung; ¶Department of Psychiatry, Tainan Hospital, Department of Health, Executive Yuan, Tainan; #Addiction Research Center, National Cheng Kung University, Tainan, Taiwan; and **Laboratory of Toxicology and Pharmacology, NIH/NIEHS, Research Triangle Park, NC. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 337 EP - 343 VL - 34 IS - 3 KW - Antimanic Agents KW - 0 KW - Cytokines KW - Excitatory Amino Acid Antagonists KW - Receptors, N-Methyl-D-Aspartate KW - Valproic Acid KW - 614OI1Z5WI KW - Memantine KW - W8O17SJF3T KW - Index Medicus KW - Severity of Illness Index KW - Young Adult KW - Double-Blind Method KW - Humans KW - Linear Models KW - Excitatory Amino Acid Antagonists -- administration & dosage KW - Drug Therapy, Combination KW - Psychiatric Status Rating Scales KW - Adult KW - Antimanic Agents -- administration & dosage KW - Excitatory Amino Acid Antagonists -- therapeutic use KW - Treatment Outcome KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Antimanic Agents -- therapeutic use KW - Female KW - Male KW - Cytokines -- drug effects KW - Memantine -- therapeutic use KW - Memantine -- administration & dosage KW - Bipolar Disorder -- drug therapy KW - Cytokines -- metabolism KW - Valproic Acid -- therapeutic use KW - Valproic Acid -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521329320?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+psychopharmacology&rft.atitle=The+effects+of+add-on+low-dose+memantine+on+cytokine+levels+in+bipolar+II+depression%3A+a+12-week+double-blind%2C+randomized+controlled+trial.&rft.au=Lee%2C+Sheng-Yu%3BChen%2C+Shiou-Lan%3BChang%2C+Yun-Hsuan%3BChen%2C+Po+See%3BHuang%2C+San-Yuan%3BTzeng%2C+Nian-Sheng%3BWang%2C+Yu-Shan%3BWang%2C+Liang-Jen%3BLee%2C+I+Hui%3BWang%2C+Tzu-Yun%3BYeh%2C+Tzung+Lieh%3BYang%2C+Yen+Kuang%3BHong%2C+Jau-Shyong%3BLu%2C+Ru-Band&rft.aulast=Lee&rft.aufirst=Sheng-Yu&rft.date=2014-06-01&rft.volume=34&rft.issue=3&rft.spage=337&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+psychopharmacology&rft.issn=1533-712X&rft_id=info:doi/10.1097%2FJCP.0000000000000109 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-09 N1 - Date created - 2014-05-05 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/JCP.0000000000000109 ER - TY - JOUR T1 - S6 kinase 2 is bound to chromatin-nuclear matrix cellular fractions and is able to phosphorylate histone H3 at threonine 45 in vitro and in vivo. AN - 1517398440; 23564320 AB - The activity of S6 kinases (S6K) is highly induced in cancer cells highlighting an essential role in carcinogenesis. The S6K family has two members: S6K1 and S6K2 which bear common as well as distinct features. In an attempt to identify S6K2 unique sequence features compared to S6K1, we applied extensive bioinformatic analysis and motif search approaches. Interestingly, we identified 14 unique protein signatures which are present in proteins directly connected to chromatin and/or involved in transcription regulation. Using chromatin binding assay, we biochemically showed that S6K2 is bound to chromatin as well as nuclear matrix cellular fractions in HEK293 cells. The presence of S6K2 in chromatin fractions raised the possibility that it may be in close proximity to a number of chromatin substrates. For that, we then searched for S6K phosphorylation consensus sites RXRXXT/S in mammalian proteins using the SWISS-PROT database. Interestingly, we identified some potential phosphorylation sites in histone H3 (Thr45). Using in vitro kinase assays and siRNA-based knockdown strategy; we confirmed that S6K2 but not S6K1 or AKT is essential for histone H3-Thr45 phosphorylation in HEK293 cells. Furthermore, we show that the nuclear localisation sequence in the S6K2 C-terminus is essential for this modification. We have found that, H3-Thr45 phosphorylation correlates to S6K activation in response to mitogens and TPA-induced cell differentiation of leukaemic cell lines U937, HL60 and THP1. Overall, we demonstrate that S6K2 is a novel kinase that can phosphorylate histone H3 at position Thr45, which may play a role during cell proliferation and/or differentiation. © 2014 Wiley Periodicals, Inc. JF - Journal of cellular biochemistry AU - Ismail, Heba M S AU - Hurd, Paul J AU - Khalil, Mahmoud I M AU - Kouzarides, Tony AU - Bannister, Andrew AU - Gout, Ivan AD - Institute of Structural and Molecular Biology, University College London, London, WC1E 6BT, United Kingdom; Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 1048 EP - 1062 VL - 115 IS - 6 KW - Chromatin KW - 0 KW - Histones KW - Threonine KW - 2ZD004190S KW - Proto-Oncogene Proteins c-akt KW - EC 2.7.11.1 KW - Ribosomal Protein S6 Kinases, 70-kDa KW - Ribosomal Protein S6 Kinases, 90-kDa KW - ribosomal protein S6 kinase, 70kD, polypeptide 1 KW - ribosomal protein S6 kinase, 90kDa, polypeptide 3 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - S6K2 KW - CHROMATIN KW - H3 PHOSPHORYLATION KW - Proto-Oncogene Proteins c-akt -- genetics KW - Proto-Oncogene Proteins c-akt -- metabolism KW - Animals KW - HL-60 Cells KW - HEK293 Cells KW - Humans KW - Amino Acid Sequence KW - Cell Line, Tumor KW - Mice KW - Ribosomal Protein S6 Kinases, 70-kDa -- metabolism KW - Protein Binding KW - Ribosomal Protein S6 Kinases, 70-kDa -- genetics KW - NIH 3T3 Cells KW - Cell Fractionation KW - Blotting, Western KW - Phosphorylation KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Middle Aged KW - RNA Interference KW - Cell Differentiation -- drug effects KW - U937 Cells KW - Ribosomal Protein S6 Kinases, 90-kDa -- metabolism KW - Chromatin -- metabolism KW - Threonine -- metabolism KW - Nuclear Matrix -- metabolism KW - Histones -- metabolism KW - Ribosomal Protein S6 Kinases, 90-kDa -- genetics KW - Chromatin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1517398440?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biochemistry&rft.atitle=S6+kinase+2+is+bound+to+chromatin-nuclear+matrix+cellular+fractions+and+is+able+to+phosphorylate+histone+H3+at+threonine+45+in+vitro+and+in+vivo.&rft.au=Ismail%2C+Heba+M+S%3BHurd%2C+Paul+J%3BKhalil%2C+Mahmoud+I+M%3BKouzarides%2C+Tony%3BBannister%2C+Andrew%3BGout%2C+Ivan&rft.aulast=Ismail&rft.aufirst=Heba+M&rft.date=2014-06-01&rft.volume=115&rft.issue=6&rft.spage=1048&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+biochemistry&rft.issn=1097-4644&rft_id=info:doi/10.1002%2Fjcb.24566 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-15 N1 - Date created - 2014-04-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/jcb.24566 ER - TY - JOUR T1 - Characterization of an anti-Bla g 1 scFv: epitope mapping and cross-reactivity. AN - 1514436205; 24667070 AB - Bla g 1 is a major allergen from Blatella germanica and one of the primary allergens used to assess cockroach allergen exposure. The epitope of an anti-Bla g 1 scFv was mapped in order to better understand cross reactivity with other group 1 cockroach allergens and patient IgE epitopes. X-ray crystallography was used to determine the structure of the scFv. The scFv epitope on Bla g 1 was located by alanine scanning site-directed mutagenesis and ELISA. Twenty-six rBla g 1-GST alanine mutants were evaluated for variations in binding to the scFv compared to the wild type allergen. Six mutants showed a significant difference in scFv binding affinity. These mutations clustered to form a discontinuous epitope mainly comprising two helices of Bla g 1. The allergen-scFv complex was modeled based on the results, and the epitope region was found to have low sequence similarity with Per a 1, especially among the residues identified as functionally important for the scFv binding to Bla g 1. Indeed, the scFv failed to bind Per a 1 in American cockroach extract. The scFv was unable to inhibit the binding of IgE antibodies from a highly cockroach allergic patient to Bla g 1. Based on the surface area of Bla g 1 occluded by the scFv, putative regions of patient IgE-Bla g 1 interactions can be inferred. This scFv could be best utilized as a capture antibody in an IgE detection ELISA, or to differentiate Bla g 1 from Per a 1 in environmental exposure assays. Published by Elsevier Ltd. JF - Molecular immunology AU - Mueller, Geoffrey A AU - Ankney, John A AU - Glesner, Jill AU - Khurana, Taruna AU - Edwards, Lori L AU - Pedersen, Lars C AU - Perera, Lalith AU - Slater, Jay E AU - Pomés, Anna AU - London, Robert E AD - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Electronic address: mueller3@niehs.nih.gov. ; National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Indoor Biotechnologies, Inc., Charlottesville, VA 22903, USA. ; U.S. Food and Drug Administration, Bethesda, MD 20892, USA. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 200 EP - 207 VL - 59 IS - 2 KW - Allergens KW - 0 KW - Epitopes KW - Single-Chain Antibodies KW - allergen Bla g 1 KW - allergen Per a I KW - Immunoglobulin E KW - 37341-29-0 KW - Index Medicus KW - Allergen KW - Epitope KW - Structure KW - Bla g 1 KW - Cockroach KW - scFv KW - Animals KW - Immunoglobulin E -- immunology KW - Models, Molecular KW - Humans KW - Epitopes -- ultrastructure KW - Crystallography, X-Ray KW - Epitopes -- immunology KW - Binding Sites, Antibody -- immunology KW - Mutation KW - Epitope Mapping KW - Cross Reactions -- immunology KW - Allergens -- immunology KW - Single-Chain Antibodies -- immunology KW - Single-Chain Antibodies -- ultrastructure KW - Cockroaches -- immunology KW - Allergens -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514436205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+immunology&rft.atitle=Characterization+of+an+anti-Bla+g+1+scFv%3A+epitope+mapping+and+cross-reactivity.&rft.au=Mueller%2C+Geoffrey+A%3BAnkney%2C+John+A%3BGlesner%2C+Jill%3BKhurana%2C+Taruna%3BEdwards%2C+Lori+L%3BPedersen%2C+Lars+C%3BPerera%2C+Lalith%3BSlater%2C+Jay+E%3BPom%C3%A9s%2C+Anna%3BLondon%2C+Robert+E&rft.aulast=Mueller&rft.aufirst=Geoffrey&rft.date=2014-06-01&rft.volume=59&rft.issue=2&rft.spage=200&rft.isbn=&rft.btitle=&rft.title=Molecular+immunology&rft.issn=1872-9142&rft_id=info:doi/10.1016%2Fj.molimm.2014.02.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-05 N1 - Date created - 2014-04-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2001 Mar 23;276(12):9359-65 [11134039] Clin Exp Allergy. 2002 May;32(5):721-7 [11994096] Eur J Immunol. 2002 Aug;32(8):2156-62 [12209627] J Am Chem Soc. 2003 Feb 19;125(7):1731-7 [12580598] Annu Rev Immunol. 1984;2:67-101 [6085753] Science. 1990 Aug 17;249(4970):755-9 [1697101] J Allergy Clin Immunol. 1991 Feb;87(2):505-10 [1993810] J Allergy Clin Immunol. 1991 Feb;87(2):511-21 [1993811] Int Arch Allergy Immunol. 1995 Mar;106(3):250-7 [7534151] J Biol Chem. 1995 Aug 18;270(33):19563-8 [7642642] J Allergy Clin Immunol. 1996 Jul;98(1):172-80 [8765832] N Engl J Med. 1997 May 8;336(19):1356-63 [9134876] J Allergy Clin Immunol. 1998 Oct;102(4 Pt 1):563-70 [9802363] J Biol Chem. 1998 Nov 13;273(46):30801-7 [9804858] J Allergy Clin Immunol. 1999 May;103(5 Pt 1):859-64 [10329820] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] J Allergy Clin Immunol. 2005 Apr;115(4):803-9 [15806002] J Mol Biol. 2005 Apr 29;348(2):433-44 [15811379] Clin Exp Allergy. 2005 Aug;35(8):1040-8 [16120086] Protein Pept Lett. 2007;14(10):960-9 [18220993] J Allergy Clin Immunol. 2008 Mar;121(3):678-684.e2 [18255132] Methods Mol Biol. 2008;426:419-35 [18542881] J Biol Chem. 2008 Aug 15;283(33):22806-14 [18519566] J Biol Chem. 2009 Nov 13;284(46):31928-35 [19776018] Allergy. 2010 Nov;65(11):1414-22 [20560910] Ann Allergy Asthma Immunol. 2010 Nov;105(5):351-8 [21055660] PLoS One. 2011;6(7):e22223 [21789239] Allergy. 2011 Oct;66(10):1261-74 [21623828] J Biol Chem. 2012 Mar 2;287(10):7388-98 [22210776] J Mol Med (Berl). 2012 Jul;90(7):837-46 [22307521] J Immunol. 2012 Jul 15;189(2):679-88 [22706084] J Allergy Clin Immunol. 2013 Dec;132(6):1420-6 [23915714] Genome Biol Evol. 2013;5(12):2344-58 [24253356] Methods. 2014 Mar 1;66(1):3-21 [23891546] Arb Paul Ehrlich Inst Bundesinstitut Impfstoffe Biomed Arzneim Langen Hess. 2013;97:37-44 [24912311] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.molimm.2014.02.003 ER - TY - JOUR T1 - Targeting STAT3 phosphorylation by neem leaf glycoprotein prevents immune evasion exerted by supraglottic laryngeal tumor induced M2 macrophages. AN - 1514435985; 24607970 AB - Tumor-associated macrophages (TAMs) are preferentially M2 skewed and promote tumor growth, angiogenesis, invasion, and/or metastasis. In this study, we have analyzed the in vitro immunomodulatory potential of a non-toxic neem leaf glycoprotein (NLGP) in reprogramming Stage III supraglottic laryngeal tumor cell lysate (SLTCL) induced M2 TAMs to their classical anti-tumor shape (M1). Data generated from this study support that NLGP is effective in preventing the SLTCL induced generation (CD68(+)CD206(+)IL-10(high) to CD68(+)CD206(-)IL-10(low) TAMs) and functions (NO(low) to NO(high), MHC-I(low) to MHC-I(high), CD80(low) to CD80(high)) of pro-tumorous M2 macrophages, which in turn associated with sustained anti-tumor effector functions by promoting cytotoxic T cell activities and suppressing regulatory T cells. Furthermore, our data also suggest that NLGP prevents M2 skewness of TAMs by downregulating phosphorylation of targeted STAT3. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - Molecular immunology AU - Goswami, K K AU - Barik, S AU - Sarkar, M AU - Bhowmick, A AU - Biswas, J AU - Bose, A AU - Baral, R AD - Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata, 700026, India. ; Department of ENT and Head-Neck Oncology, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata, 700026, India. ; Department of Surgical Oncology and Medical Oncology, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata 700026, India. ; Department of Molecular Medicine, Bose Institute, C.I.T. Scheme, Kolkata, India. ; Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata, 700026, India. Electronic address: rathindranath.baral@cnci.org.in. Y1 - 2014/06// PY - 2014 DA - June 2014 SP - 119 EP - 127 VL - 59 IS - 2 KW - Glycoproteins KW - 0 KW - IL10 protein, human KW - Immunologic Factors KW - Plant Extracts KW - RNA, Small Interfering KW - STAT3 Transcription Factor KW - STAT3 protein, human KW - Interleukin-10 KW - 130068-27-8 KW - Interleukin-12 KW - 187348-17-0 KW - Nitric Oxide KW - 31C4KY9ESH KW - NOS2 protein, human KW - EC 1.14.13.39 KW - Nitric Oxide Synthase Type II KW - Index Medicus KW - Tumor-associated macrophages KW - Supraglottic laryngeal tumor cell lysate KW - T cells KW - Neem leaf glycoprotein KW - Humans KW - Cell Line, Tumor KW - T-Lymphocytes, Cytotoxic -- immunology KW - Nitric Oxide -- biosynthesis KW - Nitric Oxide Synthase Type II -- biosynthesis KW - Plant Extracts -- pharmacology KW - Phosphorylation KW - Interleukin-12 -- biosynthesis KW - Interleukin-10 -- biosynthesis KW - Down-Regulation -- drug effects KW - RNA Interference KW - T-Lymphocytes, Regulatory -- immunology KW - Macrophages -- immunology KW - Immune Evasion -- drug effects KW - Glycoproteins -- pharmacology KW - Laryngeal Neoplasms -- immunology KW - Immunologic Factors -- pharmacology KW - Azadirachta -- chemistry KW - STAT3 Transcription Factor -- genetics KW - STAT3 Transcription Factor -- metabolism KW - Plant Leaves -- chemistry KW - Macrophages -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514435985?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+immunology&rft.atitle=Targeting+STAT3+phosphorylation+by+neem+leaf+glycoprotein+prevents+immune+evasion+exerted+by+supraglottic+laryngeal+tumor+induced+M2+macrophages.&rft.au=Goswami%2C+K+K%3BBarik%2C+S%3BSarkar%2C+M%3BBhowmick%2C+A%3BBiswas%2C+J%3BBose%2C+A%3BBaral%2C+R&rft.aulast=Goswami&rft.aufirst=K&rft.date=2014-06-01&rft.volume=59&rft.issue=2&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Molecular+immunology&rft.issn=1872-9142&rft_id=info:doi/10.1016%2Fj.molimm.2014.01.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-05 N1 - Date created - 2014-04-07 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.molimm.2014.01.015 ER - TY - JOUR T1 - Repair of DNA double-strand breaks by templated nucleotide sequence insertions derived from distant regions of the genome. AN - 1534796520; 24821809 AB - We used the I-SceI endonuclease to produce DNA double-strand breaks (DSBs) and observed that a fraction of these DSBs were repaired by insertion of sequences, which we termed "templated sequence insertions" (TSIs), derived from distant regions of the genome. These TSIs were derived from genic, retrotransposon, or telomere sequences and were not deleted from the donor site in the genome, leading to the hypothesis that they were derived from reverse-transcribed RNA. Cotransfection of RNA and an I-SceI expression vector demonstrated insertion of RNA-derived sequences at the DNA-DSB site, and TSIs were suppressed by reverse-transcriptase inhibitors. Both observations support the hypothesis that TSIs were derived from RNA templates. In addition, similar insertions were detected at sites of DNA DSBs induced by transcription activator-like effector nuclease proteins. Whole-genome sequencing of myeloma cell lines revealed additional TSIs, demonstrating that repair of DNA DSBs via insertion was not restricted to experimentally produced DNA DSBs. Analysis of publicly available databases revealed that many of these TSIs are polymorphic in the human genome. Taken together, these results indicate that insertional events should be considered as alternatives to gross chromosomal rearrangements in the interpretation of whole-genome sequence data and that this mutagenic form of DNA repair may play a role in genetic disease, exon shuffling, and mammalian evolution. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Onozawa, Masahiro AU - Zhang, Zhenhua AU - Kim, Yoo Jung AU - Goldberg, Liat AU - Varga, Tamas AU - Bergsagel, P Leif AU - Kuehl, W Michael AU - Aplan, Peter D AD - Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; and. ; Comprehensive Cancer Center, Mayo Clinic, Scottsdale, AZ 85259. ; Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; and aplanp@mail.nih.gov. Y1 - 2014/05/27/ PY - 2014 DA - 2014 May 27 SP - 7729 EP - 7734 VL - 111 IS - 21 KW - Cinnamates KW - 0 KW - DNA Primers KW - Retroelements KW - Hygromycin B KW - 3XQ2233B0B KW - hygromycin A KW - 3YJY415DDI KW - Index Medicus KW - TSIP KW - LINE-1 KW - polymorphism KW - DNA patch KW - Polymerase Chain Reaction KW - DNA Copy Number Variations KW - DNA Primers -- genetics KW - Humans KW - Cell Line, Tumor KW - Genetic Vectors -- genetics KW - Computational Biology KW - Hygromycin B -- analogs & derivatives KW - DNA Repair -- genetics KW - Retroelements -- genetics KW - Telomere -- genetics KW - DNA Breaks, Double-Stranded KW - Mutagenesis, Insertional -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534796520?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Repair+of+DNA+double-strand+breaks+by+templated+nucleotide+sequence+insertions+derived+from+distant+regions+of+the+genome.&rft.au=Onozawa%2C+Masahiro%3BZhang%2C+Zhenhua%3BKim%2C+Yoo+Jung%3BGoldberg%2C+Liat%3BVarga%2C+Tamas%3BBergsagel%2C+P+Leif%3BKuehl%2C+W+Michael%3BAplan%2C+Peter+D&rft.aulast=Onozawa&rft.aufirst=Masahiro&rft.date=2014-05-27&rft.volume=111&rft.issue=21&rft.spage=7729&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.1321889111 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-02 N1 - Date created - 2014-06-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Annu Rev Biochem. 2006;75:493-517 [16756500] Trends Genet. 2006 Jan;22(1):46-55 [16257470] J Exp Med. 2007 Mar 19;204(3):633-43 [17353367] Nature. 2007 May 17;447(7142):338-41 [17429354] PLoS One. 2008;3(2):e1547 [18253495] Genome Biol. 2007;8(12):R260 [18067655] Nat Genet. 2009 Jul;41(7):849-53 [19543269] Nat Rev Genet. 2009 Oct;10(10):691-703 [19763152] Mutat Res. 2010 Jan 5;683(1-2):115-22 [19909760] Nat Rev Mol Cell Biol. 2010 Mar;11(3):182-95 [20164840] Cell. 2010 Apr 2;141(1):27-38 [20371343] Annu Rev Biochem. 2010;79:181-211 [20192759] Cell. 2010 Jun 25;141(7):1171-82 [20602999] Semin Cancer Biol. 2010 Aug;20(4):222-33 [20541013] Bioinformatics. 2010 Nov 1;26(21):2684-8 [20876606] Cell. 2010 Nov 24;143(5):837-47 [21111241] BMC Biochem. 2011;12:18 [21545744] Cell. 2011 Sep 30;147(1):95-106 [21962510] Cell. 2011 Sep 30;147(1):107-19 [21962511] Cell. 2012 Mar 2;148(5):908-21 [22341456] Nat Biotechnol. 2012 May;30(5):460-5 [22484455] Mol Cell. 1999 Nov;4(5):873-81 [10619034] Blood. 2000 Feb 1;95(3):1032-8 [10648419] Nat Genet. 2000 Apr;24(4):363-7 [10742098] Nature. 2000 Jun 8;405(6787):697-700 [10864328] Br J Haematol. 2001 Feb;112(2):388-91 [11167836] Genetics. 2001 Aug;158(4):1665-74 [11514454] Cell. 2012 Jul 20;150(2):264-78 [22817890] Science. 2012 Aug 24;337(6097):967-71 [22745252] Nature. 2012 Nov 1;491(7422):56-65 [23128226] Annu Rev Genet. 2012;46:455-73 [23146099] Annu Rev Genet. 2013;47:433-55 [24050180] Genome Biol. 2013;14(3):R22 [23497673] Leukemia. 2014 Aug;28(8):1725-35 [24518206] Nature. 2012 Aug 9;488(7410):231-5 [22722852] Nat Genet. 2002 Jun;31(2):159-65 [12006980] Hum Genet. 2002 Jun;110(6):578-86 [12107444] Nat Genet. 2004 Oct;36(10):1065-71 [15361872] Cell. 1991 Oct 18;67(2):355-64 [1655280] Antimicrob Agents Chemother. 1994 Dec;38(12):2743-9 [7695256] Leukemia. 1996 May;10(5):866-76 [8656685] Nature. 1996 Oct 17;383(6601):641-4 [8857543] Nature. 1996 Oct 17;383(6601):644-6 [8857544] J Neurol Sci. 1997 Jul;149(1):19-25 [9168161] DNA Repair (Amst). 2005 May 2;4(5):546-55 [15811627] DNA Repair (Amst). 2005 Aug 15;4(9):1038-46 [15935739] Nature. 2007 Mar 8;446(7132):208-12 [17344853] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1321889111 ER - TY - JOUR T1 - 3,4-Methylenedioxypyrovalerone (MDPV) and metabolites quantification in human and rat plasma by liquid chromatography-high resolution mass spectrometry. AN - 1525764939; 24832995 AB - Synthetic cathinones are recreational drugs that mimic the effects of illicit stimulants like cocaine, amphetamine or Ecstasy. Among the available synthetic cathinones in the United States, 3,4-methylenedioxypyrovalerone (MDPV) is commonly abused and associated with dangerous side effects. MDPV is a dopamine transporter blocker 10-fold more potent than cocaine as a locomotor stimulant in rats. Previous in vitro and in vivo studies examining MDPV metabolism reported 3,4-dihydroxypyrovalerone (3,4-catechol-PV) and 4-hydroxy-3-methoxypyrovalerone (4-OH-3-MeO-PV) as the two primary metabolites. We developed and validated a liquid chromatography-high resolution mass spectrometry method to quantify MDPV and its primary metabolites in 100 μL human and rat plasma. Plasma hydrolysis was followed by protein precipitation before analysis. Limits of detection were 0.1 μg L(-1), with linear ranges from 0.25 to 1000 μg L(-1). Process efficiency, matrix effect, total imprecision (%CV) and accuracy (%target) were 36-93%, from -8 to 12%, 2.1 to 7.3% and 86 to 109%, respectively. MDPV and metabolites were stable at room temperature for 24 h, 4 °C for 72 h and after 3 freeze-thaw cycles with less than 10% variability. Human-rat plasma cross validation demonstrated that rat plasma could be accurately quantified against a human plasma calibration curve. As proof of this method, rat plasma specimens were analyzed after intraperitoneal and subcutaneous dosing with MDPV (0.5 mg kg(-1)). MDPV, 3,4-catechol-PV and 4-OH-3-MeO-PV concentrations ranged from not detected to 107.5 μg L(-1) prior to and up to 8h after dosing. This method provides a simultaneous quantification of MDPV and two metabolites in plasma with good selectivity and sensitivity. Published by Elsevier B.V. JF - Analytica chimica acta AU - Anizan, Sebastien AU - Ellefsen, Kayla AU - Concheiro, Marta AU - Suzuki, Masaki AU - Rice, Kenner C AU - Baumann, Michael H AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Drug Design and Synthesis Section, Intramural Research Program, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Baltimore, MD, USA; On leave from the Medicinal Chemistry Group, Qs' Research Institute, Otsuka Pharmaceutical Co., Ltd., Tokushima, Japan. ; Drug Design and Synthesis Section, Intramural Research Program, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Baltimore, MD, USA. ; Designer Drug Research Unit, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. Electronic address: mhuestis@intra.nida.nih.gov. Y1 - 2014/05/27/ PY - 2014 DA - 2014 May 27 SP - 54 EP - 63 VL - 827 KW - 3,4-methylenedioxypyrovalerone KW - 0 KW - Benzodioxoles KW - Pyrrolidines KW - Index Medicus KW - Synthetic cathinones KW - MDPV KW - Metabolites KW - HRMS KW - LC–MS/MS KW - Rats KW - Animals KW - Reproducibility of Results KW - Humans KW - Linear Models KW - Chromatography, Liquid KW - Limit of Detection KW - Hydrolysis KW - Male KW - Mass Spectrometry KW - Benzodioxoles -- blood KW - Pyrrolidines -- chemistry KW - Blood Chemical Analysis -- methods KW - Pyrrolidines -- metabolism KW - Pyrrolidines -- blood KW - Benzodioxoles -- metabolism KW - Benzodioxoles -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1525764939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytica+chimica+acta&rft.atitle=3%2C4-Methylenedioxypyrovalerone+%28MDPV%29+and+metabolites+quantification+in+human+and+rat+plasma+by+liquid+chromatography-high+resolution+mass+spectrometry.&rft.au=Anizan%2C+Sebastien%3BEllefsen%2C+Kayla%3BConcheiro%2C+Marta%3BSuzuki%2C+Masaki%3BRice%2C+Kenner+C%3BBaumann%2C+Michael+H%3BHuestis%2C+Marilyn+A&rft.aulast=Anizan&rft.aufirst=Sebastien&rft.date=2014-05-27&rft.volume=827&rft.issue=&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=Analytica+chimica+acta&rft.issn=1873-4324&rft_id=info:doi/10.1016%2Fj.aca.2014.04.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-19 N1 - Date created - 2014-05-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Chem Res Toxicol. 2001 Sep;14(9):1203-8 [11559034] Life Sci. 2014 Feb 27;97(1):2-8 [23911668] Clin Chem. 1984 Feb;30(2):290-2 [6692538] Ann Emerg Med. 1993 Dec;22(12):1897-903 [8239113] J Med Chem. 2006 Feb 23;49(4):1420-32 [16480278] J Chromatogr B Analyt Technol Biomed Life Sci. 2007 Aug 15;855(2):262-70 [17646137] Anal Bioanal Chem. 2009 Mar;393(6-7):1607-17 [19183967] Rapid Commun Mass Spectrom. 2010 Sep;24(18):2706-14 [20814976] J Mass Spectrom. 2010 Dec;45(12):1426-42 [21053377] Forensic Sci Int. 2011 Jul 15;210(1-3):195-200 [21477955] Drug Test Anal. 2011 Jul-Aug;3(7-8):439-53 [21755607] Clin Toxicol (Phila). 2011 Jul;49(6):499-505 [21824061] J Anal Toxicol. 2011 Sep;35(7):470-80 [21871156] J Miss State Med Assoc. 2011 Dec;52(12):375-7 [22329114] J Med Toxicol. 2012 Mar;8(1):33-42 [22108839] J Anal Toxicol. 2012 Jun;36(5):327-33 [22582267] Ann Emerg Med. 2012 Jul;60(1):103-5 [22387085] Br J Pharmacol. 2013 Jan;168(2):458-70 [22897747] J Anal Toxicol. 2013 Mar;37(2):51-5 [23325764] Neuropsychopharmacology. 2013 Mar;38(4):552-62 [23072836] J Anal Toxicol. 2013 Apr;37(3):135-46 [23361867] Br J Pharmacol. 2013 Apr;168(7):1750-7 [23170765] J Forensic Sci. 2013 Nov;58(6):1654-9 [23822613] Anal Bioanal Chem. 2013 Nov;405(29):9437-48 [24196122] Anal Chem. 2003 Jul 1;75(13):3019-30 [12964746] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.aca.2014.04.015 ER - TY - JOUR T1 - Divalent metal ions enhance DOPAL-induced oligomerization of alpha-synuclein. AN - 1521344182; 24670480 AB - Parkinson disease (PD) features profound striatal dopamine depletion and Lewy bodies containing abundant precipitated alpha-synuclein. Mechanisms linking alpha-synucleinopathy with the death of dopamine neurons remain incompletely understood. One such link may be 3,4-dihydroxyphenylacetaldehyde (DOPAL). All of the intra-neuronal metabolism of dopamine passes through DOPAL, which is toxic. DOPAL also potently oligomerizes alpha-synuclein and alpha-synuclein oligomers are thought to be pathogenic in PD. Another implicated factor in PD pathogenesis is metal ions, and alpha-synuclein contains binding sites for these ions. In this study we tested whether divalent metal ions augment DOPAL-induced oligomerization of alpha-synuclein in cell-free system and in PC12 cells conditionally over-expressing alpha-synuclein. Incubation with divalent metal ions augmented DOPAL-induced oligomerization of alpha-synuclein (Cu(2+)>Fe(2+)>Mn(2+)), whereas monovalent Cu(1+) and trivalent Fe(3+) were without effect. Other dopamine metabolites, dopamine itself, and metal ions alone or in combination with dopamine, also had no effect. Antioxidant treatment with ascorbic acid and divalent cation chelation with EDTA attenuated the augmentation by Cu(2+) of DOPAL-induced alpha-synuclein oligomerization. Incubation of PC12 cells with L-DOPA markedly increased intracellular DOPAL content and promoted alpha-synuclein dimerization. Co-incubation with Cu(2+) amplified (p=0.01), while monoamine oxidase inhibition prevented, L-DOPA-related dimerization of alpha-synuclein (p=0.01). We conclude that divalent metal ions augment DOPAL-induced oligomerization of alpha-synuclein. Drugs that interfere with this interaction might constitute a novel approach for future treatment or prevention approaches. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Neuroscience letters AU - Jinsmaa, Yunden AU - Sullivan, Patricia AU - Gross, Daniel AU - Cooney, Adele AU - Sharabi, Yehonatan AU - Goldstein, David S AD - Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive MSC-1620, Bethesda, MD 20892-1620, USA. ; Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive MSC-1620, Bethesda, MD 20892-1620, USA. Electronic address: goldsteind@ninds.nih.gov. Y1 - 2014/05/21/ PY - 2014 DA - 2014 May 21 SP - 27 EP - 32 VL - 569 KW - Antioxidants KW - 0 KW - Cations, Divalent KW - Chelating Agents KW - Protein Aggregates KW - alpha-Synuclein KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - 3,4-dihydroxyphenylethanol KW - 10597-60-1 KW - Manganese KW - 42Z2K6ZL8P KW - 3,4-dihydroxyphenylacetaldehyde KW - 5707-55-1 KW - Copper KW - 789U1901C5 KW - Edetic Acid KW - 9G34HU7RV0 KW - Iron KW - E1UOL152H7 KW - Phenylethyl Alcohol KW - ML9LGA7468 KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Alpha-synuclein KW - Parkinson disease KW - Oligomerization KW - DOPAL KW - Rats KW - Animals KW - Chelating Agents -- chemistry KW - Dopamine -- chemistry KW - Phenylethyl Alcohol -- analogs & derivatives KW - Humans KW - Phenylethyl Alcohol -- chemistry KW - Ascorbic Acid -- chemistry KW - Antioxidants -- chemistry KW - Protein Multimerization KW - Edetic Acid -- chemistry KW - PC12 Cells KW - 3,4-Dihydroxyphenylacetic Acid -- chemistry KW - alpha-Synuclein -- metabolism KW - alpha-Synuclein -- chemistry KW - Manganese -- chemistry KW - 3,4-Dihydroxyphenylacetic Acid -- pharmacology KW - Iron -- chemistry KW - Copper -- pharmacology KW - Copper -- chemistry KW - 3,4-Dihydroxyphenylacetic Acid -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521344182?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Divalent+metal+ions+enhance+DOPAL-induced+oligomerization+of+alpha-synuclein.&rft.au=Jinsmaa%2C+Yunden%3BSullivan%2C+Patricia%3BGross%2C+Daniel%3BCooney%2C+Adele%3BSharabi%2C+Yehonatan%3BGoldstein%2C+David+S&rft.aulast=Jinsmaa&rft.aufirst=Yunden&rft.date=2014-05-21&rft.volume=569&rft.issue=&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=1872-7972&rft_id=info:doi/10.1016%2Fj.neulet.2014.03.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-09 N1 - Date created - 2014-05-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Arch Biochem Biophys. 2000 Jun 15;378(2):269-77 [10860544] J Neurochem. 2012 Dec;123(6):932-43 [22906103] J Neurochem. 1989 Feb;52(2):515-20 [2911028] Brain. 1991 Aug;114 ( Pt 4):1953-75 [1832073] Nature. 1997 Aug 28;388(6645):839-40 [9278044] Am J Pathol. 1998 Apr;152(4):879-84 [9546347] Biochem J. 1999 Jun 15;340 ( Pt 3):821-8 [10359669] Neurotoxicology. 1999 Apr-Jun;20(2-3):239-47 [10385887] Acta Neuropathol. 2008 Feb;115(2):193-203 [17965867] Arch Neurol. 2008 Dec;65(12):1577-81 [19064744] Biochem Biophys Res Commun. 2009 Mar 6;380(2):377-81 [19250637] Chem Res Toxicol. 2009 Jul;22(7):1256-63 [19537779] FASEB J. 2009 Aug;23(8):2384-93 [19325037] Neuromolecular Med. 2009;11(4):239-51 [19669606] Neurosci Res. 2010 Jan;66(1):124-30 [19835916] J Neurochem. 2010 May;113(3):704-14 [20141569] PLoS One. 2010;5(12):e15251 [21179455] Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4194-9 [21325059] Chem Biol Interact. 2011 Jun 30;192(1-2):118-21 [21238438] J Biol Chem. 2011 Jul 29;286(30):26978-86 [21642436] J Neural Transm. 1988;74(3):199-205 [3210014] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.neulet.2014.03.016 ER - TY - JOUR T1 - Oral anticancer drugs: how limited dosing options and dose reductions may affect outcomes in comparative trials and efficacy in patients. AN - 1526127380; 24711558 AB - Historically, cancer medicine has avoided the problem of unequal dosing by comparing maximum-tolerated doses of intravenous regimens with proportionate dose reductions for toxicity. However, in recent years, with the development of numerous oral anticancer agents, dosing options are arbitrarily and increasingly limited by the size of pills. We contend that an underappreciated consequence of pill size is unequal dosing in comparative clinical trials and that this can have an impact on outcomes. We discuss how comparative effectiveness trials can be unbalanced and how the use of doses that are not sustainable might affect outcomes, especially marginal ones. We further argue that because of their poor tolerability and their limited dosing options, which often result in large dose adjustments in response to toxicity, the real-world clinical effectiveness of oral anticancer agents may be diminished and may not emulate results achieved in registration trials. © 2014 by American Society of Clinical Oncology. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Prasad, Vinay AU - Massey, Paul R AU - Fojo, Tito AD - Vinay Prasad and Tito Fojo, National Cancer Institute, National Institutes of Health, Bethesda, MD; and Paul R. Massey, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. vinayak.prasad@nih.gov. ; Vinay Prasad and Tito Fojo, National Cancer Institute, National Institutes of Health, Bethesda, MD; and Paul R. Massey, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA. Y1 - 2014/05/20/ PY - 2014 DA - 2014 May 20 SP - 1620 EP - 1629 VL - 32 IS - 15 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Administration, Oral KW - Dose-Response Relationship, Drug KW - Humans KW - Treatment Outcome KW - Neoplasms -- drug therapy KW - Antineoplastic Agents -- administration & dosage KW - Drug Dosage Calculations KW - Comparative Effectiveness Research KW - Research Design KW - Clinical Trials as Topic -- methods KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1526127380?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Oral+anticancer+drugs%3A+how+limited+dosing+options+and+dose+reductions+may+affect+outcomes+in+comparative+trials+and+efficacy+in+patients.&rft.au=Prasad%2C+Vinay%3BMassey%2C+Paul+R%3BFojo%2C+Tito&rft.aulast=Prasad&rft.aufirst=Vinay&rft.date=2014-05-20&rft.volume=32&rft.issue=15&rft.spage=1620&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2013.53.0204 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-03 N1 - Date created - 2014-05-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Cancer Res. 2011 Jun 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1;29(1):69-75 [21098323] N Engl J Med. 2011 Feb 10;364(6):501-13 [21306237] J Clin Oncol. 2011 Mar 10;29(8):1059-66 [21282542] Lancet. 2011 Mar 12;377(9769):914-23 [21376385] Br J Cancer. 2011 Apr 12;104(8):1256-61 [21448165] J Natl Cancer Inst. 2011 May 4;103(9):763-73 [21527770] Comment In: J Clin Oncol. 2014 May 20;32(15):1537-9 [24711547] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2013.53.0204 ER - TY - CPAPER T1 - HIV-Related Malignancies: Diseases at the Crossroads of Virology, Immunology, and Cancer Biology T2 - 114th General Meeting of the American Society for Microbiology (ASM 2014) AN - 1518614223; 6284225 JF - 114th General Meeting of the American Society for Microbiology (ASM 2014) AU - Yarchoan, Robert Y1 - 2014/05/17/ PY - 2014 DA - 2014 May 17 KW - Virology KW - Malignancy KW - Immunology KW - Cancer KW - Human immunodeficiency virus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518614223?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.atitle=HIV-Related+Malignancies%3A+Diseases+at+the+Crossroads+of+Virology%2C+Immunology%2C+and+Cancer+Biology&rft.au=Yarchoan%2C+Robert&rft.aulast=Yarchoan&rft.aufirst=Robert&rft.date=2014-05-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/Browse.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Spatial Organization Of Transcription Machinery In Fast-growing Bacterial Cells T2 - 114th General Meeting of the American Society for Microbiology (ASM 2014) AN - 1518610714; 6284604 JF - 114th General Meeting of the American Society for Microbiology (ASM 2014) AU - Cagliero, C AU - Zhou, Y AU - Schneider, T AU - Jin, D Y1 - 2014/05/17/ PY - 2014 DA - 2014 May 17 KW - Transcription UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518610714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.atitle=Spatial+Organization+Of+Transcription+Machinery+In+Fast-growing+Bacterial+Cells&rft.au=Cagliero%2C+C%3BZhou%2C+Y%3BSchneider%2C+T%3BJin%2C+D&rft.aulast=Cagliero&rft.aufirst=C&rft.date=2014-05-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={673511F0-C86B-432F-A387-058032B8500B} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - The Search for Permissive Cells in the Gut T2 - 114th General Meeting of the American Society for Microbiology (ASM 2014) AN - 1518610094; 6284508 JF - 114th General Meeting of the American Society for Microbiology (ASM 2014) AU - Green, Kim Y1 - 2014/05/17/ PY - 2014 DA - 2014 May 17 KW - Digestive tract KW - Permissive cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518610094?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.atitle=The+Search+for+Permissive+Cells+in+the+Gut&rft.au=Green%2C+Kim&rft.aulast=Green&rft.aufirst=Kim&rft.date=2014-05-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={673511F0-C86B-432F-A387-058032B8500B} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Small Changes Can Lead to Big Effects: Visualizing How BacteriophageT4 Appropriates Host RNA Polymerase T2 - 114th General Meeting of the American Society for Microbiology (ASM 2014) AN - 1518609777; 6284556 JF - 114th General Meeting of the American Society for Microbiology (ASM 2014) AU - Hinton, Deborah Y1 - 2014/05/17/ PY - 2014 DA - 2014 May 17 KW - DNA-directed RNA polymerase UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609777?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.atitle=Small+Changes+Can+Lead+to+Big+Effects%3A+Visualizing+How+BacteriophageT4+Appropriates+Host+RNA+Polymerase&rft.au=Hinton%2C+Deborah&rft.aulast=Hinton&rft.aufirst=Deborah&rft.date=2014-05-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=114th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={673511F0-C86B-432F-A387-058032B8500B} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - JOUR T1 - Incorrect identification of recent HIV infection in adults in the United States using a limiting-antigen avidity assay AN - 1765983245; PQ0002610787 AB - Objectives: To evaluate factors associated with misclassification by the limiting-antigen avidity (LAg-avidity) assay among individuals with long-standing HIV infection. Design: Samples were obtained from the Multicenter AIDS Cohort Study and AIDS Linked to the IntraVenous Experience cohort (1089 samples from 667 individuals, 595 samples collected 2-4 years and 494 samples collected 4-8 years after HIV seroconversion). Paired samples from both time points were available for 422 (63.3%) of the 667 individuals. Methods: Samples were considered to be misclassified if the LAg-avidity assay result was 1.5 or less normalized optical density (OD-n) units. Results: Overall, 4.8% (52/1089) of the samples were misclassified, including 1.8% [1 6/884, 95% confidence interval (Cl) 1.09-3.06%] of samples from individuals with viral loads above 400copies/ml and 1.4% (10/705) of samples from individuals with viral loads above 400copies/ml and CD4 super(+) cell counts above 200cells/ mu l (95% Cl 0.68-2.60%). Age, race, sex, and mode of HIV acquisition were not associated with misclassification. In an adjusted analysis, viral load below 400 copies/ml [adjusted odds ratio (aOR) 3.72, 95% Cl 1.61 -8.57], CD4 super(+) cell count below 50cells/ mu l (aOR 5.41, 95% Cl 1.86-15.74), and low LAg-avidity result ([< or =]1.5 OD-n) from the earlier time point (aOR 5.60, 95% Cl 1.55-20.25) were significantly associated with misclassification. Conclusions: The manufacturer of the LAg-avidity assay recommends excluding individuals from incidence surveys who are receiving antiretroviral therapy, are elite suppressors, or have AIDS (CD4 super(+) cell count <200cells/ mu l). The results of this study indicate that those exclusions do not remove all sources of assay misclassification among individuals with long-standing HIV infection. JF - AIDS AU - Longosz, Andrew F AU - Mehta, Shruti H AU - Kirk, Gregory D AU - Margolick, Joseph B AU - Brown, Joelle AU - Quinn, Thomas C AU - Eshleman, Susan H AU - Laeyendecker, Oliver AD - Laboratory of Immunoregulation, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, NIH, olaeyen1@jhmi.edu Y1 - 2014/05/15/ PY - 2014 DA - 2014 May 15 SP - 1227 EP - 1232 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 IS - 8 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - HIV KW - incidence KW - limiting-antigen avidity KW - misclassification KW - MSM KW - people who inject drugs KW - Acquired immune deficiency syndrome KW - Intravenous administration KW - Age KW - antiretroviral therapy KW - Assays KW - Infection KW - Antiretroviral agents KW - USA KW - CD4 antigen KW - Human immunodeficiency virus KW - Avidity KW - Optical density KW - Seroconversion KW - Races KW - Sex KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765983245?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Incorrect+identification+of+recent+HIV+infection+in+adults+in+the+United+States+using+a+limiting-antigen+avidity+assay&rft.au=Longosz%2C+Andrew+F%3BMehta%2C+Shruti+H%3BKirk%2C+Gregory+D%3BMargolick%2C+Joseph+B%3BBrown%2C+Joelle%3BQuinn%2C+Thomas+C%3BEshleman%2C+Susan+H%3BLaeyendecker%2C+Oliver&rft.aulast=Longosz&rft.aufirst=Andrew&rft.date=2014-05-15&rft.volume=28&rft.issue=8&rft.spage=1227&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000221 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Age; Intravenous administration; CD4 antigen; Acquired immune deficiency syndrome; Avidity; antiretroviral therapy; Optical density; Seroconversion; Infection; Races; Sex; Human immunodeficiency virus; Assays; Antiretroviral agents; USA DO - http://dx.doi.org/10.1097/QAD.0000000000000221 ER - TY - JOUR T1 - Lifespan of effector memory CD4 super(+) T cells determined by replication-incompetent integrated HIV-1 provirus AN - 1765980495; PQ0002610773 AB - Objective: Determining the precise lifespan of human T-cell is challenging due to the inability of standard techniques to distinguish between dividing and dying cells. Here, we measured the lifespan of a pool of T cells that were derived from a single cell 'naturally' labelled with a single integrated clone of a replication-incompetent HIV-1 provirus. Design/methods: Utilizing a combination of techniques, we were able to sequence/ map an integration site of a unique provirus with a stop codon at position 42 of the HIV-1 protease. In-vitro reconstruction of this provirus into an infectious clone confirmed its inability to replicate. By combining cell separation and integration site-specific PCR, we were able to follow the fate of this single provirus in multiple T-cell subsets over a 20-year period. As controls, a number of additional integrated proviruses were also sequenced. Results: The replication-incompetent HIV-1 provirus was solely contained in the pool of effector memory CD4 super(+) T cells for 17 years. The percentage of the total effector memory CD4 super(+) T cells containing the replication-incompetent provirus peaked at 1% with a functional half-life of 11.1 months. In the process of sequencing multiple proviruses, we also observed high levels of lethal mutations in the peripheral blood pool of proviruses. Conclusion: These data indicate that human effector memory CD4 super(+) T cells are able to persist in vivo for more than 1 7 years without detectably reverting to a central memory phenotype. A secondary observation is that the fraction of the pool of integrated HIV-1 proviruses capable of replicating may be considerably less than the 12% currently noted in the literature. JF - AIDS AU - Imamichi, Hiromi AU - Natarajan AU - Adelsberger, Joseph W AU - Rehm, Catherine A AU - Lempicki, Richard A AU - Das, Biswajit AU - Hazen, Allison AU - Imamichi, Tomozumi AU - Lane, H Clifford AD - Clinical and Molecular Retrovirology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, CLANE@niaid.nih.gov Y1 - 2014/05/15/ PY - 2014 DA - 2014 May 15 SP - 1091 EP - 1099 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 IS - 8 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - genetic marker KW - HIV-1 KW - in-vivo persistence of CD4-positive T lymphocytes KW - integration KW - provirus KW - replication-incompetent KW - Acquired immune deficiency syndrome KW - Data processing KW - Life span KW - Immunological memory KW - Memory cells KW - Peripheral blood KW - Integration KW - Stop codon KW - CD4 antigen KW - Human immunodeficiency virus 1 KW - Lymphocytes T KW - Polymerase chain reaction KW - Proteinase KW - Mutation KW - Proviruses KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765980495?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Lifespan+of+effector+memory+CD4+super%28%2B%29+T+cells+determined+by+replication-incompetent+integrated+HIV-1+provirus&rft.au=Imamichi%2C+Hiromi%3BNatarajan%3BAdelsberger%2C+Joseph+W%3BRehm%2C+Catherine+A%3BLempicki%2C+Richard+A%3BDas%2C+Biswajit%3BHazen%2C+Allison%3BImamichi%2C+Tomozumi%3BLane%2C+H+Clifford&rft.aulast=Imamichi&rft.aufirst=Hiromi&rft.date=2014-05-15&rft.volume=28&rft.issue=8&rft.spage=1091&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000223 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Data processing; Life span; Memory cells; Immunological memory; Peripheral blood; Integration; CD4 antigen; Stop codon; Lymphocytes T; Polymerase chain reaction; Proteinase; Mutation; Proviruses; Acquired immune deficiency syndrome; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1097/QAD.0000000000000223 ER - TY - JOUR T1 - CLPTM1L promotes growth and enhances aneuploidy in pancreatic cancer cells. AN - 1525765152; 24648346 AB - Genome-wide association studies (GWAS) of 10 different cancers have identified pleiotropic cancer predisposition loci across a region of chromosome 5p15.33 that includes the TERT and CLPTM1L genes. Of these, susceptibility alleles for pancreatic cancer have mapped to the CLPTM1L gene, thus prompting an investigation of the function of CLPTM1L in the pancreas. Immunofluorescence analysis indicated that CLPTM1L localized to the endoplasmic reticulum where it is likely embedded in the membrane, in accord with multiple predicted transmembrane domains. Overexpression of CLPTM1L enhanced growth of pancreatic cancer cells in vitro (1.3-1.5-fold; PDAY7 < 0.003) and in vivo (3.46-fold; PDAY68 = 0.039), suggesting a role in tumor growth; this effect was abrogated by deletion of two hydrophilic domains. Affinity purification followed by mass spectrometry identified an interaction between CLPTM1L and non-muscle myosin II (NMM-II), a protein involved in maintaining cell shape, migration, and cytokinesis. The two proteins colocalized in the cytoplasm and, after treatment with a DNA-damaging agent, at the centrosomes. Overexpression of CLPTM1L and depletion of NMM-II induced aneuploidy, indicating that CLPTM1L may interfere with normal NMM-II function in regulating cytokinesis. Immunohistochemical analysis revealed enhanced staining of CLPTM1L in human pancreatic ductal adenocarcinoma (n = 378) as compared with normal pancreatic tissue samples (n = 17; P = 1.7 × 10(-4)). Our results suggest that CLPTM1L functions as a growth-promoting gene in the pancreas and that overexpression may lead to an abrogation of normal cytokinesis, indicating that it should be considered as a plausible candidate gene that could explain the effect of pancreatic cancer susceptibility alleles on chr5p15.33. ©2014 American Association for Cancer Research. JF - Cancer research AU - Jia, Jinping AU - Bosley, Allen D AU - Thompson, Abbey AU - Hoskins, Jason W AU - Cheuk, Adam AU - Collins, Irene AU - Parikh, Hemang AU - Xiao, Zhen AU - Ylaya, Kris AU - Dzyadyk, Marta AU - Cozen, Wendy AU - Hernandez, Brenda Y AU - Lynch, Charles F AU - Loncarek, Jadranka AU - Altekruse, Sean F AU - Zhang, Lizhi AU - Westlake, Christopher J AU - Factor, Valentina M AU - Thorgeirsson, Snorri AU - Bamlet, William R AU - Hewitt, Stephen M AU - Petersen, Gloria M AU - Andresson, Thorkell AU - Amundadottir, Laufey T AD - Authors' Affiliations: Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics; Pediatric Oncology Branch; Laboratory of Pathology; Division of Cancer Control and Population Sciences; Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda; Laboratory of Proteomics and Analytical Technologies, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research; Laboratory of Protein Dynamics and Signaling and Laboratory of Cell & Developmental Signaling, NCI-Frederick, Frederick, Maryland; Keck School of Medicine, University of Southern California, Los Angeles, California; University of Hawaii Cancer Center, Honolulu, Hawaii; Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, Iowa; and Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota. ; Authors' Affiliations: Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics; Pediatric Oncology Branch; Laboratory of Pathology; Division of Cancer Control and Population Sciences; Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda; Laboratory of Proteomics and Analytical Technologies, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research; Laboratory of Protein Dynamics and Signaling and Laboratory of Cell & Developmental Signaling, NCI-Frederick, Frederick, Maryland; Keck School of Medicine, University of Southern California, Los Angeles, California; University of Hawaii Cancer Center, Honolulu, Hawaii; Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, Iowa; and Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota amundadottirl@mail.nih.gov. Y1 - 2014/05/15/ PY - 2014 DA - 2014 May 15 SP - 2785 EP - 2795 VL - 74 IS - 10 KW - CLPTM1L protein, human KW - 0 KW - Membrane Proteins KW - Neoplasm Proteins KW - Myosin Type II KW - EC 3.6.1.- KW - Index Medicus KW - Heterografts KW - Myosin Type II -- metabolism KW - Animals KW - Aneuploidy KW - Cell Growth Processes -- physiology KW - Humans KW - HEK293 Cells KW - Mice, Nude KW - Mice KW - Cell Line, Tumor KW - Subcellular Fractions -- metabolism KW - Female KW - Neoplasm Proteins -- biosynthesis KW - Pancreatic Neoplasms -- pathology KW - Pancreatic Neoplasms -- metabolism KW - Carcinoma, Pancreatic Ductal -- metabolism KW - Membrane Proteins -- metabolism KW - Neoplasm Proteins -- genetics KW - Membrane Proteins -- biosynthesis KW - Carcinoma, Pancreatic Ductal -- pathology KW - Carcinoma, Pancreatic Ductal -- genetics KW - Pancreatic Neoplasms -- genetics KW - Membrane Proteins -- genetics KW - Neoplasm Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1525765152?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=CLPTM1L+promotes+growth+and+enhances+aneuploidy+in+pancreatic+cancer+cells.&rft.au=Jia%2C+Jinping%3BBosley%2C+Allen+D%3BThompson%2C+Abbey%3BHoskins%2C+Jason+W%3BCheuk%2C+Adam%3BCollins%2C+Irene%3BParikh%2C+Hemang%3BXiao%2C+Zhen%3BYlaya%2C+Kris%3BDzyadyk%2C+Marta%3BCozen%2C+Wendy%3BHernandez%2C+Brenda+Y%3BLynch%2C+Charles+F%3BLoncarek%2C+Jadranka%3BAltekruse%2C+Sean+F%3BZhang%2C+Lizhi%3BWestlake%2C+Christopher+J%3BFactor%2C+Valentina+M%3BThorgeirsson%2C+Snorri%3BBamlet%2C+William+R%3BHewitt%2C+Stephen+M%3BPetersen%2C+Gloria+M%3BAndresson%2C+Thorkell%3BAmundadottir%2C+Laufey+T&rft.aulast=Jia&rft.aufirst=Jinping&rft.date=2014-05-15&rft.volume=74&rft.issue=10&rft.spage=2785&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-13-3176 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-07 N1 - Date created - 2014-05-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochem Biophys Res Commun. 2001 Feb 2;280(4):1148-54 [11162647] Hum Mol Genet. 2013 Jun 15;22(12):2520-8 [23535824] Nat Biotechnol. 2002 May;20(5):473-7 [11981560] Science. 2003 Mar 14;299(5613):1743-7 [12637748] Cell. 2004 Apr 30;117(3):361-72 [15109496] Cancer Genet Cytogenet. 2004 Oct 15;154(2):99-109 [15474144] J Cell Biol. 1977 Jul;74(1):251-63 [141455] Science. 1987 May 29;236(4805):1086-91 [3576222] Science. 1994 Dec 23;266(5193):2011-5 [7605428] Cell. 1995 Sep 22;82(6):949-57 [7553855] J Cell Sci. 2006 Oct 15;119(Pt 20):4342-52 [17038547] Methods. 2007 Apr;41(4):460-74 [17367718] BMC Cancer. 2007;7:226 [18088415] Cancer Genet Cytogenet. 2008 Apr 1;182(1):1-11 [18328944] J Cell Sci. 2008 Sep 1;121(Pt 17):2860-70 [18697832] Nat Genet. 2008 Dec;40(12):1407-9 [18978787] Nat Genet. 2008 Dec;40(12):1404-6 [18978790] Nat Genet. 2009 Feb;41(2):221-7 [19151717] Cancer Res. 2009 Apr 1;69(7):2950-5 [19276352] Nat Genet. 2009 Aug;41(8):909-14 [19578363] Nat Genet. 2009 Aug;41(8):899-904 [19578367] Cancer Res. 2009 Aug 15;69(16):6633-41 [19654303] Nat Rev Mol Cell Biol. 2009 Nov;10(11):778-90 [19851336] PLoS Genet. 2009 Nov;5(11):e1000719 [19911042] Am J Hum Genet. 2009 Nov;85(5):679-91 [19836008] Nat Genet. 2010 Mar;42(3):224-8 [20101243] Nat Cell Biol. 2010 Apr;12(4):362-71 [20208530] Nat Genet. 2010 Jul;42(7):604-7 [20543847] Nature. 2010 Jul 1;466(7302):68-76 [20562859] Nat Genet. 2010 Nov;42(11):978-84 [20972438] J Proteome Res. 2010 Dec 3;9(12):6696-704 [20968308] Nat Genet. 2011 Aug;43(8):785-91 [21743467] Biochem Soc Trans. 2011 Oct;39(5):1115-9 [21936774] Biochem Soc Trans. 2011 Oct;39(5):1131-5 [21936777] Nat Genet. 2011 Dec;43(12):1210-4 [22037553] PLoS One. 2012;7(3):e32667 [22412903] PLoS One. 2012;7(6):e36116 [22675468] J Natl Cancer Inst. 2012 Jun 6;104(11):840-54 [22523397] Arch Dermatol Res. 2013 Jan;305(1):49-52 [22893025] PLoS One. 2012;7(12):e52598 [23300716] Nat Genet. 2013 Apr;45(4):371-84, 384e1-2 [23535731] Cold Spring Harb Perspect Biol. 2013 Apr;5(4):a013227 [23545422] Bioinformatics. 2001 Dec;17(12):1228-9 [11751233] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/0008-5472.CAN-13-3176 ER - TY - JOUR T1 - Herb-drug interaction prediction based on the high specific inhibition of andrographolide derivatives towards UDP-glucuronosyltransferase (UGT) 2B7. AN - 1518241986; 24631340 AB - Herb-drug interaction strongly limits the clinical application of herbs and drugs, and the inhibition of herbal components towards important drug-metabolizing enzymes (DMEs) has been regarded as one of the most important reasons. The present study aims to investigate the inhibition potential of andrographolide derivatives towards one of the most important phase II DMEs UDP-glucuronosyltransferases (UGTs). Recombinant UGT isoforms (except UGT1A4)-catalyzed 4-methylumbelliferone (4-MU) glucuronidation reaction and UGT1A4-catalyzed trifluoperazine (TFP) glucuronidation were employed to firstly screen the andrographolide derivatives' inhibition potential. High specific inhibition of andrographolide derivatives towards UGT2B7 was observed. The inhibition type and parameters (Ki) were determined for the compounds exhibiting strong inhibition capability towards UGT2B7, and human liver microsome (HLMs)-catalyzed zidovudine (AZT) glucuronidation probe reaction was used to furtherly confirm the inhibition behavior. In combination of inhibition parameters (Ki) and in vivo concentration of andrographolide and dehydroandrographolide, the potential in vivo inhibition magnitude was predicted. Additionally, both the in vitro inhibition data and computational modeling results provide important information for the modification of andrographolide derivatives as selective inhibitors of UGT2B7. Taken together, data obtained from the present study indicated the potential herb-drug interaction between Andrographis paniculata and the drugs mainly undergoing UGT2B7-catalyzed metabolic elimination, and the andrographolide derivatives as potential candidates for the selective inhibitors of UGT2B7. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Toxicology and applied pharmacology AU - Ma, Hai-Ying AU - Sun, Dong-Xue AU - Cao, Yun-Feng AU - Ai, Chun-Zhi AU - Qu, Yan-Qing AU - Hu, Cui-Min AU - Jiang, Changtao AU - Dong, Pei-Pei AU - Sun, Xiao-Yu AU - Hong, Mo AU - Tanaka, Naoki AU - Gonzalez, Frank J AU - Ma, Xiao-Chi AU - Fang, Zhong-Ze AD - The Fourth Affiliated Hospital of China Medical University, Shenyang 110032, China. Electronic address: cmu4h-mhy@126.com. ; School of Traditional Chinese Medicine, Shenyang Pharmaceutical University, No. 103, Wenhua Road, Shenyang 110016, China. ; The First Affiliated Hospital of Liaoning Medical University, Jinzhou 121001, China; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China. ; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China. ; Thyroid Surgery, Yantaishan Hospital, Yantai, Shandong, China. ; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China; Department of Microbiology & Immunology, Georgetown University Medical Center, Washington, DC 20057, USA. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. ; Academy of Integrative Medicine, Dalian Medical University, Dalian 116044, China. ; The First Affiliated Hospital of Liaoning Medical University, Jinzhou 121001, China; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China; Academy of Integrative Medicine, Dalian Medical University, Dalian 116044, China; College of Pharmacy, Pharmacokinetic and Drug Transport Key Laboratory, Dalian, Medical University, Dalian, China. Electronic address: maxc1978@163.com. ; The First Affiliated Hospital of Liaoning Medical University, Jinzhou 121001, China; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Zhongshan Road, Dalian 116023, China; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. Electronic address: zzfang228@gmail.com. Y1 - 2014/05/15/ PY - 2014 DA - 2014 May 15 SP - 86 EP - 94 VL - 277 IS - 1 KW - Diterpenes KW - 0 KW - andrographolide KW - 410105JHGR KW - UGT2B7 protein, human KW - EC 2.4.1.- KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - UGT1A5 protein, human KW - Index Medicus KW - Andrographolide derivatives KW - Adverse effects KW - UDP-glucuronosyltransferases (UGTs) KW - Herb–drug interaction (HDI) KW - Enzyme Repression -- drug effects KW - Humans KW - Microsomes, Liver -- enzymology KW - Microsomes, Liver -- drug effects KW - Glucuronosyltransferase -- metabolism KW - Glucuronosyltransferase -- drug effects KW - Herb-Drug Interactions KW - Andrographis KW - Diterpenes -- metabolism KW - Diterpenes -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518241986?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Herb-drug+interaction+prediction+based+on+the+high+specific+inhibition+of+andrographolide+derivatives+towards+UDP-glucuronosyltransferase+%28UGT%29+2B7.&rft.au=Ma%2C+Hai-Ying%3BSun%2C+Dong-Xue%3BCao%2C+Yun-Feng%3BAi%2C+Chun-Zhi%3BQu%2C+Yan-Qing%3BHu%2C+Cui-Min%3BJiang%2C+Changtao%3BDong%2C+Pei-Pei%3BSun%2C+Xiao-Yu%3BHong%2C+Mo%3BTanaka%2C+Naoki%3BGonzalez%2C+Frank+J%3BMa%2C+Xiao-Chi%3BFang%2C+Zhong-Ze&rft.aulast=Ma&rft.aufirst=Hai-Ying&rft.date=2014-05-15&rft.volume=277&rft.issue=1&rft.spage=86&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2014.02.021 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-15 N1 - Date created - 2014-04-21 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2014.02.021 ER - TY - JOUR T1 - Breast cancer risk after radiotherapy for heritable and non-heritable retinoblastoma: a US-UK study AN - 1534855121; 19881880 AB - Background: Retinoblastoma is a rare childhood eye cancer caused by germline or somatic mutations in the RB1 gene. Previous studies observed elevated breast cancer risk among retinoblastoma survivors. However, there has been no research on breast cancer risk in relation to radiation (primarily scatter radiation from the primary treatment) and genetic susceptibility of retinoblastoma survivors. Methods: Two groups of retinoblastoma survivors from the US and UK were selected, and breast cancer risk analysed using a case-control methodology, nesting within the respective cohorts, matching on heritability (that is to say, having bilateral retinoblastoma or being unilateral cases with at least one relative with retinoblastoma), and using exact statistical methods. There were a total of 31 cases and 77 controls. Results: Overall there was no significant variation of breast cancer risk with dose (P>0.5). However, there was a pronounced and significant (P=0.047) increase in the risk of breast cancer with increasing radiation dose for non-heritable retinoblastoma patients and a slight and borderline significant (P=0.072) decrease in risk of breast cancer with increasing radiation dose for heritable retinoblastoma patients, implying significant (P=0.024) heterogeneity in radiation risk between the heritable and non-heritable retinoblastoma groups; this was unaffected by the blindness status. There was no significant effect of any type of alkylating-agent chemotherapy on breast cancer risk (P>0.5). Conclusions: There is significant radiation-related risk of breast cancer for non-heritable retinoblastoma survivors but no excess risk for heritable retinoblastoma survivors, and no significant risk overall. However, these results are based on very small numbers of cases; therefore, they must be interpreted with caution. JF - British Journal of Cancer AU - Little, M P AU - Schaeffer, M L AU - Reulen, R C AU - Abramson, D H AU - Stovall, M AU - Weathers, R AU - de Vathaire, F AU - Diallo, I AU - Seddon, J M AU - Hawkins, M M AU - Tucker, M A AU - Kleinerman, R A AD - Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2014/05/13/ PY - 2014 DA - 2014 May 13 SP - 2623 EP - 2632 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 110 IS - 10 SN - 0007-0920, 0007-0920 KW - Risk Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534855121?accountid=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=Breast+cancer+risk+after+radiotherapy+for+heritable+and+non-heritable+retinoblastoma%3A+a+US-UK+study&rft.au=Little%2C+M+P%3BSchaeffer%2C+M+L%3BReulen%2C+R+C%3BAbramson%2C+D+H%3BStovall%2C+M%3BWeathers%2C+R%3Bde+Vathaire%2C+F%3BDiallo%2C+I%3BSeddon%2C+J+M%3BHawkins%2C+M+M%3BTucker%2C+M+A%3BKleinerman%2C+R+A&rft.aulast=Little&rft.aufirst=M&rft.date=2014-05-13&rft.volume=110&rft.issue=10&rft.spage=2623&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2014.193 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2014-06-12 DO - http://dx.doi.org/10.1038/bjc.2014.193 ER - TY - CPAPER T1 - Antiviral Proteins from Natural Product Extracts: from Discovery to Development T2 - 27th International Conference on Antiviral Research (ICAR 2014) AN - 1562646591; 6301808 JF - 27th International Conference on Antiviral Research (ICAR 2014) AU - O'Keefe, Barry Y1 - 2014/05/12/ PY - 2014 DA - 2014 May 12 KW - Molecular structure KW - natural products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562646591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=27th+International+Conference+on+Antiviral+Research+%28ICAR+2014%29&rft.atitle=Antiviral+Proteins+from+Natural+Product+Extracts%3A+from+Discovery+to+Development&rft.au=O%27Keefe%2C+Barry&rft.aulast=O%27Keefe&rft.aufirst=Barry&rft.date=2014-05-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=27th+International+Conference+on+Antiviral+Research+%28ICAR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://c.ymcdn.com/sites/www.isar-icar.com/resource/resmgr/docs/ICAR_Program2014final.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-31 N1 - Last updated - 2014-09-18 ER - TY - CPAPER T1 - Progressive Ratio Responding to Palatable High Sucrose Food in Mice Lacking Adult Hippocampal Neurogenesis T2 - 2014 Keystone Symposia Conference on Adult Neurogenesis AN - 1518611697; 6280415 JF - 2014 Keystone Symposia Conference on Adult Neurogenesis AU - Karlsson, Rose-Marie Y1 - 2014/05/12/ PY - 2014 DA - 2014 May 12 KW - Neurogenesis KW - Hippocampus KW - Food KW - Sucrose KW - Mice UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611697?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Keystone+Symposia+Conference+on+Adult+Neurogenesis&rft.atitle=Progressive+Ratio+Responding+to+Palatable+High+Sucrose+Food+in+Mice+Lacking+Adult+Hippocampal+Neurogenesis&rft.au=Karlsson%2C+Rose-Marie&rft.aulast=Karlsson&rft.aufirst=Rose-Marie&rft.date=2014-05-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Keystone+Symposia+Conference+on+Adult+Neurogenesis&rft.issn=&rft_id=info:doi/ L2 - http://www.keystonesymposia.org/index.cfm?e=Web.Meeting.Flyer&MeetingID=1304 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Physical Activity and New Neuron Connectivity T2 - 2014 Keystone Symposia Conference on Adult Neurogenesis AN - 1518609647; 6280416 JF - 2014 Keystone Symposia Conference on Adult Neurogenesis AU - Van Praag, Henriette Y1 - 2014/05/12/ PY - 2014 DA - 2014 May 12 KW - Neural networks KW - Neurons KW - Physical activity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609647?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Keystone+Symposia+Conference+on+Adult+Neurogenesis&rft.atitle=Physical+Activity+and+New+Neuron+Connectivity&rft.au=Van+Praag%2C+Henriette&rft.aulast=Van+Praag&rft.aufirst=Henriette&rft.date=2014-05-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Keystone+Symposia+Conference+on+Adult+Neurogenesis&rft.issn=&rft_id=info:doi/ L2 - http://www.keystonesymposia.org/index.cfm?e=Web.Meeting.Flyer&MeetingID=1304 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - JOUR T1 - Identification of Biologically Active, HIV TAR RNA-Binding Small Molecules Using Small Molecule Microarrays AN - 1683350669; PQ0001582112 AB - Identifying small molecules that selectively bind to structured RNA motifs remains an important challenge in developing potent and specific therapeutics. Most strategies to find RNA-binding molecules have identified highly charged compounds or aminoglycosides that commonly have modest selectivity. Here we demonstrate a strategy to screen a large unbiased library of druglike small molecules in a microarray format against an RNA target. This approach has enabled the identification of a novel chemotype that selectively targets the HIV transactivation response (TAR) RNA hairpin in a manner not dependent on cationic charge. Thienopyridine 4 binds to and stabilizes the TAR hairpin with a Kd of 2.4 mu M. Structure-activity relationships demonstrate that this compound achieves activity through hydrophobic and aromatic substituents on a heterocyclic core, rather than cationic groups typically required. Selective 2'-hydroxyl acylation analyzed by primer extension (SHAPE) analysis was performed on a 365-nucleotide sequence derived from the 5' untranslated region (UTR) of the HIV-1 genome to determine global structural changes in the presence of the molecule. Importantly, the interaction of compound 4 can be mapped to the TAR hairpin without broadly disrupting any other structured elements of the 5' UTR. Cell-based anti-HIV assays indicated that 4 inhibits HIV-induced cytopathicity in T lymphocytes with an EC50 of 28 mu M, while cytotoxicity was not observed at concentrations approaching 1 mM. JF - Journal of the American Chemical Society AU - Sztuba-Solinska, Joanna AU - Shenoy, Shilpa R AU - Gareiss, Peter AU - Krumpe, Lauren RH AU - Le Grice, Stuart FJ AU - O'Keefe, Barry R AU - Schneekloth, John S AD - HIV Drug Resistance Program, National Cancer Institute, Frederick, Maryland, United States, PY - 2014 SP - 8402 EP - 8410 PB - American Chemical Society, P.O. Box 182426 Columbus OH 43218-2426 United States VL - 136 IS - 23 SN - 0002-7863, 0002-7863 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Genomes KW - Nucleotide sequence KW - Hydrophobicity KW - Acylation KW - Cytotoxicity KW - RNA KW - Human immunodeficiency virus KW - Human immunodeficiency virus 1 KW - Lymphocytes T KW - Primers KW - Structure-activity relationships KW - Aromatics KW - N 14810:Methods KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683350669?accountid=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+Chemical+Society&rft.atitle=Identification+of+Biologically+Active%2C+HIV+TAR+RNA-Binding+Small+Molecules+Using+Small+Molecule+Microarrays&rft.au=Sztuba-Solinska%2C+Joanna%3BShenoy%2C+Shilpa+R%3BGareiss%2C+Peter%3BKrumpe%2C+Lauren+RH%3BLe+Grice%2C+Stuart+FJ%3BO%27Keefe%2C+Barry+R%3BSchneekloth%2C+John+S&rft.aulast=Sztuba-Solinska&rft.aufirst=Joanna&rft.date=2014-05-02&rft.volume=136&rft.issue=23&rft.spage=8402&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Chemical+Society&rft.issn=00027863&rft_id=info:doi/10.1021%2Fja502754f LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Genomes; Cytotoxicity; RNA; Nucleotide sequence; Lymphocytes T; Hydrophobicity; Primers; Acylation; Structure-activity relationships; Aromatics; Human immunodeficiency virus; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1021/ja502754f ER - TY - CPAPER T1 - The nature of AID off-targeting activity T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AN - 1518611710; 6280542 JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AU - Casellas, Rafael Y1 - 2014/05/02/ PY - 2014 DA - 2014 May 02 KW - activation-induced cytidine deaminase UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611710?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=The+nature+of+AID+off-targeting+activity&rft.au=Casellas%2C+Rafael&rft.aulast=Casellas&rft.aufirst=Rafael&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.immunology2014.org/Program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Translational development of a malaria vaccine from bench to bedside: is it prime time for T cells? T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AN - 1518611483; 6280585 JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AU - Seder, Robert Y1 - 2014/05/02/ PY - 2014 DA - 2014 May 02 KW - Translation KW - Lymphocytes T KW - Disease control KW - Malaria KW - Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Translational+development+of+a+malaria+vaccine+from+bench+to+bedside%3A+is+it+prime+time+for+T+cells%3F&rft.au=Seder%2C+Robert&rft.aulast=Seder&rft.aufirst=Robert&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.immunology2014.org/Program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Adoptive T cell therapy: from biology to practice T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AN - 1518611444; 6280606 JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AU - Restifo, Nicholas Y1 - 2014/05/02/ PY - 2014 DA - 2014 May 02 KW - Lymphocytes T KW - Therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611444?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Adoptive+T+cell+therapy%3A+from+biology+to+practice&rft.au=Restifo%2C+Nicholas&rft.aulast=Restifo&rft.aufirst=Nicholas&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.immunology2014.org/Program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Cytokine regulation of Staphylococcus aureus infections T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AN - 1518611003; 6280502 JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AU - Datta, Sandip Y1 - 2014/05/02/ PY - 2014 DA - 2014 May 02 KW - Cytokines KW - Infection KW - Staphylococcus aureus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611003?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Cytokine+regulation+of+Staphylococcus+aureus+infections&rft.au=Datta%2C+Sandip&rft.aulast=Datta&rft.aufirst=Sandip&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.immunology2014.org/Program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - IL-7 receptor as a new target for immune intervention in inflammation and autoimmunity T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AN - 1518609676; 6280533 JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AU - Park, Hyun Y1 - 2014/05/02/ PY - 2014 DA - 2014 May 02 KW - Interleukin 7 KW - Autoimmunity KW - Intervention KW - Inflammation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609676?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=IL-7+receptor+as+a+new+target+for+immune+intervention+in+inflammation+and+autoimmunity&rft.au=Park%2C+Hyun&rft.aulast=Park&rft.aufirst=Hyun&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.immunology2014.org/Program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Visualizing the dynamics and micro-anatomy of the immune system: how this complex machine really works T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AN - 1518609517; 6280601 JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AU - Germain, Ronald Y1 - 2014/05/02/ PY - 2014 DA - 2014 May 02 KW - Immune system UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609517?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Visualizing+the+dynamics+and+micro-anatomy+of+the+immune+system%3A+how+this+complex+machine+really+works&rft.au=Germain%2C+Ronald&rft.aulast=Germain&rft.aufirst=Ronald&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.immunology2014.org/Program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Finding the molecular links between house dust and asthma T2 - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AN - 1518609512; 6280567 JF - 2014 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2014) AU - Cook, Donald Y1 - 2014/05/02/ PY - 2014 DA - 2014 May 02 KW - House dust KW - Asthma KW - Respiratory diseases KW - Dust UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609512?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.atitle=Finding+the+molecular+links+between+house+dust+and+asthma&rft.au=Cook%2C+Donald&rft.aulast=Cook&rft.aufirst=Donald&rft.date=2014-05-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.immunology2014.org/Program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - JOUR T1 - Cardiac Reactivity During the Ascending Phase of Acute Intravenous Alcohol Exposure and Association with Subjective Perceptions of Intoxication in Social Drinkers AN - 1842509609; 19774224 AB - The aim of this study was to characterize cardiac reactivity measures, heart rate (HR), and heart rate variability (HRV), following acute intravenous (IV) alcohol administration and their association with subjective responses in social drinkers. Twenty-four subjects (11 females) received IV alcohol infusions to attain and clamp the breath alcohol concentration (BrAC) at 50 mg% or placebo in separate sessions. Serial 5-minute cardiac recordings at baseline and during the infusion were analyzed to obtain frequency and time domain cardiac measures. Self-reported subjective perceptions were also obtained at the same time points. HR showed significant decreases from baseline, while the HRV measure pNN50 showed steady increases during the ascending phase of alcohol infusion. HR was inversely correlated with pNN50 across time and treatment. There was a significant association of HR with subjective feelings of high, intoxication, feeling drug effects, and liking drug effects across time during the ascending phase. Acute IV alcohol resulted in decreases in HR and increases in HRV consistent with autonomic parasympathetic activation. The association of these changes with subjective responses suggests that cardiac reactivity may serve as a physiological marker of subjective alcohol effects. This study broadens the understanding of acute cardiovascular effects of alcohol and clinically significant cardiac conditions such as arrhythmia and cardiomyopathy associated with chronic alcohol drinking. JF - Alcoholism: Clinical and Experimental Research AU - Vatsalya, Vatsalya AU - Momenan, Reza AU - Hommer, Daniel W AU - Ramchandani, Vijay A AD - Section on Human Psychopharmacology Laboratory of Clinical and Translational Studies. National Institute on Alcohol Abuse and Alcoholism Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1247 EP - 1254 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 38 IS - 5 SN - 0145-6008, 0145-6008 KW - Toxicology Abstracts KW - Intoxication KW - Heart KW - Arrhythmia KW - Intravenous administration KW - Parasympathetic nervous system KW - Heart rate KW - Drug abuse KW - Cardiomyopathy KW - Perception KW - Alcoholism KW - Drinking behavior KW - Drugs KW - Ethanol KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842509609?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%3A+Clinical+and+Experimental+Research&rft.atitle=Cardiac+Reactivity+During+the+Ascending+Phase+of+Acute+Intravenous+Alcohol+Exposure+and+Association+with+Subjective+Perceptions+of+Intoxication+in+Social+Drinkers&rft.au=Vatsalya%2C+Vatsalya%3BMomenan%2C+Reza%3BHommer%2C+Daniel+W%3BRamchandani%2C+Vijay+A&rft.aulast=Vatsalya&rft.aufirst=Vatsalya&rft.date=2014-05-01&rft.volume=38&rft.issue=5&rft.spage=1247&rft.isbn=&rft.btitle=&rft.title=Alcoholism%3A+Clinical+and+Experimental+Research&rft.issn=01456008&rft_id=info:doi/10.1111%2Facer.12377 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-11-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Heart; Intoxication; Intravenous administration; Arrhythmia; Parasympathetic nervous system; Heart rate; Drug abuse; Cardiomyopathy; Perception; Alcoholism; Drinking behavior; Drugs; Ethanol DO - http://dx.doi.org/10.1111/acer.12377 ER - TY - JOUR T1 - History of Weight Control Attempts Among Adolescent Girls With Loss of Control Eating AN - 1732808412; PQ0002227716 AB - Objective: Loss of control (LOC) eating and a weight control attempt (WCA) history during adolescence are important behavioral risk factors for eating disorders and obesity. The current study investigated the significance of the presence of a WCA history among adolescent girls with LOC eating. Method: Participants were 114 obesity-prevention-seeking 12-17-year-old (M = 14.5, SD = 1.7 years) girls who were between the 75th and 97th body mass index (BMI) percentile (BMI-z: M = 1.5, SD = 0.3) and reported LOC eating episodes during the previous month (M = 4.0, SD = 4.9 episodes; Median = 2.0). Measures included the Eating Disorder Examination to assess LOC eating, eating pathology, and WCA history, and self-report questionnaires for symptoms of general psychopathology. Eating behavior was observed during a laboratory meal designed to capture a LOC eating episode. Results: 67.5% reported a WCA history. As compared to girls without a WCA history (no-WCA), those with a WCA history (WCA) had greater disordered eating attitudes and depressive symptoms (ps .10). During the laboratory meal, WCA consumed less energy from snack-type foods than no-WCA (M = 245.0, SD = 156.1 vs. M = 341.6, SD = 192.3 kcal; p = .01). Conclusions: Reported WCAs are highly prevalent and are associated with greater psychopathology symptoms among adolescent girls with LOC eating. Prospective data are needed to determine whether these overlapping risk behaviors confer differential vulnerability for developing eating disorders and obesity. JF - Health Psychology AU - Vannucci, Anna AU - Shomaker, Lauren B AU - Field, Sara E AU - Sbrocco, Tracy AU - Stephens, Mark AU - Kozlosky, Merel AU - Reynolds, James C AU - Yanovski, Jack A AU - Tanofsky-Kraff, Marian AD - Uniformed Services University of the Health Sciences and Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, mtanofsky@usuhs.edu PY - 2014 SP - 419 EP - 423 PB - American Psychological Association, 750 First St., N.E. Washington DC 20002-4242 United States VL - 33 IS - 5 SN - 0278-6133, 0278-6133 KW - Physical Education Index KW - loss of control eating KW - dieting KW - weight control behavior KW - eating disorders KW - obesity KW - Evaluation KW - Obesity KW - Attitudes KW - Weight control KW - Eating disorders KW - Girls KW - Adolescence KW - Body mass KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732808412?accountid=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=Health+Psychology&rft.atitle=History+of+Weight+Control+Attempts+Among+Adolescent+Girls+With+Loss+of+Control+Eating&rft.au=Vannucci%2C+Anna%3BShomaker%2C+Lauren+B%3BField%2C+Sara+E%3BSbrocco%2C+Tracy%3BStephens%2C+Mark%3BKozlosky%2C+Merel%3BReynolds%2C+James+C%3BYanovski%2C+Jack+A%3BTanofsky-Kraff%2C+Marian&rft.aulast=Vannucci&rft.aufirst=Anna&rft.date=2014-05-01&rft.volume=33&rft.issue=5&rft.spage=419&rft.isbn=&rft.btitle=&rft.title=Health+Psychology&rft.issn=02786133&rft_id=info:doi/10.1037%2Fa0033184 LA - English DB - Physical Education Index N1 - Date revised - 2015-11-01 N1 - Last updated - 2015-12-09 N1 - SubjectsTermNotLitGenreText - Evaluation; Obesity; Attitudes; Weight control; Eating disorders; Body mass; Adolescence; Girls DO - http://dx.doi.org/10.1037/a0033184 ER - TY - JOUR T1 - Learning by doing: observing an interprofessional process as an interprofessional team AN - 1665161484 AB - New competencies exist for interprofessional education, which are centered on the goal of improving quality of care and patient safety through improved interprofessional collaboration. Interprofessional education and effective interprofessional collaboration are cornerstones of the Veterans Affairs Quality Scholars fellowship program. The purpose of this project was to evaluate an innovative interprofessional education strategy in which teams of physicians and nurses were "learning by doing" as they observed and analyzed the functioning of an interprofessional process, specifically, inpatient discharge. Fellows completed voluntary, anonymous surveys seeking their perspectives about the project. Fellowsʼ feedback revealed several themes, with both positive and negative characteristics related to team functioning, interprofessional understanding, microsystem knowledge, pooled knowledge and assignment challenges. The strength of this strategy is exemplified by the fact that fellows not only learned from each otherʼs separate professional observations, but also observed the emergence of a shared interprofessional perspective through working together. JF - Journal of Interprofessional Care AU - Brennan, Caitlin W AU - Olds, Danielle M AU - Dolansky, Mary AU - Estrada, Carlos A AU - Patrician, Patricia A AD - National Institutes of Health Clinical Center, Nursing Department, Research and Practice Development, 10 Center Drive, Room 2B08, Bethesda, MD 20892, USA ; National Database of Nursing Quality Indicators (NDNQI(R)), University of Kansas Medical Center, Kansas City, KS, USA ; Frances Payne Bolton School of Nursing, Case Western Reserve University, Cleveland, OH, USA ; Birmingham VA Medical Center, University of Alabama at Birmingham, Birmingham, AL, USA ; University of Alabama at Birmingham, Birmingham, AL, USA ; National Institutes of Health Clinical Center, Nursing Department, Research and Practice Development, 10 Center Drive, Room 2B08, Bethesda, MD 20892, USA Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 249 EP - 251 CY - Abingdon PB - Taylor & Francis Ltd. VL - 28 IS - 3 SN - 1356-1820 KW - Medical Sciences KW - Interprofessional collaboration KW - interprofessional education KW - interprofessional evaluation KW - teams KW - Doctors KW - Veterans KW - Feedback KW - Hospitalization KW - Interagency collaboration KW - Interdisciplinary approach KW - Interdisciplinary education KW - Interdisciplinary team work KW - Learning KW - Nurses KW - Patient care KW - Professional knowledge KW - Quality of care KW - Safety KW - Safety measures KW - Teams UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665161484?accountid=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+Interprofessional+Care&rft.atitle=Learning+by+doing%3A+observing+an+interprofessional+process+as+an+interprofessional+team&rft.au=Brennan%2C+Caitlin+W%3BOlds%2C+Danielle+M%3BDolansky%2C+Mary%3BEstrada%2C+Carlos+A%3BPatrician%2C+Patricia+A&rft.aulast=Brennan&rft.aufirst=Caitlin&rft.date=2014-05-01&rft.volume=28&rft.issue=3&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Journal+of+Interprofessional+Care&rft.issn=13561820&rft_id=info:doi/10.3109%2F13561820.2013.838750 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/10.3109/13561820.2013.838750 ER - TY - JOUR T1 - Neglected Parasitic Infections in the United States: Cysticercosis AN - 1647024281; 21184014 AB - Cysticercosis is a potentially fatal and preventable neglected parasitic infection caused by the larval form of Taenia solium. Patients with symptomatic disease usually have signs and symptoms of neurocysticercosis, which commonly manifest as seizures or increased intracranial pressure. Although there are many persons living in the United States who emigrated from highly disease-endemic countries and there are foci of autochthonous transmission of the parasite in the United States, little is known about burden and epidemiology of the disease in this country. In addition, despite advances in the diagnosis and management of neurocysticercosis, there remain many unanswered questions. Improving our understanding and management of neurocysticercosis in the United States will require improved surveillance or focused prospective studies in appropriate areas and allocation of resources towards answering some of the key questions discussed in this report. JF - American Journal of Tropical Medicine and Hygiene AU - Cantey, Paul T AU - Coyle, Christina M AU - Sorvillo, Frank J AU - Wilkins, Patricia P AU - Starr, Michelle C AU - Nash, Theodore E AD - Division of Parasitic Diseases and Malaria, Centers for Disease Control and Prevention, 1600 Clifton Road NE, Mailstop A-06, Atlanta, GA 30333; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York; Department of Pediatrics, University of Washington, Seattle, Washington; Department of Epidemiology, School of Public Health, University of California-Los Angeles, Los Angeles, California; Gastrointestinal Parasites Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, pcantey@cdc.gov Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 805 EP - 809 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 90 IS - 5 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality KW - Parasites KW - Symptoms KW - Resource management KW - Seizures KW - Surveillance and enforcement KW - Infection KW - Disease transmission KW - USA KW - Neurotransmission KW - Epidemiology KW - Cysticercosis KW - Taenia KW - Taenia solium KW - Pressure KW - Hygiene KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08502:Methods and instruments KW - J 02400:Human Diseases KW - K 03420:Plant Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647024281?accountid=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=Neglected+Parasitic+Infections+in+the+United+States%3A+Cysticercosis&rft.au=Cantey%2C+Paul+T%3BCoyle%2C+Christina+M%3BSorvillo%2C+Frank+J%3BWilkins%2C+Patricia+P%3BStarr%2C+Michelle+C%3BNash%2C+Theodore+E&rft.aulast=Cantey&rft.aufirst=Paul&rft.date=2014-05-01&rft.volume=90&rft.issue=5&rft.spage=805&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0724 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Symptoms; Parasites; Resource management; Epidemiology; Surveillance and enforcement; Hygiene; Disease transmission; Neurotransmission; Seizures; Cysticercosis; Pressure; Infection; Taenia solium; Taenia; USA DO - http://dx.doi.org/10.4269/ajtmh.13-0724 ER - TY - JOUR T1 - G6PD A- Deficiency and Severe Malaria in The Gambia: Heterozygote Advantage and Possible Homozygote Disadvantage AN - 1647024172; 21184024 AB - Glucose-6-phosphate dehydrogenase (G6PD) deficiency is frequent in Africa, because it confers resistance to Plasmodium falciparum malaria; however, the nature of the protection and the genotypes associated with it have been controversial. In 1972, Bienzle and others described protection from malaria in West African females heterozygous for G6PD A-. They determined that G6PD A- heterozygotes had lower parasite counts than A- homozygotes, hemizygous males, and normal individuals. However, other studies have reached different conclusions about the protective genotypes. DNA samples from 135 children with severe malaria and 146 children with mild malaria from The Gambia were genotyped for the G6PD A- mutation that is most frequent among Gambians (G6PD 968 T->C); there was a marked deficiency of heterozygotes and an excess of homozygotes with severe malaria, producing a strong deviation from Hardy-Weinberg equilibrium. Our results support the protective effect in G6PD A- heterozygous females and suggest that homozygotes might be more susceptible to severe malaria attacks. JF - American Journal of Tropical Medicine and Hygiene AU - Sirugo, Giorgio AU - Predazzi, Irene M AU - Bartlett, Jacquelaine AU - Tacconelli, Alessandra AU - Walther, Michael AU - Williams, Scott M AD - Centro di Ricerca, Ospedale San Pietro Fatebenefratelli, Via Cassia, 600, 00189 Rome, Italy; Center for Human Genetics Research, Vanderbilt University Medical Center, Nashville, Tennessee; Department of Genetics, Geisel School of Medicine, Dartmouth College, Hanover, New Hampshire; National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland; Medical Research Council Laboratories, Fajara, Banjul, The Gambia, sirugo.giorgio@fbfrm.it Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 856 EP - 859 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 90 IS - 5 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality KW - Parasites KW - Human diseases KW - Gambia KW - Mutations KW - Malaria KW - Plasmodium falciparum KW - Genotypes KW - Children KW - Homozygotes KW - Glucosephosphate dehydrogenase KW - Public health KW - Heterozygote advantage KW - DNA KW - Africa KW - Hygiene KW - Mutation KW - Dehydrogenases KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08502:Methods and instruments KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647024172?accountid=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=G6PD+A-+Deficiency+and+Severe+Malaria+in+The+Gambia%3A+Heterozygote+Advantage+and+Possible+Homozygote+Disadvantage&rft.au=Sirugo%2C+Giorgio%3BPredazzi%2C+Irene+M%3BBartlett%2C+Jacquelaine%3BTacconelli%2C+Alessandra%3BWalther%2C+Michael%3BWilliams%2C+Scott+M&rft.aulast=Sirugo&rft.aufirst=Giorgio&rft.date=2014-05-01&rft.volume=90&rft.issue=5&rft.spage=856&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0622 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Mutations; DNA; Malaria; Genotypes; Hygiene; Dehydrogenases; Public health; Heterozygote advantage; Children; Mutation; Homozygotes; Glucosephosphate dehydrogenase; Plasmodium falciparum; Gambia; Africa DO - http://dx.doi.org/10.4269/ajtmh.13-0622 ER - TY - JOUR T1 - Investigation of Dengue and Japanese Encephalitis Virus Transmission in Hanam, Viet Nam AN - 1647022956; 21184029 AB - This study investigated whether a large dengue epidemic that struck Hanaoi in 2009 also affected a nearby semirural area. Seroconversion (dengue virus-reactive immunoglobulin G enzyme-linked immunosorbent assay) was high during 2009 compared with 2008, but neutralization assays showed that it was caused by both dengue virus and Japanese encephalitis virus infections. The findings highlight the importance of continued Japanese encephalitis virus vaccination and dengue surveillance. JF - American Journal of Tropical Medicine and Hygiene AU - Fox, Annette AU - Whitehead, Stephen AU - Anders, Katherine L AU - Hoa, Le Nguyen Minh AU - Mai, Le Quynh AU - Thai, Pham Quang AU - Yen, Nguyen Thu AU - Duong, Tran Nhu AU - Thoang, Dang Dinh AU - Farrar, Jeremy AU - Wertheim, Heiman AU - Simmons, Cameron AU - Hien, Nguyen Tran AU - Horby, Peter AD - Oxford University Clinical Research Unit and Wellcome Trust Major Overseas Programme, Viet Nam; Centre for Tropical Medicine, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, United Kingdom; National Institute of Allergy and Infectious Diseases, Bethesda, Maryland; National Institute of Hygiene and Epidemiology, Hanaoi, Viet Nam; Hanam Centre for Preventive Medicine, Hanam, Viet Nam, afox@pacific.net.au Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 892 EP - 896 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 90 IS - 5 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts; Virology & AIDS Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality KW - Dengue virus KW - Enzyme-linked immunosorbent assay KW - Epidemics KW - Surveillance and enforcement KW - Infection KW - Vaccination KW - Encephalitis KW - Vietnam KW - Dengue KW - Immunoglobulin G KW - Seroconversion KW - Japanese encephalitis virus KW - Hygiene KW - V 22490:Miscellaneous KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08502:Methods and instruments KW - J 02350:Immunology KW - N3 11027:Neurology & neuropathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647022956?accountid=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=Investigation+of+Dengue+and+Japanese+Encephalitis+Virus+Transmission+in+Hanam%2C+Viet+Nam&rft.au=Fox%2C+Annette%3BWhitehead%2C+Stephen%3BAnders%2C+Katherine+L%3BHoa%2C+Le+Nguyen+Minh%3BMai%2C+Le+Quynh%3BThai%2C+Pham+Quang%3BYen%2C+Nguyen+Thu%3BDuong%2C+Tran+Nhu%3BThoang%2C+Dang+Dinh%3BFarrar%2C+Jeremy%3BWertheim%2C+Heiman%3BSimmons%2C+Cameron%3BHien%2C+Nguyen+Tran%3BHorby%2C+Peter&rft.aulast=Fox&rft.aufirst=Annette&rft.date=2014-05-01&rft.volume=90&rft.issue=5&rft.spage=892&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0077 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Epidemics; Surveillance and enforcement; Hygiene; Vaccination; Enzyme-linked immunosorbent assay; Dengue; Immunoglobulin G; Seroconversion; Infection; Encephalitis; Dengue virus; Japanese encephalitis virus; Vietnam DO - http://dx.doi.org/10.4269/ajtmh.13-0077 ER - TY - JOUR T1 - Immune Responses to O-Specific Polysaccharide and Lipopolysaccharide of Vibrio cholerae O1 Ogawa in Adult Bangladeshi Recipients of an Oral Killed Cholera Vaccine and Comparison to Responses in Patients with Cholera AN - 1647017392; 21184027 AB - Protective immunity to cholera is serogroup specific, and serogrouping is defined by the O-specific polysaccharide (OSP) of lipopolysaccharide (LPS). We characterized OSP-specific immune responses in adult recipients of an oral killed cholera vaccine (OCV WC-rBS) and compared these with responses in patients with cholera caused by Vibrio cholerae O1 Ogawa. Although vaccinees developed plasma immunoglobulin G (IgG), IgM, IgA antibody and antibody secreting cell (ASC, marker of mucosal response) to Ogawa OSP and LPS 7 days after vaccination, responses were significantly lower than that which occurred after cholera. Similarly, patients recovering from cholera had detectable IgA, IgM, and IgG memory B cell (MBC) responses against OSP and LPS on Day 30 and Day 90, whereas vaccinees only developed IgG responses to OSP 30 days after the second immunization. The markedly lower ASC and MBC responses to OSP and LPS observed among vaccinees might explain, in part, the lower protection of an OCV compared with natural infection. JF - American Journal of Tropical Medicine and Hygiene AU - Uddin, Taher AU - Aktar, Amena AU - Xu, Peng AU - Johnson, Russell A AU - Rahman, M Arifur AU - Leung, Daniel T AU - Afrin, Sadia AU - Akter, Aklima AU - Alam, Mohammad Murshid AU - Rahman, Atiqur AD - Centre for Vaccine Sciences, International Centre for Diarrhoeal Disease Research, Bangladesh (icddr,b), Dhaka, Bangladesh; NIDDK, LBC, National Institutes of Health, Bethesda, Maryland; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts; Departments of Medicine and Pediatrics, Harvard Medical School, Boston, Massachusetts; Department of Biochemistry and Molecular Biology, University of Dhaka, Bangladesh; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts; Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 873 EP - 881 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 90 IS - 5 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Immunology Abstracts; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality KW - Mucosa KW - Immunological memory KW - Disease control KW - Infection KW - Polysaccharides KW - Lipopolysaccharides KW - Cholera KW - Pathogenic bacteria KW - Lymphocytes B KW - Bacterial diseases KW - Memory cells KW - Immunity KW - Vaccination KW - Vibrio cholerae KW - Immunoglobulin A KW - Antibodies KW - Immunoglobulin G KW - Immune response KW - Vaccines KW - Hygiene KW - Immunoglobulin M KW - F 06905:Vaccines 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 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647017392?accountid=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=Immune+Responses+to+O-Specific+Polysaccharide+and+Lipopolysaccharide+of+Vibrio+cholerae+O1+Ogawa+in+Adult+Bangladeshi+Recipients+of+an+Oral+Killed+Cholera+Vaccine+and+Comparison+to+Responses+in+Patients+with+Cholera&rft.au=Uddin%2C+Taher%3BAktar%2C+Amena%3BXu%2C+Peng%3BJohnson%2C+Russell+A%3BRahman%2C+M+Arifur%3BLeung%2C+Daniel+T%3BAfrin%2C+Sadia%3BAkter%2C+Aklima%3BAlam%2C+Mohammad+Murshid%3BRahman%2C+Atiqur&rft.aulast=Uddin&rft.aufirst=Taher&rft.date=2014-05-01&rft.volume=90&rft.issue=5&rft.spage=873&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0498 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Antibodies; Pathogenic bacteria; Bacterial diseases; Disease control; Immunity; Vaccines; Hygiene; Polysaccharides; Vaccination; Lymphocytes B; Mucosa; Immunological memory; Memory cells; Infection; Immunoglobulin A; Immunoglobulin G; Lipopolysaccharides; Cholera; Immune response; Immunoglobulin M; Vibrio cholerae DO - http://dx.doi.org/10.4269/ajtmh.13-0498 ER - TY - JOUR T1 - Cannabis withdrawal in chronic, frequent cannabis smokers during sustained abstinence within a closed residential environment AN - 1560134539; 19654335 AB - Objectives Chronic, frequent cannabis smokers may experience residual and offset effects, withdrawal, and craving when abstaining from the drug. We characterized the prevalence, duration, and intensity of these effects in chronic frequent cannabis smokers during abstinence on a closed research unit. Methods Non-treatment-seeking participants (N=29 on admission, 66% and 34% remaining after 2 and 4 weeks) provided subjective effects data. A battery of five instruments was computer-administered daily to measure psychological, sensory, and physical symptoms associated with cannabinoid intoxication and withdrawal. Plasma and oral fluid specimens were concurrently collected and analyzed for cannabinoids. Outcome variables were evaluated as change from admission (Day 0) with regression models. Results Most abstinence effects, including irritability and anxiety were greatest on Days 0-3 and decreased thereafter. Cannabis craving significantly decreased over time, whereas decreased appetite began to normalize on Day 4. Strange dreams and difficulty getting to sleep increased over time, suggesting intrinsic sleep problems in chronic cannabis smokers. Symptoms likely induced by residual drug effects were at maximum intensity on admission and positively correlated with plasma and oral fluid cannabinoid concentrations on admission but not afterward; these symptoms showed overall prevalence higher than cannabis withdrawal symptoms. Conclusions The combined influence of residual/offset drug effects, withdrawal, and craving was observed in chronic cannabis smokers during monitored abstinence. Abstinence symptoms were generally more intense in the initial phase, implying importance of early intervention in cannabis quit attempts. Sleep disturbance persisting for an extended period suggests that hypnotic medications could be beneficial in treating cannabis dependence. (Am J Addict 2014; 23:234-242) JF - American Journal on Addictions AU - Lee, Dayong AU - Schroeder, Jennifer R AU - Karschner, Erin L AU - Goodwin, Robert S AU - Hirvonen, Jussi AU - Gorelick, David A AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, National Institute on Drug Abuse, National Institute of Health, Baltimore, Maryland. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 234 EP - 242 PB - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801 VL - 23 IS - 3 SN - 1055-0496, 1055-0496 KW - Toxicology Abstracts KW - Intoxication KW - Dreams KW - Data processing KW - Addicts KW - Anxiety KW - Sleep disorders KW - Withdrawal KW - Hypnotics KW - Drug abuse KW - Appetite KW - Models KW - Cannabinoids KW - Sleep KW - Regression analysis KW - Cannabis KW - Addiction KW - Drug addiction KW - oral fluids KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560134539?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+on+Addictions&rft.atitle=Cannabis+withdrawal+in+chronic%2C+frequent+cannabis+smokers+during+sustained+abstinence+within+a+closed+residential+environment&rft.au=Lee%2C+Dayong%3BSchroeder%2C+Jennifer+R%3BKarschner%2C+Erin+L%3BGoodwin%2C+Robert+S%3BHirvonen%2C+Jussi%3BGorelick%2C+David+A%3BHuestis%2C+Marilyn+A&rft.aulast=Lee&rft.aufirst=Dayong&rft.date=2014-05-01&rft.volume=23&rft.issue=3&rft.spage=234&rft.isbn=&rft.btitle=&rft.title=American+Journal+on+Addictions&rft.issn=10550496&rft_id=info:doi/10.1111%2Fj.1521-0391.2014.12088.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Intoxication; Dreams; Data processing; Sleep disorders; Anxiety; Addicts; Withdrawal; Hypnotics; Appetite; Drug abuse; Models; Cannabinoids; Sleep; Cannabis; Regression analysis; Addiction; Drug addiction; oral fluids DO - http://dx.doi.org/10.1111/j.1521-0391.2014.12088.x ER - TY - JOUR T1 - Reduced fatalism and increased prevention behavior after two high-profile lung cancer events AN - 1536010727; 4569283 AB - The positive impact of media coverage of high-profile cancer events on cancer prevention behaviors is well-established. However, less work has focused on potential adverse psychological reactions to such events, such as fatalism. Conducting 3 studies, the authors explored how the lung cancer death of Peter Jennings and diagnosis of Dana Reeve in 2005 related to fatalism. Analysis of a national media sample in Study 1 found that media coverage of these events often focused on reiterating the typical profile of those diagnosed with lung cancer; 38% of the media mentioned at least 1 known risk factor for lung cancer, most often smoking. Data from a nationally representative survey in Study 2 found that respondents reported lower lung cancer fatalism, after, compared with before, the events (OR = 0.16, 95% CI [0.03, 0.93]). A sustained increase in call volume to the national tobacco Quitline after these events was found in Study 3. These results suggest that there is a temporal association between high-profile cancer events, the subsequent media coverage, psychological outcomes, and cancer prevention behaviors. These results suggest that high-profile cancer events could be leveraged as an opportunity for large-scale public heath communication campaigns through the dissemination of cancer prevention messages and services. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Portnoy, David B AU - Leach, Corinne R AU - Kaufman, Annette R AU - Moser, Richard P AU - Alfano, Catherine M AD - US National Institutes of Health Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 577 EP - 592 VL - 19 IS - 5 SN - 1081-0730, 1081-0730 KW - Sociology KW - Death KW - Prevention KW - Fatalism KW - Cancer KW - Public health KW - Media coverage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1536010727?accountid=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=Reduced+fatalism+and+increased+prevention+behavior+after+two+high-profile+lung+cancer+events&rft.au=Portnoy%2C+David+B%3BLeach%2C+Corinne+R%3BKaufman%2C+Annette+R%3BMoser%2C+Richard+P%3BAlfano%2C+Catherine+M&rft.aulast=Portnoy&rft.aufirst=David&rft.date=2014-05-01&rft.volume=19&rft.issue=5&rft.spage=577&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2013.821553 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-06-16 N1 - Last updated - 2014-06-17 N1 - SubjectsTermNotLitGenreText - Media coverage; 10449 5772; 1939 3617 6220; 10072; 3303; 4825 10777 1547 10792 DO - http://dx.doi.org/10.1080/10810730.2013.821553 ER - TY - JOUR T1 - Prediagnostic lifestyle factors and survival after colon and rectal cancer diagnosis in the National Institutes of Health (NIH)-AARP Diet and Health Study AN - 1534857187; 19822178 AB - BACKGROUND Few studies have examined the relationship of lifestyle factors with mortality among patients with colorectal cancer. METHODS Among NIH-AARP Diet and Health study participants, 4213 colon and 1514 rectal cancer cases were identified through linkage to state cancer registries and determined date and cause of death using the National Death Index. Lifestyle factors were assessed at baseline and included: healthy diet (measured by Healthy Eating Index 2005 [HEI-2005]), body mass index (BMI), physical activity, alcohol consumption and smoking. The association of factors was examined individually and combined into a lifestyle score with 5-year mortality from all-causes, colorectal cancer, and cardiovascular disease (CVD). Relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models. RESULTS Among colon cancer survivors, smokers had increased risk of total mortality (RR=1.74; 95% CI=1.45-2.08) and colorectal cancer mortality (RR=1.46; 95% CI=1.17-1.82), compared to never smokers. Obese (BMI, greater than or equal to 30) individuals had increased risk of all death (RR=1.19; 95% CI=1.02-1.39) and CVD death (RR=1.84; 95% CI=1.05-3.23), compared to normal weight (BMI, 18.5 to<25) individuals. Compared to those with the lowest lifestyle score, those with the highest score had a 34% lower risk of all-cause mortality (RR=0.66; 95% CI=0.50-0.87). Among rectal cancer survivors, individuals in the highest quintile of HEI-2005 scores had reduced all-cause mortality (RR=0.60; 95% CI=0.42-0.86) compared to those in the lowest. Higher combined lifestyle scores were associated with a 46% lower risk of total mortality (0.54; 0.32-0.91). CONCLUSIONS Healthier lifestyle before cancer diagnosis was associated with improved overall survival after diagnosis with colorectal cancer. Cancer 2014; 120:1540-1547 2014. Several modifiable lifestyle factors measured prediagnosis were related to survival among patients with colorectal cancer. A combined lifestyle score consisting of meeting recommendations for diet, body weight, physical activity, alcohol intake, and smoking was also associated with reduced all-cause mortality. JF - Cancer AU - Pelser, Colleen AU - Arem, Hannah AU - Pfeiffer, Ruth M AU - Elena, Joanne W AU - Alfano, Catherine M AU - Hollenbeck, Albert R AU - Park, Yikyung AD - Cancer Prevention Fellowship Program, Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1540 EP - 1547 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 120 IS - 10 SN - 0008-543X, 0008-543X KW - Health & Safety Science Abstracts; Risk Abstracts KW - Diets KW - Risk assessment KW - Obesity KW - Alcohol KW - Mortality KW - Physical activity KW - Survival KW - Cancer KW - Smoking KW - Health risks KW - Body weight KW - Risk factors KW - Colorectal carcinoma KW - Cardiovascular diseases 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/1534857187?accountid=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=Prediagnostic+lifestyle+factors+and+survival+after+colon+and+rectal+cancer+diagnosis+in+the+National+Institutes+of+Health+%28NIH%29-AARP+Diet+and+Health+Study&rft.au=Pelser%2C+Colleen%3BArem%2C+Hannah%3BPfeiffer%2C+Ruth+M%3BElena%2C+Joanne+W%3BAlfano%2C+Catherine+M%3BHollenbeck%2C+Albert+R%3BPark%2C+Yikyung&rft.aulast=Pelser&rft.aufirst=Colleen&rft.date=2014-05-01&rft.volume=120&rft.issue=10&rft.spage=1540&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.28573 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Risk assessment; Diets; Mortality; Alcohol; Obesity; Physical activity; Survival; Cancer; Health risks; Smoking; Body weight; Risk factors; Colorectal carcinoma; Cardiovascular diseases DO - http://dx.doi.org/10.1002/cncr.28573 ER - TY - JOUR T1 - Visiting Again? Subjective Well-Being of Children in Elementary School and Repeated Visits to School Health Nurses AN - 1531918783; 201413853 AB - Children with vague complaints are without chronic illness, and who repeatedly visit the school nurse may be at risk for limited academic success. This study compares student reports of subjective well-being between children who do and do not repeatedly visit the school nurse with vague complaints. Children in grades 4 through 6 completed the School Well-Being Profile-American English (SWBP-AE), a questionnaire with 4 well-being subscales: health status, school environment, social relationships, and school as a means of self-fulfillment. School nurses extracted data on clinic visits from clinic records. Logistic regression explored associations between well-being subscales and repeated visits to the school nurse. Of the 320 students participating in the study, 33 (12.04%) students made repeated visits to the school nurse. Perception of health status (OR = 2.072; 95% CI = 1.037, 4.163) was the only significant (p < .05) predictor of repeated visits to the nurse. Children with poor perception of their health status are more likely to repeatedly visit the school nurse. Children's perceptions of their school environment, social relationships, or school as a means of self-fulfillment are not statistically significant predictors of repeated visits to the school nurse. Adapted from the source document. JF - Journal of School Health AU - Leaver, Cynthia A AD - National Institute of Nursing Research, National Institutes of Health, Division of Intramural Research Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 294 EP - 301 PB - Wiley-Blackwell, UK VL - 84 IS - 5 SN - 0022-4391, 0022-4391 KW - Social relationships KW - Wellbeing KW - Health status KW - School nurses KW - Clinics KW - Children KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1531918783?accountid=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+Health&rft.atitle=Visiting+Again%3F+Subjective+Well-Being+of+Children+in+Elementary+School+and+Repeated+Visits+to+School+Health+Nurses&rft.au=Leaver%2C+Cynthia+A&rft.aulast=Leaver&rft.aufirst=Cynthia&rft.date=2014-05-01&rft.volume=84&rft.issue=5&rft.spage=294&rft.isbn=&rft.btitle=&rft.title=Journal+of+School+Health&rft.issn=00224391&rft_id=info:doi/10.1111%2Fjosh.12150 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-06-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - School nurses; Children; Wellbeing; Health status; Clinics; Social relationships DO - http://dx.doi.org/10.1111/josh.12150 ER - TY - JOUR T1 - A problem-solving education intervention in caregivers and patients during allogeneic hematopoietic stem cell transplantation AN - 1531431165; 4565572 AB - The aim of this study was to determine the effect of problem-solving education on self-efficacy and distress in informal caregivers of allogeneic hematopoietic stem cell transplantation patients. Patient/caregiver teams attended three 1-hour problem-solving education sessions to help cope with problems during hematopoietic stem cell transplantation. Primary measures included the Cancer Self-Efficacy Scale-transplant and Brief Symptom Inventory-18. Active caregivers reported improvements in self-efficacy (p Reprinted by permission of Sage Publications Ltd JF - Journal of health psychology AU - Bevans, Margaret AU - Wehrlen, Leslie AU - Castro, Kathleen AU - Prince, Patricia AU - Shelburne, Nonniekaye AU - Soeken, Karen AU - Zabora, James AU - Wallen, Gwenyth R AD - National Institutes of Health Clinical Center ; National Cancer Institute ; University of Maryland ; Inova Health System Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 602 EP - 617 VL - 19 IS - 5 SN - 1359-1053, 1359-1053 KW - Sociology KW - Anxiety KW - Survival strategy KW - Caring KW - Problem solving KW - Family KW - Patients KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1531431165?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+psychology&rft.atitle=A+problem-solving+education+intervention+in+caregivers+and+patients+during+allogeneic+hematopoietic+stem+cell+transplantation&rft.au=Bevans%2C+Margaret%3BWehrlen%2C+Leslie%3BCastro%2C+Kathleen%3BPrince%2C+Patricia%3BShelburne%2C+Nonniekaye%3BSoeken%2C+Karen%3BZabora%2C+James%3BWallen%2C+Gwenyth+R&rft.aulast=Bevans&rft.aufirst=Margaret&rft.date=2014-05-01&rft.volume=19&rft.issue=5&rft.spage=602&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+psychology&rft.issn=13591053&rft_id=info:doi/10.1177%2F1359105313475902 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-06-02 N1 - Last updated - 2014-06-03 N1 - SubjectsTermNotLitGenreText - 1147 4196; 1939 3617 6220; 12432; 4748; 10220; 9271 7890 5792 10484; 2039 13521 DO - http://dx.doi.org/10.1177/1359105313475902 ER - TY - JOUR T1 - Assurance of neuroattenuation of a live vaccine against West Nile virus: A comprehensive study of neuropathogenesis after infection with chimeric WN/DEN4 Delta 30 vaccine in comparison to two parental viruses and a surrogate flavivirus reference vaccine AN - 1529943856; 19862597 AB - The upsurge of West Nile virus (WNV) human infections in 2012 suggests that the US can expect periodic WNV outbreaks in the future. Availability of safe and effective vaccines against WNV in endemic areas, particularly for aging populations that are at high risk of West Nile neuroinvasive disease (WNND), could be beneficial. WN/DEN4 Delta 30 is a live, attenuated chimeric vaccine against WNV produced by replacement of the genes encoding the pre-membrane and envelope protein genes of the vaccine virus against dengue virus type 4 (DEN4 Delta 30) with corresponding sequences derived from a wild type WNV. Following intrathalamic inoculation of nonhuman primates (NHPs), a comprehensive neuropathogenesis study was performed and neurovirulence of WN/DEN4 Delta 30 vaccine candidate was compared to that of two parental viruses (i.e., WNV and DEN4 Delta 30), as well as to that of an attenuated flavivirus surrogate reference (i.e., yellow fever YF 17D). Clinical and virological data, as well as results of a semi-quantitative histopathological analysis, demonstrated that WN/DEN4 Delta 30 vaccine is highly attenuated for the central nervous system (CNS) of NHPs in comparison to a wild type WNV. Importantly, based on the virus replicative ability in the CNS of NHPs and the degree of induced histopathological changes, the level of neuroattenuation of WN/DEN4 Delta 30 vaccine was similar to that of YF 17D, and therefore within an acceptable range. In addition, we show that the DEN4 Delta 30 vaccine tested in this study also has a low neurovirulence profile. In summary, our results demonstrate a high level of neuroattenuation of two vaccine candidates, WN/DEN4 Delta 30 and DEN4 Delta 30. We also show here a remarkable sensitivity of our WNV-NY99 NHP model, as well as striking resemblance of the observed neuropathology to that seen in human WNND. These results support the use of this NHP model for translational studies of WNV neuropathogenesis and/or testing the effectiveness of vaccines and therapeutic approaches. JF - Vaccine AU - Maximova, Olga A AU - Speicher, James M AU - Skinner, Jeff R AU - Murphy, Brian R AU - St Claire, Marisa C AU - Ragland, Danny R AU - Herbert, Richard L AU - Pare, Dan R AU - Moore, Rashida M AU - Pletnev, Alexander G AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, United States Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 3187 EP - 3197 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 32 IS - 26 SN - 0264-410X, 0264-410X KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Virology & AIDS Abstracts; Immunology Abstracts KW - West Nile virus (WNV) KW - Live attenuated WNV vaccine KW - Neuropathogenesis KW - Neurovirulence KW - Nonhuman primates KW - Translation KW - Central nervous system KW - Invasiveness KW - Viruses KW - Aging KW - Animal models KW - Disease control KW - Histopathology KW - Infection KW - Flavivirus KW - Public health KW - Endemic species KW - Risk factors KW - Yellow fever KW - Envelope protein KW - Neuropathology KW - Dengue virus type 4 KW - Data processing KW - Environmental impact KW - Inoculation KW - Vaccines KW - West Nile virus KW - F 06905:Vaccines KW - Q1 08423:Behaviour KW - Q5 08524:Public health, medicines, dangerous organisms KW - V 22310:Genetics, Taxonomy & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1529943856?accountid=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=Assurance+of+neuroattenuation+of+a+live+vaccine+against+West+Nile+virus%3A+A+comprehensive+study+of+neuropathogenesis+after+infection+with+chimeric+WN%2FDEN4+Delta+30+vaccine+in+comparison+to+two+parental+viruses+and+a+surrogate+flavivirus+reference+vaccine&rft.au=Maximova%2C+Olga+A%3BSpeicher%2C+James+M%3BSkinner%2C+Jeff+R%3BMurphy%2C+Brian+R%3BSt+Claire%2C+Marisa+C%3BRagland%2C+Danny+R%3BHerbert%2C+Richard+L%3BPare%2C+Dan+R%3BMoore%2C+Rashida+M%3BPletnev%2C+Alexander+G&rft.aulast=Maximova&rft.aufirst=Olga&rft.date=2014-05-01&rft.volume=32&rft.issue=26&rft.spage=3187&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2014.04.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Central nervous system; Endemic species; Aging; Viruses; Environmental impact; Disease control; Histopathology; Vaccines; Public health; Translation; Invasiveness; Data processing; Neuropathogenesis; Animal models; Neurovirulence; Infection; Yellow fever; Risk factors; Envelope protein; Inoculation; Neuropathology; West Nile virus; Flavivirus; Dengue virus type 4 DO - http://dx.doi.org/10.1016/j.vaccine.2014.04.002 ER - TY - JOUR T1 - Humans and Ferrets with Prior H1N1 Influenza Virus Infections Do Not Exhibit Evidence of Original Antigenic Sin after Infection or Vaccination with the 2009 Pandemic H1N1 Influenza Virus AN - 1529934374; 19846340 AB - The hypothesis of original antigenic sin (OAS) states that the imprint established by an individual's first influenza virus infection governs the antibody response thereafter. Subsequent influenza virus infection results in an antibody response against the original infecting virus and an impaired immune response against the newer influenza virus. The purpose of our study was to seek evidence of OAS after infection or vaccination with the 2009 pandemic H1N1 (2009 pH1N1) virus in ferrets and humans previously infected with H1N1 viruses with various antigenic distances from the 2009 pH1N1 virus, including viruses from 1935 through 1999. In ferrets, seasonal H1N1 priming did not diminish the antibody response to infection or vaccination with the 2009 pH1N1 virus, nor did it diminish the T-cell response, indicating the absence of OAS in seasonal H1N1 virus-primed ferrets. Analysis of paired samples of human serum taken before and after vaccination with a monovalent inactivated 2009 pH1N1 vaccine showed a significantly greater-fold rise in the titer of antibody against the 2009 pH1N1 virus than against H1N1 viruses that circulated during the childhood of each subject. Thus, prior experience with H1N1 viruses did not result in an impairment of the antibody response against the 2009 pH1N1 vaccine. Our data from ferrets and humans suggest that prior exposure to H1N1 viruses did not impair the immune response against the 2009 pH1N1 virus. JF - Clinical and Vaccine Immunology AU - O'Donnell, Christopher D AU - Wright, Amber AU - Vogel, Leatrice AU - Boonnak, Kobporn AU - Treanor, John J AU - Subbarao, Kanta AD - Laboratory of Infectious Diseases, NIAID, Bethesda, Maryland, USA, ksubbarao@niaid.nih.gov. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 737 EP - 746 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 21 IS - 5 SN - 1556-679X, 1556-679X KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts KW - Data processing KW - Immunology KW - Viruses KW - Antibody response KW - Infection KW - Children KW - Vaccination KW - Influenza KW - pandemics KW - Influenza virus KW - Sulfur dioxide KW - Mustela KW - Lymphocytes T KW - Vaccines KW - Immune response KW - Seasonal variations KW - V 22350:Immunology KW - F 06905:Vaccines KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1529934374?accountid=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=Clinical+and+Vaccine+Immunology&rft.atitle=Humans+and+Ferrets+with+Prior+H1N1+Influenza+Virus+Infections+Do+Not+Exhibit+Evidence+of+Original+Antigenic+Sin+after+Infection+or+Vaccination+with+the+2009+Pandemic+H1N1+Influenza+Virus&rft.au=O%27Donnell%2C+Christopher+D%3BWright%2C+Amber%3BVogel%2C+Leatrice%3BBoonnak%2C+Kobporn%3BTreanor%2C+John+J%3BSubbarao%2C+Kanta&rft.aulast=O%27Donnell&rft.aufirst=Christopher&rft.date=2014-05-01&rft.volume=21&rft.issue=5&rft.spage=737&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=1556679X&rft_id=info:doi/10.1128%2FCVI.00790-13 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Number of references - 55 N1 - Last updated - 2014-08-21 N1 - SubjectsTermNotLitGenreText - Influenza; pandemics; Data processing; Lymphocytes T; Immune response; Vaccines; Antibody response; Children; Infection; Vaccination; Sulfur dioxide; Immunology; Viruses; Seasonal variations; Influenza virus; Mustela DO - http://dx.doi.org/10.1128/CVI.00790-13 ER - TY - JOUR T1 - Consultation on dengue vaccines: Progress in understanding protection, 26-28 June 2013, Rockville, Maryland AN - 1529927661; 19862614 AB - There is an unmet need for a dengue vaccine to further prevent the spread of this disease and contain the growing pandemic. To this end several vaccine companies and academic groups are actively pursuing the development of a tetravalent vaccine to prevent dengue. In the last few years progress has been made in this area, including the first results of a vaccine efficacy trial and improved understanding of the immune responses to the infection. Despite this progress, development of dengue vaccines faces important challenges including the need for a vaccine that induces balanced immune responses against all dengue strains and an incomplete understanding of the mechanism(s) of protection against infection and disease. This is a summary of a Consultation on dengue vaccines held in June 26-28, 2013 by the National Institute of Allergy and Infectious Diseases (part of the US National Institutes of Health) and the Dengue Vaccine Initiative (part of the International Vaccine Institute). The primary goal of this consultation was to review the progress in dengue vaccine development, evaluate the known mechanism of protection of dengue vaccines and discuss avenues for future research. JF - Vaccine AU - Cassetti, MCristina AU - Halstead, Scott B AD - National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 3115 EP - 3121 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 32 IS - 26 SN - 0264-410X, 0264-410X KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts KW - Dengue KW - Dengue virus KW - Dengue hemorrhagic fever KW - Severe dengue KW - Vaccine KW - Immunopathogenesis KW - Acquired immunity KW - T cell immunity KW - Innate immunity KW - Human diseases KW - Disease control KW - Infection KW - Allergies KW - Public health KW - Disease transmission KW - Allergic reactions KW - Hypersensitivity KW - pandemics KW - Infectious diseases KW - USA, Maryland, Rockville KW - USA, Maryland KW - Strains KW - ANW, USA, Maryland KW - Reviews KW - Immune response KW - Vaccines KW - V 22350:Immunology KW - Q1 08423:Behaviour KW - F 06910:Microorganisms & Parasites 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/1529927661?accountid=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=Consultation+on+dengue+vaccines%3A+Progress+in+understanding+protection%2C+26-28+June+2013%2C+Rockville%2C+Maryland&rft.au=Cassetti%2C+MCristina%3BHalstead%2C+Scott+B&rft.aulast=Cassetti&rft.aufirst=MCristina&rft.date=2014-05-01&rft.volume=32&rft.issue=26&rft.spage=3115&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2014.04.017 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Allergic reactions; Human diseases; Infectious diseases; Disease control; Vaccines; Strains; Disease transmission; Public health; pandemics; Hypersensitivity; Dengue; Reviews; Immune response; Infection; Allergies; USA, Maryland, Rockville; USA, Maryland; ANW, USA, Maryland DO - http://dx.doi.org/10.1016/j.vaccine.2014.04.017 ER - TY - JOUR T1 - Nucleophosmin modulates stability, activity, and nucleolar accumulation of base excision repair proteins. AN - 1524821577; 24648491 AB - Nucleophosmin (NPM1) is a multifunctional protein that controls cell growth and genome stability via a mechanism that involves nucleolar-cytoplasmic shuttling. It is clear that NPM1 also contributes to the DNA damage response, yet its exact function is poorly understood. We recently linked NPM1 expression to the functional activation of the major abasic endonuclease in mammalian base excision repair (BER), apurinic/apyrimidinic endonuclease 1 (APE1). Here we unveil a novel role for NPM1 as a modulator of the whole BER pathway by 1) controlling BER protein levels, 2) regulating total BER capacity, and 3) modulating the nucleolar localization of several BER enzymes. We find that cell treatment with the genotoxin cisplatin leads to concurrent relocalization of NPM1 and BER components from nucleoli to the nucleoplasm, and cellular experiments targeting APE1 suggest a role for the redistribution of nucleolar BER factors in determining cisplatin toxicity. Finally, based on the use of APE1 as a representative protein of the BER pathway, our data suggest a function for BER proteins in the regulation of ribogenesis. © 2014 Poletto et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). JF - Molecular biology of the cell AU - Poletto, Mattia AU - Lirussi, Lisa AU - Wilson, David M AU - Tell, Gianluca AD - Department of Medical and Biological Sciences, University of Udine, Udine 33100, Italy. ; Laboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224. ; Department of Medical and Biological Sciences, University of Udine, Udine 33100, Italy gianluca.tell@uniud.it. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1641 EP - 1652 VL - 25 IS - 10 KW - Cross-Linking Reagents KW - 0 KW - Nuclear Proteins KW - RNA, Small Interfering KW - Tumor Suppressor Protein p53 KW - nucleophosmin KW - 117896-08-9 KW - Fen1 protein, mouse KW - EC 3.1.- KW - Flap Endonucleases KW - Apex1 protein, mouse KW - EC 4.2.99.18 KW - DNA-(Apurinic or Apyrimidinic Site) Lyase KW - DNA Ligases KW - EC 6.5.1.- KW - DNA Ligase ATP KW - EC 6.5.1.1 KW - Doxycycline KW - N12000U13O KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Animals KW - Flap Endonucleases -- biosynthesis KW - HeLa Cells KW - Humans KW - Cell Nucleolus -- genetics KW - Cross-Linking Reagents -- pharmacology KW - Doxycycline -- pharmacology KW - Mice KW - DNA Damage -- genetics KW - DNA Ligases -- biosynthesis KW - Ribosomes -- genetics KW - Protein Transport -- genetics KW - Cisplatin -- pharmacology KW - DNA Ligases -- metabolism KW - Tumor Suppressor Protein p53 -- genetics KW - RNA Interference KW - Flap Endonucleases -- metabolism KW - DNA Repair -- genetics KW - DNA-(Apurinic or Apyrimidinic Site) Lyase -- genetics KW - Nuclear Proteins -- genetics KW - DNA-(Apurinic or Apyrimidinic Site) Lyase -- metabolism KW - DNA-(Apurinic or Apyrimidinic Site) Lyase -- biosynthesis KW - Nuclear Proteins -- biosynthesis KW - Nuclear Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524821577?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nucleophosmin+modulates+stability%2C+activity%2C+and+nucleolar+accumulation+of+base+excision+repair+proteins.&rft.au=Poletto%2C+Mattia%3BLirussi%2C+Lisa%3BWilson%2C+David+M%3BTell%2C+Gianluca&rft.aulast=Poletto&rft.aufirst=Mattia&rft.date=2014-05-01&rft.volume=25&rft.issue=10&rft.spage=1641&rft.isbn=&rft.btitle=&rft.title=Molecular+biology+of+the+cell&rft.issn=1939-4586&rft_id=info:doi/10.1091%2Fmbc.E13-12-0717 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-13 N1 - Date created - 2014-05-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2005 Sep 1;437(7055):147-53 [16007073] Mol Biol Cell. 2005 May;16(5):2395-413 [15758027] Mol Cell Biol. 2006 May;26(10):3798-809 [16648475] Hum Mol Genet. 2006 Jul 15;15(14):2239-49 [16777843] Int J Cancer. 2002 Jan 20;97(3):297-305 [11774280] Toxicology. 2002 Sep 30;179(1-2):85-93 [12204545] EMBO J. 2003 Nov 17;22(22):6068-77 [14609953] Biochem J. 2004 Mar 15;378(Pt 3):929-37 [14678012] Cancer Cell. 2004 May;5(5):465-75 [15144954] Environ Health Perspect. 2004 May;112(7):799-804 [15159209] Cancer Res. 1991 Dec 15;51(24):6506-9 [1660340] Cancer Detect Prev. 2006;30(6):481-90 [17113241] Nature. 2007 Jun 7;447(7145):730-4 [17554310] Mol Cell Biol. 2008 Feb;28(3):1068-80 [18070929] Mol Cell. 2008 Feb 29;29(4):477-87 [18313385] Mol Cell Biol. 2008 May;28(10):3114-26 [18332108] Mol Cell Biol. 2008 Jul;28(13):4310-9 [18443037] DNA Repair (Amst). 2009 Mar 1;8(3):286-97 [19144573] EMBO Rep. 2009 Mar;10(3):231-8 [19229283] Mol Cell Biol. 2009 Apr;29(7):1834-54 [19188445] Oncogene. 2009 Apr 2;28(13):1616-25 [19219073] J Biol Chem. 2010 Apr 16;285(16):12416-25 [20159984] Biol Pharm Bull. 2010;33(4):697-701 [20410608] Trends Biochem Sci. 2010 May;35(5):247-52 [20172733] Cancer Res. 2010 Sep 1;70(17):6746-56 [20713529] Nucleic Acids Res. 2010 Dec;38(22):8239-56 [20699270] Biochemistry. 2011 Apr 12;50(14):2780-9 [21425800] Oncogene. 2011 Jun 9;30(23):2595-609 [21278791] Mol Cell Proteomics. 2011 Oct;10(10):M111.009241 [21778410] Clin Cancer Res. 2011 Oct 15;17(20):6490-9 [21878537] Methods Mol Biol. 2012;809:519-33 [22113298] Nucleic Acids Res. 2012 Jan;40(2):701-11 [21933813] Mol Biol Cell. 2012 Oct;23(20):4079-96 [22918947] Mol Cell. 2013 Jan 24;49(2):339-45 [23246433] Hepatology. 2013 May;57(5):1893-905 [23258611] DNA Repair (Amst). 2013 May 1;12(5):326-33 [23473643] Mutat Res. 2013 Mar-Apr;743-744:44-52 [23219605] Antioxid Redox Signal. 2014 Feb 1;20(4):621-39 [23879289] Oncogene. 2014 May 29;33(22):2876-87 [23831574] Nucleic Acids Res. 1995 Oct 11;23(19):3974-9 [7479045] Cancer Res. 1999 Sep 1;59(17):4369-74 [10485485] J Cell Sci. 2005 Jan 1;118(Pt 1):211-22 [15615785] Mol Cell Biol. 2005 Feb;25(4):1258-71 [15684379] J Biol Chem. 2005 Mar 11;280(10):9586-94 [15613478] Mol Cell Biol. 2005 Oct;25(20):8874-86 [16199867] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1091/mbc.E13-12-0717 ER - TY - JOUR T1 - Fine-tuning of epigenetic regulation with respect to promoter CpG content in a cell type-specific manner. AN - 1524817136; 24521667 AB - Epigenetic regulation of gene expression is fundamental for cell type-specific gene expression. However, integrated comparative transcriptomic and epigenomic analyses in various adult primary differentiated cells remain underrepresented. We generated promoter landscapes of DNA methylation and three important histone methylation marks (H3K4me3, H3K9me2, and H3K27me3) in two primary cell types (B lymphocytes and liver) from adult mice. In line with previous studies, we also observed distinct H3K4me3 patterns at promoters dictated by CpG content in differentiated primary cells. We further explored the distribution of initiating RNA polymerase II and elongating RNA polymerase II across genes within different promoter classes, suggesting different rate-limiting steps at CpG-rich vs. CpG-poor genes. Examination of differentially expressed genes revealed that regulation of tissue-specific genes is closely related to gene function regardless of promoter type. Although repressive chromatin marks displayed differential preference to promoters based on CpG content, we observed fine-tuning of the pattern of association of these marks with specific promoter types in a cell type-specific manner. The distribution of H3K9me2 and H3K27me3, relative to CpG content, differed substantially between the two cell types. Cell-type specific accumulation of repressive chromatin marks was also observed at silent genes in both cell types, suggesting that differentiated primary cells may exhibit cell-type specificity in the distribution of repressive chromatin marks. Epigenetic regulation of gene expression and the association of specific histone marks with promoter sequence classes are fine-tuned in a cell type-specific manner. This unexpected finding underscores the value of extensive study of epigenetic marks across cell and tissue types. JF - Epigenetics AU - Li, Ruifang AU - Mav, Deepak AU - Grimm, Sara A AU - Jothi, Raja AU - Shah, Ruchir AU - Wade, Paul A AD - Laboratory of Molecular Carcinogenesis; National Institute of Environmental Health Sciences; Research Triangle Park, NC USA. ; SRA International; Research Triangle Park, NC USA. ; Integrative Bioinformatics; National Institute of Environmental Health Sciences; Research Triangle Park, NC USA. ; Laboratory of Molecular Carcinogenesis; National Institute of Environmental Health Sciences; Research Triangle Park, NC USA; Biostatistics Branch; National Institute of Environmental Health Sciences; Research Triangle Park, NC USA. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 747 EP - 759 VL - 9 IS - 5 KW - Histones KW - 0 KW - RNA Polymerase II KW - EC 2.7.7.- KW - Index Medicus KW - CpG content KW - promoter KW - epigenetics KW - transcription regulation KW - CpG island KW - RNA Polymerase II -- metabolism KW - Animals KW - DNA Methylation KW - Histones -- metabolism KW - Mice, Inbred C57BL KW - Organ Specificity KW - Gene Expression Regulation KW - Male KW - Histones -- genetics KW - Promoter Regions, Genetic KW - Liver -- cytology KW - B-Lymphocytes -- cytology KW - CpG Islands KW - Liver -- metabolism KW - B-Lymphocytes -- metabolism KW - Epigenesis, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524817136?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epigenetics&rft.atitle=Fine-tuning+of+epigenetic+regulation+with+respect+to+promoter+CpG+content+in+a+cell+type-specific+manner.&rft.au=Li%2C+Ruifang%3BMav%2C+Deepak%3BGrimm%2C+Sara+A%3BJothi%2C+Raja%3BShah%2C+Ruchir%3BWade%2C+Paul+A&rft.aulast=Li&rft.aufirst=Ruifang&rft.date=2014-05-01&rft.volume=9&rft.issue=5&rft.spage=747&rft.isbn=&rft.btitle=&rft.title=Epigenetics&rft.issn=1559-2308&rft_id=info:doi/10.4161%2Fepi.28075 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-10 N1 - Date created - 2014-05-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Genes Dev. 2011 May 15;25(10):1010-22 [21576262] Nature. 2010 Apr 15;464(7291):1082-6 [20393567] Genome Res. 2012 Dec;22(12):2399-408 [23100115] Cell. 1999 Oct 29;99(3):247-57 [10555141] Science. 2001 Aug 10;293(5532):1074-80 [11498575] Curr Opin Genet Dev. 2002 Apr;12(2):198-209 [11893494] Mol Cell Biol. 2004 Oct;24(20):8862-71 [15456861] Cell. 1992 Jun 12;69(6):915-26 [1606615] Lab Invest. 2005 Sep;85(9):1172-80 [16025148] Nat Rev Mol Cell Biol. 2005 Nov;6(11):838-49 [16261189] Genome Res. 2006 May;16(5):595-605 [16606705] Cancer Res. 2006 Aug 15;66(16):7939-47 [16912168] Methods Enzymol. 2006;411:270-82 [16939795] Cell. 2007 Feb 23;128(4):669-81 [17320505] Cell. 2007 Feb 23;128(4):707-19 [17320508] Proc Natl Acad Sci U S A. 2007 Mar 27;104(13):5521-6 [17376869] Nat Genet. 2007 Apr;39(4):457-66 [17334365] Cell. 2007 May 18;129(4):823-37 [17512414] Nature. 2007 Aug 2;448(7153):553-60 [17603471] Curr Opin Plant Biol. 2007 Oct;10(5):528-33 [17692561] Mol Cell. 2008 Jun 20;30(6):755-66 [18514006] Annu Rev Genet. 2008;42:733-72 [18729722] Nat Genet. 2009 Feb;41(2):246-50 [19151716] Genome Biol. 2009;10(3):R25 [19261174] Nature. 2009 Sep 10;461(7261):186-92 [19741698] Annu Rev Genet. 2009;43:559-99 [19886812] Genes Dev. 2012 May 1;26(9):933-44 [22549956] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4161/epi.28075 ER - TY - JOUR T1 - Single-dose live-attenuated Nipah virus vaccines confer complete protection by eliciting antibodies directed against surface glycoproteins AN - 1524434240; 19753917 AB - Background Nipah virus (NiV), a zoonotic pathogen causing severe respiratory illness and encephalitis in humans, emerged in Malaysia in 1998 with subsequent outbreaks on an almost annual basis since 2001 in parts of the Indian subcontinent. The high case fatality rate, human-to-human transmission, wide-ranging reservoir distribution and lack of licensed intervention options are making NiV a serious regional and potential global public health problem. The objective of this study was to develop a fast-acting, single-dose NiV vaccine that could be implemented in a ring vaccination approach during outbreaks. Methods In this study we have designed new live-attenuated vaccine vectors based on recombinant vesicular stomatitis viruses (rVSV) expressing NiV glycoproteins (G or F) or nucleoprotein (N) and evaluated their protective efficacy in Syrian hamsters, an established NiV animal disease model. We further characterized the humoral immune response to vaccination in hamsters using ELISA and neutralization assays and performed serum transfer studies. Results Vaccination of Syrian hamsters with a single dose of the rVSV vaccine vectors resulted in strong humoral immune responses with neutralizing activities found only in those animals vaccinated with rVSV expressing NiV G or F proteins. Vaccinated animals with neutralizing antibody responses were completely protected from lethal NiV disease, whereas animals vaccinated with rVSV expressing NiV N showed only partial protection. Protection of NiV G or F vaccinated animals was conferred by antibodies, most likely the neutralizing fraction, as demonstrated by serum transfer studies. Protection of N-vaccinated hamsters was not antibody-dependent indicating a role of adaptive cellular responses for protection. Conclusions The rVSV vectors expressing Nipah virus G or F are prime candidates for new 'emergency vaccines' to be utilized for NiV outbreak management. JF - Vaccine AU - DeBuysscher, Blair L AU - Scott, Dana AU - Marzi, Andrea AU - Prescott, Joseph AU - Feldmann, Heinz AD - Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, USA Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 2637 EP - 2644 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 32 IS - 22 SN - 0264-410X, 0264-410X KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts KW - glycoprotein G KW - Viruses KW - Nucleoproteins KW - Animal models KW - Intervention KW - Disease transmission KW - Public health KW - Vesicular stomatitis KW - Glycoproteins KW - Immune response (humoral) KW - Neutralization KW - Reservoirs KW - Mortality KW - Enzyme-linked immunosorbent assay KW - F protein KW - Vectors KW - Pathogens KW - ISEW, Malaysia KW - Encephalitis KW - Antibodies KW - Nipah virus KW - Proteins KW - Immune response KW - Outbreaks KW - Vaccines KW - Animal diseases KW - V 22350:Immunology KW - F 06905:Vaccines KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524434240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Single-dose+live-attenuated+Nipah+virus+vaccines+confer+complete+protection+by+eliciting+antibodies+directed+against+surface+glycoproteins&rft.au=DeBuysscher%2C+Blair+L%3BScott%2C+Dana%3BMarzi%2C+Andrea%3BPrescott%2C+Joseph%3BFeldmann%2C+Heinz&rft.aulast=DeBuysscher&rft.aufirst=Blair&rft.date=2014-05-01&rft.volume=32&rft.issue=22&rft.spage=2637&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2014.02.087 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-08-21 N1 - SubjectsTermNotLitGenreText - glycoprotein G; Enzyme-linked immunosorbent assay; Nucleoproteins; F protein; Animal models; Vectors; Pathogens; Encephalitis; Public health; Disease transmission; Vesicular stomatitis; Antibodies; Glycoproteins; Vaccines; Immune response (humoral); Mortality; Viruses; Intervention; Proteins; Outbreaks; Immune response; Reservoirs; Neutralization; Animal diseases; Nipah virus; ISEW, Malaysia DO - http://dx.doi.org/10.1016/j.vaccine.2014.02.087 ER - TY - JOUR T1 - Brief Report: Loss of p15Ink4b Accelerates Development of Myeloid Neoplasms in Nup98-HoxD13 Transgenic Mice AN - 1524416715; 19752648 AB - Homeostasis of hematopoietic stem and progenitor cells is a tightly regulated process. The disturbance of the balance in the hematopoietic progenitor pool can result in favorable conditions for development of diseases such as myelodysplastic syndromes and leukemia. It has been shown recently that mice lacking p15Ink4b have skewed differentiation of common myeloid progenitors toward the myeloid lineage at the expense of erythroid progenitors. The lack of p15INK4B expression in human leukemic blasts has been linked to poor prognosis and increased risk of myelodysplastic syndromes transformation to acute myeloid leukemia. However, the role of p15Ink4b in disease development is just beginning to be elucidated. This study examines the collaboration of the loss of p15Ink4b with Nup98-HoxD13 translocation in the development of hematological malignancies in a mouse model. Here, we report that loss of p15Ink4b collaborates with Nup98-HoxD13 transgene in the development of predominantly myeloid neoplasms, namely acute myeloid leukemia, myeloproliferative disease, and myelodysplastic syndromes. This mouse model could be a very valuable tool for studying p15Ink4b function in tumorigenesis as well as preclinical drug testing. Stem Cells 2014; 32:1361-1366 JF - Stem Cells AU - Humeniuk, Rita AU - Koller, Richard AU - Bies, Juraj AU - Aplan, Peter AU - Wolff, Linda AD - National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1361 EP - 1366 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 32 IS - 5 SN - 1066-5099, 1066-5099 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Transformation KW - Acute myeloid leukemia KW - Tumorigenesis KW - Transgenes KW - Animal models KW - Prognosis KW - Homeostasis KW - Transgenic mice KW - Differentiation KW - Myelodysplastic syndrome KW - Malignancy KW - Stem cells KW - Hemopoiesis KW - Myeloproliferative diseases KW - Blast KW - Translocation KW - Drugs KW - W 30910:Imaging KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524416715?accountid=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=Brief+Report%3A+Loss+of+p15Ink4b+Accelerates+Development+of+Myeloid+Neoplasms+in+Nup98-HoxD13+Transgenic+Mice&rft.au=Humeniuk%2C+Rita%3BKoller%2C+Richard%3BBies%2C+Juraj%3BAplan%2C+Peter%3BWolff%2C+Linda&rft.aulast=Humeniuk&rft.aufirst=Rita&rft.date=2014-05-01&rft.volume=32&rft.issue=5&rft.spage=1361&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1635 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-05-29 N1 - SubjectsTermNotLitGenreText - Transformation; Acute myeloid leukemia; Transgenes; Tumorigenesis; Prognosis; Animal models; Homeostasis; Transgenic mice; Myelodysplastic syndrome; Differentiation; Stem cells; Malignancy; Hemopoiesis; Myeloproliferative diseases; Blast; Drugs; Translocation DO - http://dx.doi.org/10.1002/stem.1635 ER - TY - JOUR T1 - Pesticides, chemical and industrial exposures in relation to systemic Lupus erythematosus AN - 1524414831; 19778858 AB - Growing evidence suggests exposure to chemicals and industrial pollutants may increase risk of systemic Lupus erythematosus (SLE). Here we review research on SLE associations with occupational and industrial exposures, primarily drawing on studies in human populations and summarizing epidemiologic research published in the past decade. The association of occupational silica exposure with SLE is well established, but key questions remain, including the required dose and susceptibility factors, and SLE risk due to other silicate exposures. Research on SLE and other exposures is less well developed, though several potential associations merit further consideration because of the consistency of preliminary human findings, experimental animal research, and biologic plausibility. These include pesticides and solvents, for which experimental findings also support investigation of specific agents, including organochlorines and trichloroethylene. Experimental findings and biologic plausibility suggest research on SLE and occupational exposure to hydrocarbons (i.e. mineral oils) is warranted, especially given the widespread exposures in the population. Experimental and limited human findings support further investigation of SLE related to mercury exposure, especially in dental occupations. Research on environmental risk factors in risk-enriched cohorts (family-based) is recommended, as is further investigation of exposures in relation to intermediate markers of effect (e.g. antinuclear antibodies), clinical features (e.g. nephritis), and outcomes. JF - Lupus AU - Parks, C G AU - De Roos, AJ AD - Epidemiology Branch, National Institute of Environmental Health Sciences, NC, USA, Parks1@mail.nih.gov Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 527 EP - 536 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 23 IS - 6 SN - 0961-2033, 0961-2033 KW - Risk Abstracts; Health & Safety Science Abstracts; Pollution Abstracts; Immunology Abstracts KW - Antinuclear antibodies KW - mineral oil KW - Organochlorine compounds KW - Oil KW - Pollutants KW - Risk factors KW - Trichloroethylene KW - Systemic lupus erythematosus KW - Occupational exposure KW - Hydrocarbons KW - Human populations KW - Silicic acid KW - Solvents KW - Population studies KW - Silica KW - Reviews KW - Nephritis KW - Pesticides KW - Mercury KW - Minerals KW - F 06930:Autoimmunity KW - R2 23060:Medical and environmental health KW - H 1000:Occupational Safety and Health KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524414831?accountid=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=Lupus&rft.atitle=Pesticides%2C+chemical+and+industrial+exposures+in+relation+to+systemic+Lupus+erythematosus&rft.au=Parks%2C+C+G%3BDe+Roos%2C+AJ&rft.aulast=Parks&rft.aufirst=C&rft.date=2014-05-01&rft.volume=23&rft.issue=6&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=Lupus&rft.issn=09612033&rft_id=info:doi/10.1177%2F0961203313511680 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Number of references - 58 N1 - Last updated - 2014-08-21 N1 - SubjectsTermNotLitGenreText - mineral oil; Antinuclear antibodies; Organochlorine compounds; Hydrocarbons; Silicic acid; Solvents; Population studies; Silica; Pollutants; Nephritis; Risk factors; Reviews; Pesticides; Mercury; Systemic lupus erythematosus; Trichloroethylene; Occupational exposure; Oil; Human populations; Minerals DO - http://dx.doi.org/10.1177/0961203313511680 ER - TY - JOUR T1 - International Society for the Advancement of Cytometry cell sorter biosafety standards AN - 1524399826; 19752542 AB - Flow cytometric cell sorting of biological specimens has become prevalent in basic and clinical research laboratories. These specimens may contain known or unknown infectious agents, necessitating precautions to protect instrument operators and the environment from biohazards arising from the use of sorters. To this end the International Society of Analytical Cytology (ISAC) was proactive in establishing biosafety guidelines in 1997 (Schmid et al., Cytometry 1997; 28:99-117) and subsequently published revised biosafety standards for cell sorting of unfixed samples in 2007 (Schmid et al., Cytometry Part A J Int Soc Anal Cytol 2007; 71A:414-437). Since their publication, these documents have become recognized worldwide as the standard of practice and safety precautions for laboratories performing cell sorting experiments. However, the field of cytometry has progressed since 2007, and the document requires an update. The new Standards provides guidance: (1) for laboratory design for cell sorter laboratories; (2) for the creation of laboratory or instrument specific Standard Operating Procedures (SOP); and (3) on procedures for the safe operation of cell sorters, including personal protective equipment (PPE) and validation of aerosol containment. Published copyright 2013 Wiley Periodicals Inc. super() JF - Cytometry Part A AU - Holmes, Kevin L AU - Fontes, Benjamin AU - Hogarth, Philip AU - Konz, Richard AU - Monard, Simon AU - Pletcher, Charles H AU - Wadley, Robert B AU - Schmid, Ingrid AU - Perfetto, Stephen P AD - Flow Cytometry Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 434 EP - 453 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 85 IS - 5 SN - 1552-4922, 1552-4922 KW - Biotechnology and Bioengineering Abstracts KW - Flow cytometry KW - Aerosols KW - Cytometry KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524399826?accountid=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=International+Society+for+the+Advancement+of+Cytometry+cell+sorter+biosafety+standards&rft.au=Holmes%2C+Kevin+L%3BFontes%2C+Benjamin%3BHogarth%2C+Philip%3BKonz%2C+Richard%3BMonard%2C+Simon%3BPletcher%2C+Charles+H%3BWadley%2C+Robert+B%3BSchmid%2C+Ingrid%3BPerfetto%2C+Stephen+P&rft.aulast=Holmes&rft.aufirst=Kevin&rft.date=2014-05-01&rft.volume=85&rft.issue=5&rft.spage=434&rft.isbn=&rft.btitle=&rft.title=Cytometry+Part+A&rft.issn=15524922&rft_id=info:doi/10.1002%2Fcyto.a.22454 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-05-29 N1 - SubjectsTermNotLitGenreText - Flow cytometry; Aerosols; Cytometry DO - http://dx.doi.org/10.1002/cyto.a.22454 ER - TY - JOUR T1 - Role of ventral subiculum in context-induced reinstatement of heroin seeking in rats AN - 1524395888; 19744645 AB - In rats, reexposure to heroin-paired contexts after extinction of lever responding in a different context reinstates heroin seeking. Previous reports indicate that ventral hippocampus/Ca1 region plays a critical role in cocaine-, cue- and context-induced reinstatement of cocaine seeking. Here, we examined whether ventral subiculum, the output region of ventral hippocampus, is involved in context-induced reinstatement of heroin seeking. We found that reversible inactivation of ventral subiculum, but not posterior Ca1, with the gamma-aminobutyric acid agonists muscimol+baclofen decreased context-induced reinstatement of heroin seeking. Our findings, together with previous studies on cocaine seeking, indicate a critical role of ventral subiculum in context-induced relapse across drug classes. In rats, re-exposure to heroin-paired contexts after extinction of lever-pressing in a different context reinstates heroin seeking. Previous reports indicate that ventral hippocampus plays a critical role in cocaine-, cue-, and context-induced reinstatement of cocaine seeking. Here, we found that reversible inactivation of ventral subiculum, the output region of ventral hippocampus, decreased context-induced reinstatement of heroin seeking. Our findings, together with previous studies on cocaine seeking, indicate a critical role of ventral subiculum in context-induced relapse across drug classes. JF - Addiction Biology AU - Bossert, Jennifer M AU - Stern, Anna L AD - Behavioral Neuroscience Branch, Intramural Research Program, National Institute on Drug Abuse, NIH/DHHS, Baltimore, MD, USA. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 338 EP - 342 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 19 IS - 3 SN - 1355-6215, 1355-6215 KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - Conditioned cues KW - drug environment KW - heroin self-administration KW - hippocampus KW - muscimol+baclofen KW - reinstatement KW - relapse KW - Extinction KW - Hippocampus KW - Heroin KW - gamma -Aminobutyric acid KW - Addiction KW - Cocaine KW - Drug abuse KW - Reinstatement 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/1524395888?accountid=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=Role+of+ventral+subiculum+in+context-induced+reinstatement+of+heroin+seeking+in+rats&rft.au=Bossert%2C+Jennifer+M%3BStern%2C+Anna+L&rft.aulast=Bossert&rft.aufirst=Jennifer&rft.date=2014-05-01&rft.volume=19&rft.issue=3&rft.spage=338&rft.isbn=&rft.btitle=&rft.title=Addiction+Biology&rft.issn=13556215&rft_id=info:doi/10.1111%2Fadb.12015 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Extinction; Heroin; Hippocampus; gamma -Aminobutyric acid; Addiction; Drug abuse; Cocaine; Reinstatement DO - http://dx.doi.org/10.1111/adb.12015 ER - TY - JOUR T1 - Virus nomenclature below the species level: a standardized nomenclature for filovirus strains and variants rescued from cDNA. AN - 1521909806; 24190508 AB - Specific alterations (mutations, deletions, insertions) of virus genomes are crucial for the functional characterization of their regulatory elements and their expression products, as well as a prerequisite for the creation of attenuated viruses that could serve as vaccine candidates. Virus genome tailoring can be performed either by using traditionally cloned genomes as starting materials, followed by site-directed mutagenesis, or by de novo synthesis of modified virus genomes or parts thereof. A systematic nomenclature for such recombinant viruses is necessary to set them apart from wild-type and laboratory-adapted viruses, and to improve communication and collaborations among researchers who may want to use recombinant viruses or create novel viruses based on them. A large group of filovirus experts has recently proposed nomenclatures for natural and laboratory animal-adapted filoviruses that aim to simplify the retrieval of sequence data from electronic databases. Here, this work is extended to include nomenclature for filoviruses obtained in the laboratory via reverse genetics systems. The previously developed template for natural filovirus genetic variant naming, (/)///-, is retained, but we propose to adapt the type of information added to each field for cDNA clone-derived filoviruses. For instance, the full-length designation of an Ebola virus Kikwit variant rescued from a plasmid developed at the US Centers for Disease Control and Prevention could be akin to "Ebola virus H.sapiens-rec/COD/1995/Kikwit-abc1" (with the suffix "rec" identifying the recombinant nature of the virus and "abc1" being a placeholder for any meaningful isolate designator). Such a full-length designation should be used in databases and the methods section of publications. Shortened designations (such as "EBOV H.sap/COD/95/Kik-abc1") and abbreviations (such as "EBOV/Kik-abc1") could be used in the remainder of the text, depending on how critical it is to convey information contained in the full-length name. "EBOV" would suffice if only one EBOV strain/variant/isolate is addressed. JF - Archives of virology AU - Kuhn, Jens H AU - Bào, Yīmíng AU - Bavari, Sina AU - Becker, Stephan AU - Bradfute, Steven AU - Brauburger, Kristina AU - Rodney Brister, J AU - Bukreyev, Alexander A AU - Caì, Yíngyún AU - Chandran, Kartik AU - Davey, Robert A AU - Dolnik, Olga AU - Dye, John M AU - Enterlein, Sven AU - Gonzalez, Jean-Paul AU - Formenty, Pierre AU - Freiberg, Alexander N AU - Hensley, Lisa E AU - Hoenen, Thomas AU - Honko, Anna N AU - Ignatyev, Georgy M AU - Jahrling, Peter B AU - Johnson, Karl M AU - Klenk, Hans-Dieter AU - Kobinger, Gary AU - Lackemeyer, Matthew G AU - Leroy, Eric M AU - Lever, Mark S AU - Mühlberger, Elke AU - Netesov, Sergey V AU - Olinger, Gene G AU - Palacios, Gustavo AU - Patterson, Jean L AU - Paweska, Janusz T AU - Pitt, Louise AU - Radoshitzky, Sheli R AU - Ryabchikova, Elena I AU - Saphire, Erica Ollmann AU - Shestopalov, Aleksandr M AU - Smither, Sophie J AU - Sullivan, Nancy J AU - Swanepoel, Robert AU - Takada, Ayato AU - Towner, Jonathan S AU - van der Groen, Guido AU - Volchkov, Viktor E AU - Volchkova, Valentina A AU - Wahl-Jensen, Victoria AU - Warren, Travis K AU - Warfield, Kelly L AU - Weidmann, Manfred AU - Nichol, Stuart T AD - Integrated Research Facility at Fort Detrick (IRF-Frederick), Division of Clinical Research (DCR), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), B-8200 Research Plaza, Fort Detrick, Frederick, MD, 21702, USA, kuhnjens@mail.nih.gov. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1229 EP - 1237 VL - 159 IS - 5 KW - Index Medicus KW - Genome, Viral KW - Filoviridae -- classification KW - Reassortant Viruses -- classification KW - Filoviridae -- genetics KW - Reassortant Viruses -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521909806?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+virology&rft.atitle=Virus+nomenclature+below+the+species+level%3A+a+standardized+nomenclature+for+filovirus+strains+and+variants+rescued+from+cDNA.&rft.au=Kuhn%2C+Jens+H%3BB%C3%A0o%2C+Y%C4%ABm%C3%ADng%3BBavari%2C+Sina%3BBecker%2C+Stephan%3BBradfute%2C+Steven%3BBrauburger%2C+Kristina%3BRodney+Brister%2C+J%3BBukreyev%2C+Alexander+A%3BCa%C3%AC%2C+Y%C3%ADngy%C3%BAn%3BChandran%2C+Kartik%3BDavey%2C+Robert+A%3BDolnik%2C+Olga%3BDye%2C+John+M%3BEnterlein%2C+Sven%3BGonzalez%2C+Jean-Paul%3BFormenty%2C+Pierre%3BFreiberg%2C+Alexander+N%3BHensley%2C+Lisa+E%3BHoenen%2C+Thomas%3BHonko%2C+Anna+N%3BIgnatyev%2C+Georgy+M%3BJahrling%2C+Peter+B%3BJohnson%2C+Karl+M%3BKlenk%2C+Hans-Dieter%3BKobinger%2C+Gary%3BLackemeyer%2C+Matthew+G%3BLeroy%2C+Eric+M%3BLever%2C+Mark+S%3BM%C3%BChlberger%2C+Elke%3BNetesov%2C+Sergey+V%3BOlinger%2C+Gene+G%3BPalacios%2C+Gustavo%3BPatterson%2C+Jean+L%3BPaweska%2C+Janusz+T%3BPitt%2C+Louise%3BRadoshitzky%2C+Sheli+R%3BRyabchikova%2C+Elena+I%3BSaphire%2C+Erica+Ollmann%3BShestopalov%2C+Aleksandr+M%3BSmither%2C+Sophie+J%3BSullivan%2C+Nancy+J%3BSwanepoel%2C+Robert%3BTakada%2C+Ayato%3BTowner%2C+Jonathan+S%3Bvan+der+Groen%2C+Guido%3BVolchkov%2C+Viktor+E%3BVolchkova%2C+Valentina+A%3BWahl-Jensen%2C+Victoria%3BWarren%2C+Travis+K%3BWarfield%2C+Kelly+L%3BWeidmann%2C+Manfred%3BNichol%2C+Stuart+T&rft.aulast=Kuhn&rft.aufirst=Jens&rft.date=2014-05-01&rft.volume=159&rft.issue=5&rft.spage=1229&rft.isbn=&rft.btitle=&rft.title=Archives+of+virology&rft.issn=1432-8798&rft_id=info:doi/10.1007%2Fs00705-013-1877-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-24 N1 - Date created - 2014-05-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 2001 Mar 9;291(5510):1965-9 [11239157] J Infect Dis. 2011 Nov;204 Suppl 3:S934-40 [21987772] Virus Res. 2004 Nov;106(1):43-50 [15522446] J Infect Dis. 2011 Nov;204 Suppl 3:S941-6 [21987773] Arch Virol. 2012 Jul;157(7):1411-22 [22481600] PLoS Pathog. 2012;8(8):e1002847 [22876185] J Virol. 2012 Nov;86(21):11779-88 [22915810] Arch Virol. 2013 Jan;158(1):301-11 [23001720] Cell Microbiol. 2013 Feb;15(2):270-84 [23186212] PLoS Pathog. 2013 Jan;9(1):e1003147 [23382680] Arch Virol. 2013 Jun;158(6):1425-32 [23358612] J Virol. 2013 Jul;87(13):7471-85 [23616668] Antiviral Res. 2013 Sep;99(3):207-13 [23751367] Virology. 2005 Feb 5;332(1):20-7 [15661137] J Virol. 2005 Aug;79(16):10300-7 [16051823] J Virol. 2006 Jan;80(2):1038-43 [16379005] J Virol. 2006 Jul;80(13):6430-40 [16775331] PLoS Pathog. 2006 Jul;2(7):e73 [16848640] Virus Res. 2006 Nov;121(2):205-14 [16839637] J Infect Dis. 2007 Nov 15;196 Suppl 2:S313-22 [17940966] J Virol. 2008 Mar;82(6):2699-704 [18199658] J Virol. 2008 Dec;82(24):12569-73 [18829754] J Virol. 2009 May;83(9):4508-19 [19225002] J Virol. 2010 Mar;84(6):3004-15 [20071589] PLoS Negl Trop Dis. 2010;4(8):e802 [20808767] Arch Virol. 2010 Dec;155(12):2083-103 [21046175] Antiviral Res. 2011 Aug;91(2):195-208 [21699921] J Infect Dis. 2011 Nov;204 Suppl 3:S1011-20 [21987737] J Infect Dis. 2011 Nov;204 Suppl 3:S861-70 [21987762] J Infect Dis. 2011 Nov;204 Suppl 3:S892-6 [21987766] J Virol. 2002 Jan;76(1):406-10 [11739705] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00705-013-1877-2 ER - TY - JOUR T1 - Lower NLRP3 inflammasome activity in NAG-1 transgenic mice is linked to a resistance to obesity and increased insulin sensitivity. AN - 1521338508; 24124102 AB - The NLRP3 inflammasome plays an important regulatory role in obesity-induced insulin resistance. NSAID activated gene-1 (NAG-1) is a divergent member of the TGF-β superfamily. NAG-1 Tg mice are resistant to dietary- and genetic-induced obesity and have improved insulin sensitivity. The objective was to examine whether NLRP3 inflammasome activity is associated with this observed phenotype in NAG-1 Tg mice. Key components of the NLRP3 inflammasome were examined in NAG-1 Tg mice on both regular and high fat diet (HFD) conditions. The expression of caspase-1 and ASC, key components of the NLRP3 inflammasome, is significantly reduced at mRNA and protein levels in white adipose tissue (WAT) of NAG-1 Tg mice. HFD increases the expression of caspase-1 and ASC in WT mice, but their expression is reduced in NAG-1 Tg mice. Furthermore, there is reduced IL-18, IL-1β, and TNF-α expression in the WAT of NAG-1 Tg mice. NAG-1 Tg mice have significantly lower serum leptin and insulin levels and reduced expression of macrophage infiltration markers (F4/80, CD11b, and CD11c) in WAT. The study suggests the lower NLRP3 inflammasome activity may play a role in the resistance of NAG-1 Tg mice to diet-induced obesity and improved insulin sensitivity. Copyright © 2013 The Obesity Society. JF - Obesity (Silver Spring, Md.) AU - Wang, Xingya AU - Chrysovergis, Kali AU - Kosak, Justin AU - Eling, Thomas E AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences (NIEHS), 111. T.W. Alexander Dr, Research Triangle Park, North Carolina, USA. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1256 EP - 1263 VL - 22 IS - 5 KW - Antigens, CD11b KW - 0 KW - Antigens, CD11c KW - Carrier Proteins KW - Inflammasomes KW - Insulin KW - Interleukin-18 KW - Interleukin-1beta KW - Leptin KW - NLR Family, Pyrin Domain-Containing 3 Protein KW - Nlrp3 protein, mouse KW - RNA, Messenger KW - Transforming Growth Factor beta KW - Tumor Necrosis Factor-alpha KW - Caspase 1 KW - EC 3.4.22.36 KW - Index Medicus KW - Animals KW - Caspase 1 -- metabolism KW - Interleukin-1beta -- genetics KW - Antigens, CD11b -- metabolism KW - Diet, High-Fat KW - Mice, Transgenic KW - RNA, Messenger -- genetics KW - Tumor Necrosis Factor-alpha -- genetics KW - Leptin -- blood KW - Adipose Tissue, White -- metabolism KW - Caspase 1 -- genetics KW - Antigens, CD11c -- genetics KW - Transforming Growth Factor beta -- genetics KW - Interleukin-18 -- genetics KW - Male KW - Antigens, CD11b -- genetics KW - Insulin -- blood KW - Mice KW - Interleukin-18 -- metabolism KW - Antigens, CD11c -- metabolism KW - RNA, Messenger -- metabolism KW - Interleukin-1beta -- metabolism KW - Mice, Inbred C57BL KW - Tumor Necrosis Factor-alpha -- metabolism KW - Transforming Growth Factor beta -- metabolism KW - Female KW - Obesity -- metabolism KW - Carrier Proteins -- metabolism KW - Obesity -- genetics KW - Carrier Proteins -- genetics KW - Insulin Resistance -- genetics KW - Inflammasomes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521338508?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Obesity+%28Silver+Spring%2C+Md.%29&rft.atitle=Lower+NLRP3+inflammasome+activity+in+NAG-1+transgenic+mice+is+linked+to+a+resistance+to+obesity+and+increased+insulin+sensitivity.&rft.au=Wang%2C+Xingya%3BChrysovergis%2C+Kali%3BKosak%2C+Justin%3BEling%2C+Thomas+E&rft.aulast=Wang&rft.aufirst=Xingya&rft.date=2014-05-01&rft.volume=22&rft.issue=5&rft.spage=1256&rft.isbn=&rft.btitle=&rft.title=Obesity+%28Silver+Spring%2C+Md.%29&rft.issn=1930-739X&rft_id=info:doi/10.1002%2Foby.20638 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-02 N1 - Date created - 2014-05-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Physiol Endocrinol Metab. 2010 Sep;299(3):E486-96 [20570821] Science. 2010 Jan 15;327(5963):296-300 [20075245] Nat Rev Immunol. 2011 Feb;11(2):98-107 [21233852] Clin Chem. 2011 Feb;57(2):309-16 [21164037] J Immunol. 2011 Feb 15;186(4):2529-34 [21257968] Nat Med. 2011 Feb;17(2):179-88 [21217695] Nat Med. 2011 Feb;17(2):164-5 [21297609] Nat Immunol. 2011 May;12(5):408-15 [21478880] Diabetes. 2011 Jun;60(6):1688-98 [21515850] Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15324-9 [21876127] Endocrinology. 2011 Oct;152(10):3769-78 [21862623] Clin Endocrinol (Oxf). 2012 Jan;76(1):46-50 [21645023] Prostate. 2012 May 1;72(6):677-89 [21809352] Mediators Inflamm. 2013;2013:641851 [23737651] Diabetes. 2013 Sep;62(9):3064-74 [23670974] J Clin Invest. 2003 Dec;112(12):1796-808 [14679176] Diabetes Obes Metab. 2005 Jul;7(4):406-13 [15955127] J Clin Invest. 2006 Jun;116(6):1494-505 [16691291] Nat Med. 2006 Jun;12(6):650-6 [16732281] Immunol Rev. 2012 Sep;249(1):239-52 [22889226] J Lipid Res. 2013 Feb;54(2):448-56 [23160218] Biochem Pharmacol. 2013 Mar 1;85(5):597-606 [23220538] PLoS One. 2013;8(5):e63944 [23675517] Obesity (Silver Spring). 2006 Aug;14 Suppl 5:242S-249S [17021375] Gastroenterology. 2006 Nov;131(5):1553-60 [17101328] Endocrinology. 2007 Jan;148(1):241-51 [17038556] Int J Obes (Lond). 2007 Feb;31(2):213-20 [16755284] Nat Med. 2007 Nov;13(11):1333-40 [17982462] Nat Rev Mol Cell Biol. 2008 May;9(5):367-77 [18401346] Endocrinology. 2009 Apr;150(4):1688-96 [19074584] Diabetologia. 2009 May;52(5):882-90 [19252892] Eur J Endocrinol. 2009 Sep;161(3):397-404 [19515791] Cell Metab. 2010 Dec 1;12(6):593-605 [21109192] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/oby.20638 ER - TY - JOUR T1 - The histone-fold complex MHF is remodeled by FANCM to recognize branched DNA and protect genome stability. AN - 1521330494; 24699063 AB - Histone-fold proteins typically assemble in multiprotein complexes to bind duplex DNA. However, one histone-fold complex, MHF, associates with Fanconi anemia (FA) protein FANCM to form a branched DNA remodeling complex that senses and repairs stalled replication forks and activates FA DNA damage response network. How the FANCM-MHF complex recognizes branched DNA is unclear. Here, we solved the crystal structure of MHF and its complex with the MHF-interaction domain (referred to as MID) of FANCM, and performed structure-guided mutagenesis. We found that the MID-MHF complex consists of one histone H3-H4-like MHF heterotetramer wrapped by a single polypeptide of MID. We identified a zinc atom-liganding structure at the central interface between MID and MHF that is critical for stabilization of the complex. Notably, the DNA-binding surface of MHF was altered by MID in both electrostatic charges and allosteric conformation. This leads to a switch in the DNA-binding preference - from duplex DNA by MHF alone, to branched DNA by the MID-MHF complex. Mutations that disrupt either the composite DNA-binding surface or the protein-protein interface of the MID-MHF complex impaired activation of the FA network and genome stability. Our data provide the structural basis of how FANCM and MHF work together to recognize branched DNA, and suggest a novel mechanism by which histone-fold complexes can be remodeled by their partners to bind special DNA structures generated during DNA metabolism. JF - Cell research AU - Fox, David AU - Yan, Zhijiang AU - Ling, Chen AU - Zhao, Ye AU - Lee, Duck-Yeon AU - Fukagawa, Tatsuo AU - Yang, Wei AU - Wang, Weidong AD - Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. ; Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, Bethesda, MD 20892, USA. ; Biochemistry Core Facility, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Molecular Genetics, National Institute of Genetics and the Graduate University for Advanced Studies, Mishima 411-8540, Japan. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 560 EP - 575 VL - 24 IS - 5 KW - APITD1 protein, human KW - 0 KW - Apoptosis Regulatory Proteins KW - DNA, Cruciform KW - DNA-Binding Proteins KW - Histones KW - Multiprotein Complexes KW - Nuclear Proteins KW - STRA13 protein, human KW - Tumor Suppressor Proteins KW - DNA KW - 9007-49-2 KW - FANCM protein, human KW - EC 3.6.1.- KW - DNA Helicases KW - EC 3.6.4.- KW - Index Medicus KW - Models, Molecular KW - HeLa Cells KW - Humans KW - Histones -- metabolism KW - HEK293 Cells KW - Protein Multimerization KW - Protein Interaction Domains and Motifs KW - Nucleic Acid Conformation KW - Fanconi Anemia -- metabolism KW - DNA Helicases -- chemistry KW - DNA Repair KW - DNA Helicases -- metabolism KW - DNA-Binding Proteins -- chemistry KW - DNA Damage KW - Apoptosis Regulatory Proteins -- chemistry KW - DNA -- metabolism KW - Tumor Suppressor Proteins -- chemistry KW - Genomic Instability KW - Tumor Suppressor Proteins -- metabolism KW - Apoptosis Regulatory Proteins -- metabolism KW - DNA -- genetics KW - DNA -- chemistry KW - Nuclear Proteins -- chemistry KW - Nuclear Proteins -- metabolism KW - Fanconi Anemia -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521330494?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+research&rft.atitle=The+histone-fold+complex+MHF+is+remodeled+by+FANCM+to+recognize+branched+DNA+and+protect+genome+stability.&rft.au=Fox%2C+David%3BYan%2C+Zhijiang%3BLing%2C+Chen%3BZhao%2C+Ye%3BLee%2C+Duck-Yeon%3BFukagawa%2C+Tatsuo%3BYang%2C+Wei%3BWang%2C+Weidong&rft.aulast=Fox&rft.aufirst=David&rft.date=2014-05-01&rft.volume=24&rft.issue=5&rft.spage=560&rft.isbn=&rft.btitle=&rft.title=Cell+research&rft.issn=1748-7838&rft_id=info:doi/10.1038%2Fcr.2014.42 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-23 N1 - Date created - 2014-05-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Genes Dev. 2012 Jul 1;26(13):1393-408 [22751496] Nat Commun. 2012;3:782 [22510687] Nature. 2013 Jan 17;493(7432):356-63 [23325218] Mol Cell. 2013 Mar 7;49(5):997-1009 [23333308] Am J Hum Genet. 2013 May 2;92(5):800-6 [23623386] Am J Hum Genet. 2013 May 2;92(5):807-19 [23623389] Open Biol. 2013 Sep;3(9):130102 [24026537] Nat Commun. 2014;5:2987 [24390579] Nucleic Acids Res. 2000 Jan 1;28(1):235-42 [10592235] Gene. 2000 Jan 25;242(1-2):1-13 [10721692] J Cell Sci. 2003 Aug 15;116(Pt 16):3347-62 [12829748] Nat Struct Biol. 2003 Dec;10(12):980 [14634627] Proteins. 1988;3(2):71-84 [3399495] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] Nat Genet. 2005 Sep;37(9):958-63 [16116422] Nat Struct Mol Biol. 2005 Sep;12(9):763-71 [16116434] Mol Cell. 2007 Feb 9;25(3):331-43 [17289582] Nat Rev Genet. 2007 Oct;8(10):735-48 [17768402] Mol Cell. 2008 Jan 18;29(1):141-8 [18206976] Hum Mol Genet. 2008 Jun 1;17(11):1641-52 [18285517] Mol Cell. 2008 Oct 10;32(1):118-28 [18851838] Proc Natl Acad Sci U S A. 2008 Oct 21;105(42):16107-12 [18843105] Cell. 2008 Dec 12;135(6):1039-52 [19070575] Blood. 2009 Jul 2;114(1):174-80 [19423727] Nucleic Acids Res. 2009 Jul;37(13):4360-70 [19465393] J Cell Biol. 2009 Jul 27;186(2):173-82 [19620631] Structure. 2009 Nov 11;17(11):1442-52 [19913479] Acta Crystallogr D Biol Crystallogr. 2010 Jan;66(Pt 1):12-21 [20057044] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):125-32 [20124692] EMBO J. 2010 Feb 17;29(4):795-805 [20010692] Mol Cell. 2010 Mar 26;37(6):865-78 [20347428] Mol Cell. 2010 Mar 26;37(6):879-86 [20347429] Obstet Gynecol. 2010 Oct;116(4):1008-10 [20859177] Chembiochem. 2011 Jan 24;12(2):196-204 [21243709] Acta Crystallogr D Biol Crystallogr. 2011 Apr;67(Pt 4):235-42 [21460441] Cell. 2012 Feb 3;148(3):487-501 [22304917] Structure. 2012 Feb 8;20(2):364-70 [22325783] Hum Mol Genet. 2012 May 1;21(9):2005-16 [22279085] J Biol Chem. 2012 Aug 3;287(32):26563-75 [22696213] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/cr.2014.42 ER - TY - JOUR T1 - Suppressive oligodeoxynucleotides reduce lung cancer susceptibility in mice with silicosis. AN - 1520347928; 24403310 AB - Silicosis is an inflammatory lung disease induced by the inhalation of silica-containing dust particles. There is conflicting data on whether patients with silicosis are more susceptible to lung cancer induced by cigarette smoke. To examine this issue experimentally, a model was developed in which one of the most abundant and potent carcinogens present in cigarette smoke [4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)] was administered to mice at the peak of silica-induced pulmonary inflammation. Results show that the incidence of lung tumors in silicotic mice treated with NNK was significantly increased compared with mice exposed to silica or NNK alone. Synthetic oligonucleotides (ODN) containing repetitive TTAGGG motifs can block pathologic inflammation. We therefore examined whether treatment with these suppressive (Sup) ODN could block silica-induced pulmonary inflammation and thereby reduce susceptibility to lung cancer. Results show that Sup (but not control) ODN inhibit pulmonary fibrosis and other inflammatory manifestations of chronic silicosis. Of greater import, Sup ODN reduced lung tumor incidence and multiplicity in silicotic mice exposed to NNK. These findings establish an experimental model for examining the role of silicotic inflammation in cancer susceptibility and demonstrate that Sup ODN represent a novel therapy for chronic silicosis. JF - Carcinogenesis AU - Bode, Christian AU - Kinjo, Takeshi AU - Alvord, W Gregory AU - Klinman, Dennis M AD - Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1078 EP - 1083 VL - 35 IS - 5 KW - Anti-Inflammatory Agents KW - 0 KW - Biomarkers KW - Interleukin-1beta KW - Nitrosamines KW - Oligodeoxyribonucleotides KW - RNA, Messenger KW - Silicon Dioxide KW - 7631-86-9 KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Index Medicus KW - Animals KW - Interleukin-1beta -- genetics KW - Humans KW - Gene Expression KW - Nitrosamines -- adverse effects KW - Disease Models, Animal KW - Mice KW - RNA, Messenger -- genetics KW - Pneumonia -- drug therapy KW - Pneumonia -- pathology KW - Pneumonia -- etiology KW - Silicon Dioxide -- adverse effects KW - RNA, Messenger -- metabolism KW - Interleukin-1beta -- metabolism KW - Female KW - Pneumonia -- complications KW - Lung Neoplasms -- prevention & control KW - Lung Neoplasms -- etiology KW - Silicosis -- pathology KW - Disease Susceptibility KW - Silicosis -- complications KW - Oligodeoxyribonucleotides -- pharmacology KW - Anti-Inflammatory Agents -- administration & dosage KW - Oligodeoxyribonucleotides -- administration & dosage KW - Lung Neoplasms -- pathology KW - Anti-Inflammatory Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520347928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Suppressive+oligodeoxynucleotides+reduce+lung+cancer+susceptibility+in+mice+with+silicosis.&rft.au=Bode%2C+Christian%3BKinjo%2C+Takeshi%3BAlvord%2C+W+Gregory%3BKlinman%2C+Dennis+M&rft.aulast=Bode&rft.aufirst=Christian&rft.date=2014-05-01&rft.volume=35&rft.issue=5&rft.spage=1078&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-24 N1 - Date created - 2014-04-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Dis Mon. 2007 Aug;53(8):394-416 [17976433] Nat Med. 2007 Sep;13(9):1050-9 [17704786] J Immunol. 2008 Jun 1;180(11):7648-54 [18490767] Nature. 2008 Jul 24;454(7203):436-44 [18650914] J Mol Cell Cardiol. 2008 Aug;45(2):168-75 [18502445] Mutat Res. 2008 Sep-Oct;659(3):221-31 [18495523] Occup Med (Lond). 2009 Mar;59(2):89-95 [19233828] Clin Exp Immunol. 2009 Jun;156(3):528-34 [19438607] Cancer Causes Control. 2009 Aug;20(6):925-33 [19184475] Nat Protoc. 2009;4(9):1350-62 [19713956] Cell. 2011 Mar 4;144(5):646-74 [21376230] Anticancer Res. 2011 Sep;31(9):2877-82 [21868532] Risk Anal. 2011 Oct;31(10):1543-60 [21477084] Lancet. 2012 May 26;379(9830):2008-18 [22534002] Int J Epidemiol. 2012 Jun;41(3):711-21 [22467291] Cancer Prev Res (Phila). 2012 Aug;5(8):1061-71 [22700853] J Immunol. 2012 Oct 1;189(7):3734-40 [22914048] J Immunol. 2013 Oct 1;191(7):3876-83 [23986531] Am J Respir Cell Mol Biol. 2000 Apr;22(4):491-501 [10745030] Annu Rev Med. 2000;51:511-23 [10774479] Toxicol Appl Pharmacol. 2000 Oct 15;168(2):131-9 [11032768] Cancer Res. 2000 Oct 15;60(20):5599-602 [11059745] Arthritis Rheum. 2003 Jun;48(6):1701-7 [12794839] J Immunol. 2003 Aug 1;171(3):1393-400 [12874230] Arthritis Rheum. 2004 May;50(5):1686-9 [15146440] Inhal Toxicol. 2004 Mar;16(3):133-9 [15204774] Ind Health. 2004 Jul;42(3):303-14 [15295901] J Immunol. 2004 Oct 15;173(8):5002-7 [15470043] Carcinogenesis. 1989 Jan;10(1):91-6 [2910536] Cancer Res. 1989 Oct 1;49(19):5305-11 [2670201] Carcinogenesis. 1989 Oct;10(10):1901-4 [2791206] Am J Respir Cell Mol Biol. 1998 Jan;18(1):51-9 [9448045] Cancer Res. 1998 Feb 1;58(3):409-12 [9458081] Chem Res Toxicol. 1998 Jun;11(6):559-603 [9625726] Mol Carcinog. 1998 Sep;23(1):36-44 [9766436] Cancer Res. 1998 Dec 1;58(23):5354-60 [9850065] Mol Carcinog. 1999 Aug;25(4):231-40 [10449029] Carcinogenesis. 1999 Oct;20(10):1939-44 [10506108] Curr Opin Pulm Med. 2005 Mar;11(2):169-73 [15699791] Arthritis Rheum. 2005 Feb;52(2):651-8 [15692999] J Immunol. 2005 Apr 15;174(8):4579-83 [15814679] Am J Physiol Lung Cell Mol Physiol. 2005 Aug;289(2):L186-95 [15849212] Epidemiology. 2001 Jan;12(1):88-93 [11138826] Lancet. 2001 Feb 17;357(9255):539-45 [11229684] Occup Environ Med. 2002 Mar;59(3):205-13; quiz 214 [11886955] J Immunol. 2002 Sep 1;169(5):2653-61 [12193738] Arthritis Rheum. 2002 Aug;46(8):2219-24 [12209528] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959] Clin Exp Immunol. 2003 May;132(2):232-8 [12699410] Free Radic Biol Med. 2003 Jun 15;34(12):1507-16 [12788471] Respir Res. 2005;6:112 [16212659] Ann N Y Acad Sci. 2005 Nov;1058:87-95 [16394128] Curr Opin Allergy Clin Immunol. 2007 Apr;7(2):168-73 [17351471] Science. 2008 May 2;320(5876):674-7 [18403674] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu005 ER - TY - JOUR T1 - Tamoxifen-DNA adduct formation in monkey and human reproductive organs. AN - 1520347749; 24501327 AB - The estrogen analog tamoxifen (TAM), used for adjuvant therapy of breast cancer, induces endometrial and uterine tumors in breast cancer patients. Proliferation stimulus of the uterine endometrium is likely involved in tumor induction, but genotoxicity may also play a role. Formation of TAM-DNA adducts in human tissues has been reported but remains controversial. To address this issue, we examined TAM-DNA adducts in uteri from two species of monkeys, Erythrocebus patas (patas) and Macaca fascicularis (macaque), and in human endometrium and myometrium. Monkeys were given 3-4 months of chronic TAM dosing scaled to be equivalent to the daily human dose. In the uteri, livers and brains from the patas (n = 3), and endometrium from the macaques (n = 4), TAM-DNA adducts were measurable by TAM-DNA chemiluminescence immunoassay. Average TAM-DNA adduct values for the patas uteri (23 adducts/10(8) nucleotides) were similar to those found in endometrium of the macaques (19 adducts/10(8) nucleotides). Endometrium of macaques exposed to both TAM and low-dose estradiol (n = 5) averaged 34 adducts/10(8) nucleotides. To examine TAM-DNA persistence in the patas, females (n = 3) were exposed to TAM for 3 months and to no drug for an additional month, resulting in low or non-detectable TAM-DNA in livers and uteri. Human endometrial and myometrial samples from women receiving (n = 8) and not receiving (n = 8) TAM therapy were also evaluated. Women receiving TAM therapy averaged 10.3 TAM-DNA adducts/10(8) nucleotides, whereas unexposed women showed no detectable TAM-DNA. The data indicate that genotoxicity, in addition to estrogen agonist effects, may contribute to TAM-induced human endometrial cancer. JF - Carcinogenesis AU - Hernandez-Ramon, Elena E AU - Sandoval, Nicole A AU - John, Kaarthik AU - Cline, J Mark AU - Wood, Charles E AU - Woodward, Ruth A AU - Poirier, Miriam C AD - Carcinogen-DNA Interactions Section, LCBG, CCR, National Cancer Institute, NIH, Building 37, Room 4032, NIH 37 Convent Drive, MSC-4255, Bethesda, MD 20892, USA. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1172 EP - 1176 VL - 35 IS - 5 KW - DNA Adducts KW - 0 KW - Tamoxifen KW - 094ZI81Y45 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Humans KW - Erythrocebus patas KW - Myometrium -- metabolism KW - Female KW - Endometrium -- metabolism KW - Uterus -- metabolism KW - DNA Adducts -- chemistry KW - DNA -- metabolism KW - Tamoxifen -- chemistry KW - DNA Adducts -- adverse effects KW - Tamoxifen -- metabolism KW - DNA -- chemistry KW - DNA Adducts -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520347749?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tamoxifen-DNA+adduct+formation+in+monkey+and+human+reproductive+organs.&rft.au=Hernandez-Ramon%2C+Elena+E%3BSandoval%2C+Nicole+A%3BJohn%2C+Kaarthik%3BCline%2C+J+Mark%3BWood%2C+Charles+E%3BWoodward%2C+Ruth+A%3BPoirier%2C+Miriam+C&rft.aulast=Hernandez-Ramon&rft.aufirst=Elena&rft.date=2014-05-01&rft.volume=35&rft.issue=5&rft.spage=1172&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu029 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-24 N1 - Date created - 2014-04-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Carcinogenesis. 2000 Aug;21(8):1461-7 [10910945] Lancet. 2013 Mar 9;381(9869):805-16 [23219286] Arch Toxicol. 2001 Aug;75(6):375-80 [11570696] J Natl Cancer Inst. 2002 Aug 7;94(15):1122 [12165635] Annu Rev Pharmacol Toxicol. 2003;43:149-73 [12171978] Mutagenesis. 2003 Jul;18(4):395-9 [12840114] Cancer Res. 2003 Sep 15;63(18):5999-6003 [14522927] Cancer Res. 2003 Dec 1;63(23):8461-5 [14679010] J Natl Cancer Inst. 2004 Jul 21;96(14):1099-104 [15265972] Cancer Res. 1993 Sep 1;53(17):3919-24 [8358718] Carcinogenesis. 1995 Jun;16(6):1299-304 [7788846] Cancer Res. 1996 Apr 1;56(7):1475-9 [8603387] Cancer Res. 1996 Oct 1;56(19):4374-7 [8813128] Br J Clin Pharmacol. 2014 Apr;77(4):673-83 [24033670] Lancet. 1998 May 16;351(9114):1451-67 [9605801] J Natl Cancer Inst. 1998 Sep 16;90(18):1371-88 [9747868] Carcinogenesis. 1999 Feb;20(2):339-42 [10069474] Chem Res Toxicol. 1999 Jul;12(7):646-53 [10409405] Cancer Res. 1999 Oct 1;59(19):4829-33 [10519392] Mutagenesis. 2005 Mar;20(2):115-24 [15755801] Cardiovasc Toxicol. 2005;5(3):333-46 [16244378] Cancer Res. 2007 Jul 15;67(14):6995-7002 [17638912] Toxicol Sci. 2007 Sep;99(1):203-13 [17545213] Pharmacogenet Genomics. 2007 Sep;17(9):731-42 [17700362] Mutagenesis. 2008 Jan;23(1):1-18 [17989146] Mutagenesis. 2009 Sep;24(5):391-404 [19505894] Drug Metab Dispos. 2010 Jan;38(1):200-7 [19812351] Clin Cancer Res. 2010 Feb 1;16(3):946-56 [20103679] Toxicol Sci. 2010 Nov;118(1):191-201 [20702595] Drug Metab Dispos. 2013 Jun;41(6):1187-94 [23491640] Carcinogenesis. 2001 Jun;22(6):839-49 [11375888] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu029 ER - TY - JOUR T1 - A nested case-control study of leukocyte mitochondrial DNA copy number and renal cell carcinoma in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. AN - 1520345985; 24398668 AB - Mitochondrial DNA (mtDNA) is vulnerable to mutations, and the number of copies of mtDNA per cell may increase to compensate for DNA damage. Case-control studies have reported associations between altered mtDNA copy number and risk of renal cell carcinoma (RCC); however, this association has not been investigated prospectively. We conducted a nested case-control study (252 cases and 504 controls) of RCC risk in relation to pre-diagnostic leukocyte mtDNA copy number in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. mtDNA copy number was measured in triplicate using a fluorescence-based quantitative PCR assay; samples from 22 cases and 36 controls could not be assayed, leaving 230 cases and 468 controls for analysis. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression. High mtDNA copy number was associated with an increased risk of RCC, both overall (highest quartile versus lowest: OR = 2.0, 95% CI = 1.2-3.2; P trend = 0.002) and among cases diagnosed ≥6 years after blood collection (OR = 2.6, 95% CI = 1.4-5.0; P trend = 0.003). These findings did not differ significantly by sex, body mass index, history of hypertension or smoking status (P interaction ≥ 0.3). Results of this study suggest that high pre-diagnostic leukocyte mtDNA copy number, a suspected marker of oxidative DNA damage and mitochondrial dysfunction, is associated with increased future RCC risk. JF - Carcinogenesis AU - Hofmann, Jonathan N AU - Hosgood, H Dean AU - Liu, Chin-San AU - Chow, Wong-Ho AU - Shuch, Brian AU - Cheng, Wen-Ling AU - Lin, Ta-Tsung AU - Moore, Lee E AU - Lan, Qing AU - Rothman, Nathaniel AU - Purdue, Mark P AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1028 EP - 1031 VL - 35 IS - 5 KW - DNA, Mitochondrial KW - 0 KW - Index Medicus KW - Odds Ratio KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Male KW - Female KW - Leukocytes -- metabolism KW - Kidney Neoplasms -- genetics KW - DNA Copy Number Variations KW - Kidney Neoplasms -- diagnosis KW - Carcinoma, Renal Cell -- diagnosis KW - Carcinoma, Renal Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520345985?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+nested+case-control+study+of+leukocyte+mitochondrial+DNA+copy+number+and+renal+cell+carcinoma+in+the+Prostate%2C+Lung%2C+Colorectal+and+Ovarian+Cancer+Screening+Trial.&rft.au=Hofmann%2C+Jonathan+N%3BHosgood%2C+H+Dean%3BLiu%2C+Chin-San%3BChow%2C+Wong-Ho%3BShuch%2C+Brian%3BCheng%2C+Wen-Ling%3BLin%2C+Ta-Tsung%3BMoore%2C+Lee+E%3BLan%2C+Qing%3BRothman%2C+Nathaniel%3BPurdue%2C+Mark+P&rft.aulast=Hofmann&rft.aufirst=Jonathan&rft.date=2014-05-01&rft.volume=35&rft.issue=5&rft.spage=1028&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt495 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-24 N1 - Date created - 2014-04-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biomed Sci. 2000 Jan-Feb;7(1):2-15 [10644884] Cancer Epidemiol Biomarkers Prev. 2012 Sep;21(9):1574-81 [22787200] Control Clin Trials. 2000 Dec;21(6 Suppl):349S-355S [11189687] Mutat Res. 2001 May;488(2):119-33 [11344040] Cancer Causes Control. 2002 Apr;13(3):287-93 [12020111] Free Radic Res. 2003 Dec;37(12):1307-17 [14753755] Int J Cancer. 1994 Apr 1;57(1):123-8 [8150530] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8739-46 [8090716] APMIS. 2006 May;114(5):329-37 [16725008] J Natl Cancer Inst. 2008 Aug 6;100(15):1104-12 [18664653] Blood. 2008 Nov 15;112(10):4247-9 [18711000] Carcinogenesis. 2010 May;31(5):847-9 [20176654] Cancer Prev Res (Phila). 2011 May;4(5):638-54 [21543342] Cancer Epidemiol Biomarkers Prev. 2011 Sep;20(9):1944-9 [21784958] Cancer Prev Res (Phila). 2011 Nov;4(11):1912-9 [21859925] PLoS One. 2012;7(8):e43149 [22937019] Biochem J. 2000 Jun 1;348 Pt 2:425-32 [10816438] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgt495 ER - TY - JOUR T1 - Photoimmunotherapy: comparative effectiveness of two monoclonal antibodies targeting the epidermal growth factor receptor. AN - 1519846665; 24508062 AB - Photoimmunotherapy (PIT) is a new cancer treatment that combines the specificity of antibodies for targeting tumors with the toxicity induced by photosensitizers after exposure to near infrared (NIR) light. Herein we compare two commonly available anti-EGFR monoclonal antibodies, cetuximab and panitumumab, for their effectiveness as PIT agents in EGFR positive tumor models. A photosensitizer, IR-700, conjugated to either cetuximab (cet-IR700) or panitumumab (pan-IR700), was evaluated using EGFR-expressing A431 and MDAMB468-luc cells in 2D- and 3D-culture. PIT was conducted with irradiation of NIR light after exposure of the sample or animal to each conjugate. In vivo PIT was performed with fractionated exposure of NIR light after injection of each agent into A431 xenografts or a MDAMB468-luc orthotopic tumor bearing model. Cet-IR700 and pan-IR700 bound with equal affinity to the cells in 2D-culture and penetrated equally into the 3D-spheroid, resulting in identical PIT cytotoxic effects in vitro. In contrast, in vivo anti-tumor effects of PIT with cet-IR700 were inferior to that of pan-IR700. Assessment of the biodistribution showed lower accumulation into the tumors and more rapid hepatic catabolism of cet-IR700 compared to pan-IR700. Although cet-IR700 and pan-IR700 showed identical in vitro characteristics, pan-IR700 showed better therapeutic tumor responses than cet-IR700 in in vivo mice models due to the prolonged retention of the conjugate in the circulation, suggesting that retention in the circulation is advantageous for tumor responses to PIT. These results suggest that the choice of monoclonal antibody in photosensitizer conjugates may influence the effectiveness of PIT. Published by Elsevier B.V. JF - Molecular oncology AU - Sato, Kazuhide AU - Watanabe, Rira AU - Hanaoka, Hirofumi AU - Harada, Toshiko AU - Nakajima, Takahito AU - Kim, Insook AU - Paik, Chang H AU - Choyke, Peter L AU - Kobayashi, Hisataka AD - Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, MD 20892, United States. ; Applied/Developmental Research Directorate, Leidos Biomedical Research Inc., Frederick, MD 20892, United States. ; Nuclear Medicine Department, Warren Grant Magnuson Clinical Center, MD 20892, United States. ; Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, MD 20892, United States. Electronic address: Kobayash@mail.nih.gov. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 620 EP - 632 VL - 8 IS - 3 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Monoclonal, Humanized KW - Photosensitizing Agents KW - panitumumab KW - 6A901E312A KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Cetuximab KW - PQX0D8J21J KW - Index Medicus KW - NIR-fluorescence KW - Monoclonal antibody KW - Epidermal growth factor receptor KW - Photoimmunotherapy KW - Pharmacokinetics KW - Animals KW - Humans KW - Xenograft Model Antitumor Assays KW - Mice KW - Cell Line, Tumor KW - Female KW - Antibodies, Monoclonal, Humanized -- pharmacokinetics KW - Receptor, Epidermal Growth Factor -- antagonists & inhibitors KW - Photosensitizing Agents -- therapeutic use KW - Antibodies, Monoclonal -- chemistry KW - Neoplasms -- therapy KW - Antibodies, Monoclonal, Humanized -- chemistry KW - Photosensitizing Agents -- pharmacokinetics KW - Antibodies, Monoclonal -- therapeutic use KW - Immunotherapy -- methods KW - Antibodies, Monoclonal, Humanized -- therapeutic use KW - Photosensitizing Agents -- chemistry KW - Neoplasms -- pathology KW - Antibodies, Monoclonal -- pharmacokinetics KW - Phototherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1519846665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+oncology&rft.atitle=Photoimmunotherapy%3A+comparative+effectiveness+of+two+monoclonal+antibodies+targeting+the+epidermal+growth+factor+receptor.&rft.au=Sato%2C+Kazuhide%3BWatanabe%2C+Rira%3BHanaoka%2C+Hirofumi%3BHarada%2C+Toshiko%3BNakajima%2C+Takahito%3BKim%2C+Insook%3BPaik%2C+Chang+H%3BChoyke%2C+Peter+L%3BKobayashi%2C+Hisataka&rft.aulast=Sato&rft.aufirst=Kazuhide&rft.date=2014-05-01&rft.volume=8&rft.issue=3&rft.spage=620&rft.isbn=&rft.btitle=&rft.title=Molecular+oncology&rft.issn=1878-0261&rft_id=info:doi/10.1016%2Fj.molonc.2014.01.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-17 N1 - Date created - 2014-04-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Crit Rev Oncol Hematol. 2000 Nov-Dec;36(2-3):179-92 [11033305] Curr Top Med Chem. 2012;12(15):1678-82 [22978338] Cancer Res. 2003 Mar 15;63(6):1288-96 [12649189] J Immunol. 1983 Mar;130(3):1473-7 [6185591] Br J Cancer. 1992 Feb;65(2):157-62 [1739610] Cancer Res. 1994 Feb 1;54(3):838-43 [8306347] Nat Biotechnol. 2005 Sep;23(9):1073-8 [16151394] Nat Biotechnol. 2007 Dec;25(12):1369-72 [18066027] Methods Enzymol. 2009;453:417-49 [19216919] Curr Med Chem. 2009;16(29):3797-804 [19747140] BMC Cancer. 2012;12:345 [22873679] ACS Nano. 2013 Jan 22;7(1):717-24 [23214407] Bioconjug Chem. 2013 May 15;24(5):811-6 [23600922] J Biomed Opt. 2013 Oct;18(10):101304 [23752742] J Nucl Med. 2013 May;54(5):770-5 [23536226] Theranostics. 2013;3(6):357-65 [23781283] Nat Rev Cancer. 2013 Sep;13(9):663-73 [23949426] Oncogene. 2014 Feb 27;33(9):1073-81 [23542173] Bioconjug Chem. 2009 Nov;20(11):2177-84 [19919110] Oncologist. 2010;15(1):73-84 [20067946] Nat Rev Clin Oncol. 2010 Aug;7(8):426-8 [20668478] Analyst. 2011 Feb 7;136(3):473-8 [20967331] Mol Biol Cell. 2011 Sep;22(17):3103-19 [21775625] Mol Cancer. 2011;10:113 [21917150] Exp Cell Res. 2011 Nov 15;317(19):2765-71 [21925171] Nat Med. 2011 Dec;17(12):1685-91 [22057348] MAbs. 2011 Nov-Dec;3(6):584-95 [22123060] Bioconjug Chem. 2012 Mar 21;23(3):604-9 [22369484] Methods Mol Biol. 2012;889:85-103 [22669661] Nat Rev Cancer. 2012 Aug;12(8):553-63 [22785351] Cancer Res. 2012 Sep 15;72(18):4622-8 [22800710] Expert Rev Anticancer Ther. 2012 Sep;12(9):1149-59 [23098115] Nat Med. 2003 Mar;9(3):269-77 [12612576] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.molonc.2014.01.006 ER - TY - JOUR T1 - Impact on survival and toxicity by duration of weight extremes during treatment for pediatric acute lymphoblastic leukemia: A report from the Children's Oncology Group. AN - 1519838217; 24687836 AB - Previous studies regarding the influence of weight on event-free survival (EFS) and treatment-related toxicity (TRT) in childhood acute lymphoblastic leukemia (ALL) considered only weight at diagnosis. Inasmuch as weight varies substantially over treatment, we hypothesized its impact on EFS is instead determined by cumulative time spent at an extreme weight during therapy and on TRT by weight at the time of toxicity. In a cohort of 2,008 children treated for high-risk ALL in Children's Oncology Group study CCG-1961, we determined the effect on EFS of cumulative time receiving therapy at an extreme weight (either obese or underweight) between end of induction and start of maintenance therapy. We also evaluated the association between weight category and incidence and patterns of TRT during 13,946 treatment courses. Being obese or underweight at diagnosis and for ≥ 50% of the time between end of induction and start of maintenance therapy resulted in inferior EFS (hazard ratios, 1.43 and 2.30, respectively; global P < .001). Normalization of weight during that period resulted in mitigation of this risk comparable to never being obese or underweight. Obese or underweight status at start of each treatment course was significantly associated with specific patterns of TRT. Influence of weight extremes on EFS and TRT is not set at diagnosis as previously reported but is moderated by subsequent weight status during intensive postinduction treatment phases. These observations suggest that weight is a potentially addressable risk factor to improve EFS and morbidity in pediatric ALL. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Orgel, Etan AU - Sposto, Richard AU - Malvar, Jemily AU - Seibel, Nita L AU - Ladas, Elena AU - Gaynon, Paul S AU - Freyer, David R AD - Etan Orgel, Jonathan Jaques Children's Cancer Center, Miller Children's Hospital, Long Beach; Etan Orgel, Paul S. Gaynon, and David R. Freyer, Keck School of Medicine, University of Southern California; Etan Orgel, Richard Sposto, Jemily Malvar, Paul S. Gaynon, and David R. Freyer, Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles; Richard Sposto, University of Southern California, Los Angeles, CA; Nita L. Seibel, Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD; and Elena Ladas, Center for Comprehensive Wellness, Columbia University, New York, NY. Y1 - 2014/05/01/ PY - 2014 DA - 2014 May 01 SP - 1331 EP - 1337 VL - 32 IS - 13 KW - Vincristine KW - 5J49Q6B70F KW - Asparaginase KW - EC 3.5.1.1 KW - Prednisone KW - VB0R961HZT KW - Daunorubicin KW - ZS7284E0ZP KW - Index Medicus KW - Young Adult KW - Daunorubicin -- administration & dosage KW - Randomized Controlled Trials as Topic KW - Disease-Free Survival KW - Vincristine -- adverse effects KW - Humans KW - Daunorubicin -- adverse effects KW - Vincristine -- administration & dosage KW - Asparaginase -- administration & dosage KW - Child KW - Child, Preschool KW - Infant KW - Asparaginase -- adverse effects KW - Prednisone -- adverse effects KW - Cohort Studies KW - Adolescent KW - Time Factors KW - Prednisone -- administration & dosage KW - Male KW - Female KW - Thinness -- complications KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Thinness -- physiopathology KW - Obesity -- physiopathology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- complications KW - Obesity -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1519838217?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Impact+on+survival+and+toxicity+by+duration+of+weight+extremes+during+treatment+for+pediatric+acute+lymphoblastic+leukemia%3A+A+report+from+the+Children%27s+Oncology+Group.&rft.au=Orgel%2C+Etan%3BSposto%2C+Richard%3BMalvar%2C+Jemily%3BSeibel%2C+Nita+L%3BLadas%2C+Elena%3BGaynon%2C+Paul+S%3BFreyer%2C+David+R&rft.aulast=Orgel&rft.aufirst=Etan&rft.date=2014-05-01&rft.volume=32&rft.issue=13&rft.spage=1331&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2013.52.6962 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-18 N1 - Date created - 2014-04-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Adv Data. 2000 Jun 8;(314):1-27 [11183293] Am J Clin Nutr. 2002 Jun;75(6):978-85 [12036802] Blood. 2002 Sep 15;100(6):1957-64 [12200352] Rev Invest Clin. 2003 Jan-Feb;55(1):31-5 [12708161] Arch Dis Child. 2004 Jan;89(1):64-8 [14709512] Cancer. 1983 Aug 15;52(4):587-98 [6407749] Cancer. 1984 Nov 15;54(10):2268-71 [6488146] Clin Pharmacol Ther. 1991 May;49(5):536-49 [1827621] Ther Drug Monit. 1991 Jan;13(1):37-41 [2057989] Basic Life Sci. 1993;60:71-4 [8110167] Am J Pediatr Hematol Oncol. 1994 Aug;16(3):225-30 [8037340] Arch Dis Child. 1994 Oct;71(4):304-10 [7979521] Ann Hum Biol. 1997 May-Jun;24(3):209-15 [9158840] J Pediatr Hematol Oncol. 1998 Nov-Dec;20(6):534-8 [9856673] JAMA. 2005 Jan 12;293(2):203-11 [15644547] Nutr Clin Pract. 2005 Aug;20(4):377-93 [16207678] J Pediatr Hematol Oncol. 2006 Sep;28(9):575-8 [17006263] Blood. 2006 Dec 15;108(13):3997-4002 [16917005] Blood. 2007 Feb 1;109(3):926-35 [17003380] J Clin Oncol. 2007 May 20;25(15):2063-9 [17513811] Blood. 2008 Mar 1;111(5):2548-55 [18039957] Head Neck. 2008 Apr;30(4):503-8 [18098310] Clin Infect Dis. 2008 May 15;46(10):1582-8 [18419494] Diabetes Care. 2008 Nov;31(11):2211-21 [18955718] J Clin Endocrinol Metab. 2008 Nov;93(11 Suppl 1):S74-80 [18987273] Cancer Chemother Pharmacol. 2009 Jul;64(2):243-51 [19020877] N Engl J Med. 2009 Jun 25;360(26):2730-41 [19553647] Cancer Res. 2009 Oct 1;69(19):7867-74 [19773440] Pediatr Blood Cancer. 2009 Dec 15;53(7):1249-54 [19688832] Leukemia. 2010 Feb;24(2):285-97 [20016531] Pharmacol Res. 2010 May;61(5):385-90 [20083201] Obesity (Silver Spring). 2011 Sep;19(9):1908-11 [21720424] JAMA. 2012 Feb 1;307(5):483-90 [22253364] J Clin Oncol. 2012 May 10;30(14):1663-9 [22412151] J Pediatr Gastroenterol Nutr. 2012 Jun;54(6):720-6 [22157928] Leuk Lymphoma. 2012 Sep;53(9):1677-81 [22390648] Leuk Res. 2013 May;37(5):503-9 [23332453] Pediatr Blood Cancer. 2013 Jun;60(6):911-5 [23109269] Comment In: J Clin Oncol. 2014 May 1;32(13):1293-4 [24687820] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2013.52.6962 ER - TY - JOUR T1 - Phase II trial on cisplatin-adriamycin-paclitaxel combination as neoadjuvant chemotherapy for locally advanced cervical adenocarcinoma. AN - 1518817289; 24662130 AB - Neoadjuvant chemotherapy (NACT) followed by surgery is a different therapeutic approach to locally advanced cervical adenocarcinoma (LACA) and seems to offer specific advantages over chemoradiation. This phase II trial was designed to evaluate the toxicity and activity of NACT with cisplatin-adriamycin-paclitaxel (TAP) in patients with LACA. Patients with International Federation of Gynecology and Obstetrics stage IB2-IIB uterine adenocarcinoma were treated with NACT TAP for 3 cycles. After the last cycle, patients underwent radical surgery with lymph node dissection. Pathological response was classified as no residual tumor (pCR), residual disease with less than 3-mm stromal invasion (pR1), or residual disease with more than 3-mm stromal invasion (pR2). Between 2003 and 2010, 30 women were enrolled. Fourteen complete clinical responses, 10 partial responses, and 6 stabilizations of disease were registered. Three patients achieved a pCR, 6 a pR1 response, and 21 a pR2 response. At a median follow-up of 45 months, progression-free survival and overall survival were 37 and 48 months, respectively. Hematologic toxicity was the most relevant adverse effect. The TAP combination seems to be feasible with an acceptable toxicity profile and a promising response rate for the treatment of LACA. JF - International journal of gynecological cancer : official journal of the International Gynecological Cancer Society AU - Lorusso, Domenica AU - Ramondino, Stefano AU - Mancini, Maria AU - Zanaboni, Flavia AU - Ditto, Antonino AU - Raspagliesi, Francesco AD - Department of Gynecologic Oncology, Fondazione "IRCCS" National Cancer Institute, Milan, Italy. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 729 EP - 734 VL - 24 IS - 4 KW - Doxorubicin KW - 80168379AG KW - Paclitaxel KW - P88XT4IS4D KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Paclitaxel -- administration & dosage KW - Young Adult KW - Neoplasm Staging KW - Lymphatic Metastasis KW - Humans KW - Prognosis KW - Aged KW - Doxorubicin -- administration & dosage KW - Cisplatin -- administration & dosage KW - Survival Rate KW - Adult KW - Neoplasm Grading KW - Follow-Up Studies KW - Middle Aged KW - Adolescent KW - Female KW - Adenocarcinoma, Mucinous -- mortality KW - Uterine Cervical Neoplasms -- mortality KW - Neoadjuvant Therapy KW - Adenocarcinoma -- mortality KW - Adenocarcinoma, Clear Cell -- drug therapy KW - Cystadenocarcinoma, Serous -- mortality KW - Adenocarcinoma, Clear Cell -- mortality KW - Adenocarcinoma -- pathology KW - Cystadenocarcinoma, Serous -- secondary KW - Adenocarcinoma, Mucinous -- secondary KW - Adenocarcinoma, Clear Cell -- secondary KW - Cystadenocarcinoma, Serous -- drug therapy KW - Uterine Cervical Neoplasms -- drug therapy KW - Adenocarcinoma, Mucinous -- drug therapy KW - Adenocarcinoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Uterine Cervical Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518817289?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+gynecological+cancer+%3A+official+journal+of+the+International+Gynecological+Cancer+Society&rft.atitle=Phase+II+trial+on+cisplatin-adriamycin-paclitaxel+combination+as+neoadjuvant+chemotherapy+for+locally+advanced+cervical+adenocarcinoma.&rft.au=Lorusso%2C+Domenica%3BRamondino%2C+Stefano%3BMancini%2C+Maria%3BZanaboni%2C+Flavia%3BDitto%2C+Antonino%3BRaspagliesi%2C+Francesco&rft.aulast=Lorusso&rft.aufirst=Domenica&rft.date=2014-05-01&rft.volume=24&rft.issue=4&rft.spage=729&rft.isbn=&rft.btitle=&rft.title=International+journal+of+gynecological+cancer+%3A+official+journal+of+the+International+Gynecological+Cancer+Society&rft.issn=1525-1438&rft_id=info:doi/10.1097%2FIGC.0000000000000115 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-13 N1 - Date created - 2014-04-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/IGC.0000000000000115 ER - TY - JOUR T1 - Efficacy of glucarpidase (carboxypeptidase g2) in patients with acute kidney injury after high-dose methotrexate therapy. AN - 1518814536; 24132809 AB - Because the incidence rate of renal impairment is 2-10% for patients treated with high-dose methotrexate and renal impairment develops in 0-12.4% of patients treated for osteosarcoma, we sought to evaluate the efficacy of glucarpidase, a recently approved drug that rapidly hydrolyzes methotrexate to inactive metabolites, which allows for nonrenal clearance in patients with delayed renal methotrexate elimination. Pooled analysis of efficacy data from four multicenter single-arm compassionate-use clinical trials using protocols from 1993 to 2007. Of 476 patients with renal toxicity and delayed methotrexate elimination who were treated with intravenous glucarpidase for rescue after high-dose methotrexate, 169 patients had at least one preglucarpidase (baseline) plasma methotrexate concentration greater than 1 μmol/L and one postglucarpidase methotrexate concentration measurement by high-performance liquid chromatography and were included in the efficacy analysis; renal recovery was assessed in 436 patients who had at least one recorded preglucarpidase and postglucarpidase serum creatinine concentration measurement. Efficacy was defined as rapid and sustained clinically important reduction (RSCIR) in plasma methotrexate concentration, with a concentration of 1 μmol/L or lower at all postglucarpidase determinations. Median age of efficacy-evaluable patients was 20 years (range 5 weeks-84 years). Osteosarcoma (36%), non-Hodgkin lymphoma (27%), and acute lymphoblastic leukemia (20%) were the most frequent underlying diagnoses. Median preglucarpidase serum methotrexate was 11.7 μmol/L. At the first (median 15 minutes) through the last (median 40 hours) postglucarpidase measurement, plasma methotrexate concentrations demonstrated consistent 99% median reduction. RSCIR was achieved by 83 (59%) of 140 patients. A total of 64% of patients with renal impairment greater than or equal to Common Terminology Criteria for Adverse Events grade 2 recovered to grade 0 or 1 at a median of 12.5 days after glucarpidase administration. Glucarpidase caused a clinically important 99% or greater sustained reduction of serum methotrexate levels and provided noninvasive rescue from methotrexate toxicity in renally impaired patients. © 2013 Pharmacotherapy Publications, Inc. JF - Pharmacotherapy AU - Widemann, Brigitte C AU - Schwartz, Stefan AU - Jayaprakash, Nalini AU - Christensen, Robbin AU - Pui, Ching-Hon AU - Chauhan, Nikhil AU - Daugherty, Claire AU - King, Thomas R AU - Rush, Janet E AU - Howard, Scott C AD - National Cancer Institute, Bethesda, Maryland. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 427 EP - 439 VL - 34 IS - 5 KW - Antimetabolites, Antineoplastic KW - 0 KW - gamma-Glutamyl Hydrolase KW - EC 3.4.19.9 KW - Leucovorin KW - Q573I9DVLP KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - acute kidney injury KW - glucarpidase KW - methotrexate KW - carboxypeptidase KW - Osteosarcoma -- drug therapy KW - Drug Administration Schedule KW - Bone Neoplasms -- blood KW - Leucovorin -- administration & dosage KW - Humans KW - Bone Neoplasms -- drug therapy KW - Treatment Outcome KW - Osteosarcoma -- blood KW - Compassionate Use Trials KW - Osteosarcoma -- complications KW - Bone Neoplasms -- complications KW - Leucovorin -- therapeutic use KW - gamma-Glutamyl Hydrolase -- administration & dosage KW - Antimetabolites, Antineoplastic -- administration & dosage KW - Methotrexate -- blood KW - Methotrexate -- adverse effects KW - Antimetabolites, Antineoplastic -- adverse effects KW - Acute Kidney Injury -- chemically induced KW - Methotrexate -- therapeutic use KW - Antimetabolites, Antineoplastic -- blood KW - Acute Kidney Injury -- prevention & control KW - gamma-Glutamyl Hydrolase -- therapeutic use KW - Methotrexate -- administration & dosage KW - Antimetabolites, Antineoplastic -- therapeutic use KW - Acute Kidney Injury -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518814536?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacotherapy&rft.atitle=Efficacy+of+glucarpidase+%28carboxypeptidase+g2%29+in+patients+with+acute+kidney+injury+after+high-dose+methotrexate+therapy.&rft.au=Widemann%2C+Brigitte+C%3BSchwartz%2C+Stefan%3BJayaprakash%2C+Nalini%3BChristensen%2C+Robbin%3BPui%2C+Ching-Hon%3BChauhan%2C+Nikhil%3BDaugherty%2C+Claire%3BKing%2C+Thomas+R%3BRush%2C+Janet+E%3BHoward%2C+Scott+C&rft.aulast=Widemann&rft.aufirst=Brigitte&rft.date=2014-05-01&rft.volume=34&rft.issue=5&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Pharmacotherapy&rft.issn=1875-9114&rft_id=info:doi/10.1002%2Fphar.1360 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-09 N1 - Date created - 2014-04-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer. 1969 Jan;23(1):126-31 [5763245] Biochem Pharmacol. 1968 Nov;17(11):2265-70 [5718139] Cancer Res. 1972 Oct;32(10):2114-9 [5080761] Cancer Treat Rep. 1977 Jul;61(4):695-701 [18282] Cancer Treat Rep. 1977 Jul;61(4):745-8 [301783] Cancer Treat Rep. 1977 Aug;61(5):779-83 [302143] Cancer. 1978 Jan;41(1):36-51 [342086] J Bacteriol. 1978 May;134(2):506-13 [26657] Clin Pharmacol Ther. 1979 Jul;26(1):63-72 [445963] Am J Med. 1980 Mar;68(3):370-6 [6965819] Eur J Clin Pharmacol. 1981;19(6):453-6 [7250179] Cancer. 2004 May 15;100(10):2222-32 [15139068] Pediatr Nephrol. 2002 Oct;17(10):825-9 [12376811] J Pharmacol Exp Ther. 2000 Sep;294(3):894-901 [10945838] J Clin Oncol. 1983 Mar;1(3):208-16 [6607976] J Clin Oncol. 1988 Aug;6(8):1216-9 [2842462] J Clin Oncol. 1994 Aug;12(8):1667-72 [8040679] Clin Chem. 1996 Jan;42(1):39-44 [8565230] Am J Kidney Dis. 1996 Dec;28(6):846-54 [8957036] J Clin Oncol. 1997 May;15(5):2125-34 [9164227] Am J Med. 1999 Apr;106(4):459-65 [10225250] Br J Cancer. 2005 Feb 14;92(3):480-7 [15668713] Expert Rev Neurother. 2006 May;6(5):635-52 [16734512] Oncologist. 2006 Jun;11(6):694-703 [16794248] Oncologist. 2007 Nov;12(11):1299-308 [18055849] Cancer Chemother Pharmacol. 2009 Mar;63(4):599-604 [18504579] Pharmacotherapy. 2010 Jan;30(1):111 [20030480] Expert Opin Biol Ther. 2010 Jan;10(1):105-11 [19925307] J Clin Oncol. 2010 Sep 1;28(25):3979-86 [20679598] Semin Nephrol. 2010 Nov;30(6):570-81 [21146122] Cancer. 2012 Sep 1;118(17):4321-30 [22252903] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/phar.1360 ER - TY - JOUR T1 - Tempol protects cardiomyocytes from nucleoside reverse transcriptase inhibitor-induced mitochondrial toxicity. AN - 1518242332; 24591154 AB - Nucleoside reverse transcriptase inhibitors (NRTIs), essential components of combinational therapies used for treatment of human immunodeficiency virus-1, damage heart mitochondria. Here, we have shown mitochondrial compromise in H9c2 rat cardiomyocytes exposed for 16 passages (P) to the NRTIs zidovudine (AZT, 50μM) and didanosine (ddI, 50μM), and we have demonstrated protection from mitochondrial compromise in cells treated with 200μM 1-oxyl-2,2,6,6-tetramethyl-4-hydroxypiperidine (Tempol) or 200μM 1-hydroxy-4-[2-triphenylphosphonio)-acetamido]-2,2,6,6-tetramethylpiperidine (Tempol-H), along with AZT/ddI, for 16P. Exposure to AZT/ddI caused a moderate growth inhibition at P3, P5, P7, and P13, which was not altered by addition of Tempol or Tempol-H. Mitochondrial oxidative phosphorylation capacity was determined as uncoupled oxygen consumption rate (OCR) by Seahorse XF24 Analyzer. At P5, P7, and P13, AZT/ddI-exposed cells showed an OCR reduction of 8.8-57.2% in AZT/ddI-exposed cells, compared with unexposed cells. Addition of Tempol or Tempol-H, along with AZT/ddI, resulted in OCR levels increased by about 300% above the values seen with AZT/ddI alone. The Seahorse data were further supported by electron microscopy (EM) studies in which P16 cells exposed to AZT/ddI/Tempol had less mitochondrial pathology than P16 cells exposed to AZT/ddI. Western blots of P5 cells showed that Tempol and Tempol-H upregulated expression of mitochondrial uncoupling protein-2 (UCP-2). However, Complex I activity that was reduced by AZT/ddI, was not restored in the presence of AZT/ddI/Tempol. Superoxide levels were increased in the presence of AZT/ddI and significantly decreased in cells exposed to AZT/3TC/Tempol at P3, P7, and P10. In conclusion, Tempol protects against NRTI-induced mitochondrial compromise, and UCP-2 plays a role through mild uncoupling. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Liu, Yongmin AU - Shim, Eunwoo AU - Nguyen, Phuonggiang AU - Gibbons, Alexander T AU - Mitchell, James B AU - Poirier, Miriam C AD - Carcinogen-DNA Interactions Section, Laboratory of Cancer Biology and Genetics, CCR, National Cancer Institute, NIH, Bethesda, Maryland 20892-4255. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 133 EP - 141 VL - 139 IS - 1 KW - Cyclic N-Oxides KW - 0 KW - Reverse Transcriptase Inhibitors KW - Spin Labels KW - Superoxides KW - 11062-77-4 KW - Zidovudine KW - 4B9XT59T7S KW - Didanosine KW - K3GDH6OH08 KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - mitochondria KW - superoxide KW - Seahorse extracellular flux analyzer KW - antiretroviral therapy KW - electron microscopy KW - oxidative phosphorylation KW - Rats KW - Didanosine -- toxicity KW - Animals KW - Superoxides -- metabolism KW - Zidovudine -- toxicity KW - Microscopy, Electron KW - Cell Line KW - Myocytes, Cardiac -- drug effects KW - Mitochondria -- drug effects KW - Cyclic N-Oxides -- pharmacology KW - Myocytes, Cardiac -- ultrastructure KW - Reverse Transcriptase Inhibitors -- toxicity KW - Myocytes, Cardiac -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518242332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tempol+protects+cardiomyocytes+from+nucleoside+reverse+transcriptase+inhibitor-induced+mitochondrial+toxicity.&rft.au=Liu%2C+Yongmin%3BShim%2C+Eunwoo%3BNguyen%2C+Phuonggiang%3BGibbons%2C+Alexander+T%3BMitchell%2C+James+B%3BPoirier%2C+Miriam+C&rft.aulast=Liu&rft.aufirst=Yongmin&rft.date=2014-05-01&rft.volume=139&rft.issue=1&rft.spage=133&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%2Fkfu034 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-28 N1 - Date created - 2014-04-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cardiovasc Toxicol. 2012 Dec;12(4):326-40 [22744233] Mol Cell. 2012 Oct 26;48(2):158-67 [23102266] Free Radic Biol Med. 2003 Jun 1;34(11):1359-68 [12757846] AIDS. 2003 Aug 15;17(12):1769-85 [12891063] Nat Rev Drug Discov. 2003 Oct;2(10):812-22 [14526384] Clin Infect Dis. 2004 Mar 1;38(5):743-53 [14986261] AIDS. 2004 Jan 23;18(2):137-51 [15075530] Cancer Res. 1991 Dec 15;51(24):6622-8 [1660344] Lancet. 1999 Sep 25;354(9184):1084-9 [10509500] Antivir Ther. 2005;10 Suppl 2:M13-27 [16152703] Cardiovasc Toxicol. 2005;5(3):333-46 [16244378] Toxicol In Vitro. 2006 Aug;20(5):535-46 [16406476] AIDS. 2006 Aug 22;20(13):1685-90 [16931932] Free Radic Biol Med. 2007 Jun 1;42(11):1632-50 [17462532] Oncogene. 2008 Dec 4;27(53):6729-37 [18794809] J Bioenerg Biomembr. 2009 Apr;41(2):133-6 [19365715] Mitochondrion. 2010 Apr;10(3):243-52 [20005987] Pharmacol Ther. 2010 May;126(2):119-45 [20153367] Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):785-91 [20211596] Expert Opin Drug Metab Toxicol. 2010 Dec;6(12):1493-504 [20929279] Curr Drug Targets. 2011 Jun;12(6):783-9 [21275885] Br J Cancer. 2011 Aug 9;105(4):469-74 [21712825] J Cardiovasc Pharmacol. 2011 Oct;58(4):380-91 [21697725] Cardiovasc Toxicol. 2012 Jun;12(2):123-34 [22170576] Adv Exp Med Biol. 2012;748:145-69 [22729857] Free Radic Biol Med. 2003 Jan 1;34(1):93-102 [12498984] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kfu034 ER - TY - JOUR T1 - Biomarkers of coordinate metabolic reprogramming in colorectal tumors in mice and humans. AN - 1517883853; 24440673 AB - There are no robust noninvasive methods for colorectal cancer screening and diagnosis. Metabolomic and gene expression analyses of urine and tissue samples from mice and humans were used to identify markers of colorectal carcinogenesis. Mass spectrometry-based metabolomic analysis of urine and tissues from wild-type C57BL/6J and Apc(Min/+) mice, as well as from mice with azoxymethane-induced tumors, was employed in tandem with gene expression analysis. Metabolic profiling was also performed on colon tumor and adjacent nontumor tissues from 39 patients. The effects of β-catenin activity on metabolic profiles were assessed in mice with colon-specific disruption of Apc. Thirteen markers were found in urine associated with development of colorectal tumors in Apc(Min/+) mice. Metabolites related to polyamine metabolism, nucleic acid metabolism, and methylation, identified tumor-bearing mice with 100% accuracy, and also accurately identified mice with polyps. Changes in gene expression in tumor samples from mice revealed that derangement of metabolites were a reflection of coordinate metabolic reprogramming in tumor tissue. Similar changes in urinary metabolites were observed in mice with azoxymethane-induced tumors and in mice with colon-specific activation of β-catenin. The metabolic alterations indicated by markers in urine, therefore, appear to occur during early stages of tumorigenesis, when cancer cells are proliferating. In tissues from patients, tumors had stage-dependent increases in 17 metabolites associated with the same metabolic pathways identified in mice. Ten metabolites that were increased in tumor tissues, compared with nontumor tissues (proline, threonine, glutamic acid, arginine, N1-acetylspermidine, xanthine, uracil, betaine, symmetric dimethylarginine, and asymmetric-dimethylarginine), were also increased in urine from tumor-bearing mice. Gene expression and metabolomic profiles of urine and tissue samples from mice with colorectal tumors and of colorectal tumor samples from patients revealed pathways associated with derangement of specific metabolic pathways that are indicative of early-stage tumor development. These urine and tissue markers might be used in early detection of colorectal cancer. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved. JF - Gastroenterology AU - Manna, Soumen K AU - Tanaka, Naoki AU - Krausz, Kristopher W AU - Haznadar, Majda AU - Xue, Xiang AU - Matsubara, Tsutomu AU - Bowman, Elise D AU - Fearon, Eric R AU - Harris, Curtis C AU - Shah, Yatrik M AU - Gonzalez, Frank J AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan. ; Departments of Internal Medicine, Pathology and Human Genetics, University of Michigan, Ann Arbor, Michigan. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Electronic address: gonzalef@mail.nih.gov. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1313 EP - 1324 VL - 146 IS - 5 KW - Biomarkers, Tumor KW - 0 KW - Azoxymethane KW - MO0N1J0SEN KW - Abridged Index Medicus KW - Index Medicus KW - Metabolic Reprogramming KW - Colorectal Cancer KW - Cancer Biomarker KW - Metabolomics KW - Apc(Min/+) KW - Real-Time Polymerase Chain Reaction KW - Spectrometry, Mass, Electrospray Ionization KW - Animals KW - High-Throughput Screening Assays KW - Reproducibility of Results KW - Neoplasm Staging KW - Protein Interaction Maps KW - Humans KW - Disease Models, Animal KW - Predictive Value of Tests KW - Mice KW - Cell Proliferation KW - Mice, Transgenic KW - Genes, APC KW - Gene Expression Regulation, Neoplastic KW - Protein Interaction Mapping KW - Mice, Inbred C57BL KW - Chromatography, Reverse-Phase KW - Biomarkers, Tumor -- metabolism KW - Metabolomics -- methods KW - Biomarkers, Tumor -- genetics KW - Colorectal Neoplasms -- pathology KW - Colorectal Neoplasms -- metabolism KW - Colorectal Neoplasms -- urine KW - Biomarkers, Tumor -- urine KW - Colorectal Neoplasms -- genetics KW - Colorectal Neoplasms -- chemically induced KW - Gene Expression Profiling -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1517883853?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=Biomarkers+of+coordinate+metabolic+reprogramming+in+colorectal+tumors+in+mice+and+humans.&rft.au=Manna%2C+Soumen+K%3BTanaka%2C+Naoki%3BKrausz%2C+Kristopher+W%3BHaznadar%2C+Majda%3BXue%2C+Xiang%3BMatsubara%2C+Tsutomu%3BBowman%2C+Elise+D%3BFearon%2C+Eric+R%3BHarris%2C+Curtis+C%3BShah%2C+Yatrik+M%3BGonzalez%2C+Frank+J&rft.aulast=Manna&rft.aufirst=Soumen&rft.date=2014-05-01&rft.volume=146&rft.issue=5&rft.spage=1313&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2014.01.017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-05 N1 - Date created - 2014-04-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Gut. 2007 Jan;56(1):140-8 [16840508] Prostate Cancer Prostatic Dis. 2006;9(3):230-4 [16683009] Cancer Res. 2007 Oct 15;67(20):9721-30 [17942902] Cell Metab. 2008 Jan;7(1):11-20 [18177721] Mol Cancer. 2008;7:72 [18799019] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18782-7 [19033189] J Proteome Res. 2009 Oct;8(10):4844-50 [19678709] Cancer Biol Ther. 2009 Jul;8(14):1313-7 [19502780] J Proteome Res. 2010 Mar 5;9(3):1627-34 [20121166] Anticancer Res. 2010 Feb;30(2):369-74 [20332441] Genes Dev. 2010 Jul 15;24(14):1507-18 [20634317] Future Oncol. 2010 Sep;6(9):1395-406 [20919825] J Biol Chem. 2010 Nov 19;285(47):36267-74 [20813845] Nucleic Acids Res. 2011 Jan;39(Database issue):D561-8 [21045058] Oncogene. 2011 May 19;30(20):2379-89 [21242974] J Proteome Res. 2011 Sep 2;10(9):4120-33 [21749142] CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29 [22237781] Cancer Cell. 2012 Mar 20;21(3):297-308 [22439925] N Engl J Med. 2012 Jun 21;366(25):2345-57 [22612596] Lancet. 2012 Nov 24;380(9856):1840-50 [23079588] J Natl Cancer Inst. 2001 Jun 6;93(11):858-65 [11390535] Am J Physiol Cell Physiol. 2001 Sep;281(3):C941-53 [11502571] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):29-39 [15000147] Inflamm Bowel Dis. 2004 Sep;10(5):529-35 [15472512] Metabolism. 1979 Aug;28(8):801-4 [454517] Dis Colon Rectum. 1986 Dec;29(12):873-7 [3792170] Cell. 1996 Oct 18;87(2):159-70 [8861899] Cancer Lett. 1998 Feb 27;124(2):187-91 [9500209] Science. 1956 Feb 24;123(3191):309-14 [13298683] N Engl J Med. 2004 Dec 23;351(26):2704-14 [15616205] Mol Cell. 2005 Apr 29;18(3):263-72 [15866169] Front Biosci. 2006;11:344-55 [16146736] Nat Protoc. 2007;2(8):1998-2004 [17703211] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1053/j.gastro.2014.01.017 ER - TY - JOUR T1 - Antiangiogenesis beyond VEGF inhibition: a journey from antiangiogenic single-target to broad-spectrum agents. AN - 1517883597; 24360358 AB - Although the inhibition of angiogenesis is an established modality of cancer treatment, concerns regarding toxicity and drug resistance still constitute barriers to be overcome. For almost a decade since the approval of bevacizumab in 2004, the efforts on antiangiogenic therapeutics have been mainly focused in inhibiting the VEGF pathway. The ongoing understanding of the complexity of the angiogenic process has broadened the spotlight to include concurrent and downstream players to the list of targeted inhibitors. In this review, we summarize the currently existing and the promising antiangiogenic treatments, envisioning an apparent evolutionary trend towards the development of angiogenesis inhibitors of three modalities: single-target, multi-target, and broad-spectrum agents. The clinical efficacy and some structural aspects of monoclonal antibodies, small molecules, endogenous and synthetic angiogenesis inhibitors and their molecular targets are discussed, and the targeting of endothelial cells with the use of cytotoxic drugs in a metronomic schedule is appraised. The reader is invited to revisit current expectations about antiangiogenic therapy in an attempt to set consistent clinical endpoints from which patients could gain real and lasting clinical benefits. Copyright © 2013 Elsevier Ltd. All rights reserved. JF - Cancer treatment reviews AU - Limaverde-Sousa, Gabriel AU - Sternberg, Cinthya AU - Ferreira, Carlos Gil AD - Coordination of Clinical Research and Technology Incorporation, National Cancer Institute of Brazil (INCA), Rio de Janeiro, Brazil. Electronic address: gabriel.sousa@inca.gov.br. ; Coordination of Clinical Research and Technology Incorporation, National Cancer Institute of Brazil (INCA), Rio de Janeiro, Brazil. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 548 EP - 557 VL - 40 IS - 4 KW - Angiogenesis Inhibitors KW - 0 KW - Vascular Endothelial Growth Factor A KW - Index Medicus KW - Vascular endothelial growth factor KW - Protein-tyrosine kinases KW - Endostatin KW - Sunitinib KW - Monoclonal antibodies KW - Drug therapy KW - Angiogenesis inhibitors KW - Bevacizumab KW - Animals KW - Neovascularization, Pathologic -- drug therapy KW - Humans KW - Vascular Endothelial Growth Factor A -- antagonists & inhibitors KW - Angiogenesis Inhibitors -- therapeutic use KW - Neoplasms -- drug therapy KW - Angiogenesis Inhibitors -- pharmacology KW - Neoplasms -- blood supply UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1517883597?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+treatment+reviews&rft.atitle=Antiangiogenesis+beyond+VEGF+inhibition%3A+a+journey+from+antiangiogenic+single-target+to+broad-spectrum+agents.&rft.au=Limaverde-Sousa%2C+Gabriel%3BSternberg%2C+Cinthya%3BFerreira%2C+Carlos+Gil&rft.aulast=Limaverde-Sousa&rft.aufirst=Gabriel&rft.date=2014-05-01&rft.volume=40&rft.issue=4&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=Cancer+treatment+reviews&rft.issn=1532-1967&rft_id=info:doi/10.1016%2Fj.ctrv.2013.11.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-21 N1 - Date created - 2014-03-10 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ctrv.2013.11.009 ER - TY - JOUR T1 - Bone marrow mesenchymal stromal cells to treat tissue damage in allogeneic stem cell transplant recipients: correlation of biological markers with clinical responses. AN - 1517880573; 24452962 AB - Bone marrow mesenchymal stromal cells (BMSCs) have been used to treat acute graft-versus-host disease (GVHD) and other complications following allogeneic hematopoietic stem cell transplantation (SCT). We conducted a phase I trial using third party, early passage BMSCs for patients with steroid-refractory GVHD, tissue injury, or marrow failure following SCT to investigate safety and efficacy. To identify mechanisms of BMSC immunomodulation and tissue repair, patients were serially monitored for plasma GVHD biomarkers, cytokines, and lymphocyte phenotype. Ten subjects were infused a fixed dose of 2 × 10(6) BMSCs/kg intravenously weekly for three doses. There was no treatment-related toxicity (primary endpoint). Eight subjects were evaluable for response at 4 weeks after the last infusion. Five of the seven patients with steroid-refractory acute GVHD achieved a complete response, two of two patients with tissue injury (pneumomediastinum/pneumothorax) achieved resolution but there was no response in two subjects with delayed marrow failure. Rapid reductions in inflammatory cytokines were observed. Clinical responses correlated with a fall in biomarkers (Reg 3α, CK18, and Elafin) relevant for the site of GVHD or tissue injury. The GVHD complete responders survived significantly longer and had higher baseline absolute lymphocyte and central memory CD4 and CD8 counts. Cytokine changes also segregated with survival. These results confirm that BMSCs are associated with rapid clinical and biomarker responses in GVHD and tissue injury. However, BMSCs were ineffective in patients with prolonged GVHD with lower lymphocyte counts, which suggest that effective GVHD control by BMSCs requires a relatively intact immune system. © 2014 AlphaMed Press. JF - Stem cells (Dayton, Ohio) AU - Yin, Fang AU - Battiwalla, Minoo AU - Ito, Sawa AU - Feng, Xingmin AU - Chinian, Fariba AU - Melenhorst, Jan Joseph AU - Koklanaris, Eleftheria AU - Sabatino, Marianna AU - Stroncek, David AU - Samsel, Leigh AU - Klotz, Jeffrey AU - Hensel, Nancy F AU - Robey, Pamela G AU - Barrett, A John AD - Hematology Branch, NHLBI, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 1278 EP - 1288 VL - 32 IS - 5 KW - Antigens, Neoplasm KW - 0 KW - Biomarkers, Tumor KW - Cytokines KW - Elafin KW - Keratin-18 KW - Lectins, C-Type KW - pancreatitis-associated protein KW - Index Medicus KW - Mesenchymal stromal cell KW - Allogeneic stem cell transplantation KW - Graft-versus-host disease KW - Biomarkers KW - Cytokines -- blood KW - Young Adult KW - CD4-Positive T-Lymphocytes -- cytology KW - Pneumothorax -- therapy KW - Humans KW - Pneumothorax -- blood KW - Pneumothorax -- etiology KW - Aged KW - Lymphocyte Count KW - Adult KW - Treatment Outcome KW - Mediastinal Emphysema -- etiology KW - Biomarkers, Tumor -- blood KW - Male KW - Keratin-18 -- blood KW - Survival Analysis KW - Infusions, Intravenous KW - Antigens, Neoplasm -- blood KW - Lectins, C-Type -- blood KW - Elafin -- blood KW - Mediastinal Emphysema -- blood KW - Transplantation, Homologous KW - CD8-Positive T-Lymphocytes -- cytology KW - Middle Aged KW - Mediastinal Emphysema -- therapy KW - Female KW - Graft vs Host Disease -- therapy KW - Mesenchymal Stem Cell Transplantation -- methods KW - Graft vs Host Disease -- blood KW - Bone Marrow Cells -- cytology KW - Graft vs Host Disease -- etiology KW - Hematopoietic Stem Cell Transplantation -- methods KW - Hematopoietic Stem Cell Transplantation -- adverse effects KW - Mesenchymal Stromal Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1517880573?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Bone+marrow+mesenchymal+stromal+cells+to+treat+tissue+damage+in+allogeneic+stem+cell+transplant+recipients%3A+correlation+of+biological+markers+with+clinical+responses.&rft.au=Yin%2C+Fang%3BBattiwalla%2C+Minoo%3BIto%2C+Sawa%3BFeng%2C+Xingmin%3BChinian%2C+Fariba%3BMelenhorst%2C+Jan+Joseph%3BKoklanaris%2C+Eleftheria%3BSabatino%2C+Marianna%3BStroncek%2C+David%3BSamsel%2C+Leigh%3BKlotz%2C+Jeffrey%3BHensel%2C+Nancy+F%3BRobey%2C+Pamela+G%3BBarrett%2C+A+John&rft.aulast=Yin&rft.aufirst=Fang&rft.date=2014-05-01&rft.volume=32&rft.issue=5&rft.spage=1278&rft.isbn=&rft.btitle=&rft.title=Stem+cells+%28Dayton%2C+Ohio%29&rft.issn=1549-4918&rft_id=info:doi/10.1002%2Fstem.1638 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-15 N1 - Date created - 2014-04-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Immunother. 2009 Sep;32(7):755-64 [19561533] Bone Marrow Transplant. 2009 Mar;43(6):447-54 [18955980] Biol Blood Marrow Transplant. 2011 Apr;17(4):534-41 [20457269] Cytotherapy. 2011 Jul;13(6):661-74 [21250865] Blood. 2012 Mar 22;119(12):2960-3 [22286196] J Transl Med. 2012;10:23 [22309358] Biol Blood Marrow Transplant. 2012 Apr;18(4):557-64 [21820393] Blood. 2012 Apr 19;119(16):3854-60 [22383800] Blood. 2013 Jan 24;121(4):585-94 [23165480] Stem Cells. 2013 Aug;31(8):1715-25 [23554294] Br J Haematol. 2004 Mar;124(6):777-86 [15009066] Lancet. 2004 May 1;363(9419):1439-41 [15121408] Leukemia. 2007 Nov;21(11):2271-6 [17611560] Lancet. 2008 May 10;371(9624):1579-86 [18468541] Cytotherapy. 2009;11(5):503-15 [19728189] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/stem.1638 ER - TY - JOUR T1 - Phase 2 randomized, flexible crossover, double-blinded, placebo-controlled trial of the farnesyltransferase inhibitor tipifarnib in children and young adults with neurofibromatosis type 1 and progressive plexiform neurofibromas. AN - 1516722580; 24500418 AB - RAS is dysregulated in neurofibromatosis type 1 (NF1) related plexiform neurofibromas (PNs). The activity of tipifarnib, which blocks RAS signaling by inhibiting its farnesylation, was tested in children and young adults with NF1 and progressive PNs. Patients aged 3-25 years with NF1-related PNs and imaging evidence of tumor progression were randomized in a double-blinded fashion to receive tipifarnib (200 mg/m(2) orally every 12 h) or placebo (phase A) and crossed over to the opposite treatment arm at the time of tumor progression (phase B). PN volumes were measured with MRI, and progression was defined as ≥20% volume increase. Time to progression (TTP) in phase A was the primary endpoint, and the trial was powered to detect whether tipifarnib doubled TTP compared with placebo. Toxicity, response, and quality of life were also monitored. Sixty-two patients were enrolled. Tipifarnib and placebo were well tolerated. On phase A, the median TTP was 10.6 months on the placebo arm and 19.2 months on the tipifarnib arm (P = .12; 1-sided). Quality of life improved significantly compared with baseline on the tipifarnib arm but not on the placebo arm. Volumetric tumor measurement detected tumor progression earlier than conventional 2-dimensional (WHO) and 1-dimensional (RECIST) methods. Tipifarnib was well tolerated but did not significantly prolong TTP of PNs compared with placebo. The randomized, flexible crossover design and volumetric PN assessment provided a feasible and efficient means of assessing the efficacy of tipifarnib. The placebo arm serves as an historical control group for phase 2 single-arm trials directed at progressive PNs. JF - Neuro-oncology AU - Widemann, Brigitte C AU - Dombi, Eva AU - Gillespie, Andrea AU - Wolters, Pamela L AU - Belasco, Jean AU - Goldman, Stewart AU - Korf, Bruce R AU - Solomon, Jeffrey AU - Martin, Staci AU - Salzer, Wanda AU - Fox, Elizabeth AU - Patronas, Nicholas AU - Kieran, Mark W AU - Perentesis, John P AU - Reddy, Alyssa AU - Wright, John J AU - Kim, AeRang AU - Steinberg, Seth M AU - Balis, Frank M AD - Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland (B.W., E.D., A.G., P.W., S.M., E.F., F.B.); Cancer Therapy Evaluation Program, Investigational Drug Branch, National Cancer Institute, Bethesda, Maryland (J.W.); Biostatistics and Data Management Section, National Cancer Institute, Bethesda, Maryland (S.S.); Diagnostic Radiology Department, National Institutes of Health, Bethesda, Maryland (N.P.); The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania (J.B., E.F., F.B.); Ann and Robert H. Lurie Children's Hospital, Chicago, Illinois (S.G.); Department of Genetics, University of Alabama at Birmingham, South Birmingham, Alabama (B.K.); Expert Image Analysis LC, Potomac, Maryland (J.S.); Dana-Farber/Children's Hospital Cancer Center, Boston, Massachusetts (M.K.); Cincinnati Children's Hospital, Cincinnati, Ohio (J.P.); Children's National Medical Center, Washington, DC (A.K.); US Army Medical Research and Material Command, Fort Detrick, Maryland (W.S.); Children's Hospital of Alabama, Birmingham, Alabama (A.R.). Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 707 EP - 718 VL - 16 IS - 5 KW - Antineoplastic Agents KW - 0 KW - Enzyme Inhibitors KW - Quinolones KW - Farnesyltranstransferase KW - EC 2.5.1.29 KW - tipifarnib KW - MAT637500A KW - Index Medicus KW - neurofibromatosis type 1 KW - RAS signaling KW - trial design KW - phase 2 trial KW - plexiform neurofibroma KW - Young Adult KW - Double-Blind Method KW - Humans KW - Adult KW - Treatment Outcome KW - Disease Progression KW - Cross-Over Studies KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Neurofibromatosis 1 -- drug therapy KW - Enzyme Inhibitors -- therapeutic use KW - Quinolones -- therapeutic use KW - Neurofibroma, Plexiform -- drug therapy KW - Farnesyltranstransferase -- antagonists & inhibitors KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516722580?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+2+randomized%2C+flexible+crossover%2C+double-blinded%2C+placebo-controlled+trial+of+the+farnesyltransferase+inhibitor+tipifarnib+in+children+and+young+adults+with+neurofibromatosis+type+1+and+progressive+plexiform+neurofibromas.&rft.au=Widemann%2C+Brigitte+C%3BDombi%2C+Eva%3BGillespie%2C+Andrea%3BWolters%2C+Pamela+L%3BBelasco%2C+Jean%3BGoldman%2C+Stewart%3BKorf%2C+Bruce+R%3BSolomon%2C+Jeffrey%3BMartin%2C+Staci%3BSalzer%2C+Wanda%3BFox%2C+Elizabeth%3BPatronas%2C+Nicholas%3BKieran%2C+Mark+W%3BPerentesis%2C+John+P%3BReddy%2C+Alyssa%3BWright%2C+John+J%3BKim%2C+AeRang%3BSteinberg%2C+Seth+M%3BBalis%2C+Frank+M&rft.aulast=Widemann&rft.aufirst=Brigitte&rft.date=2014-05-01&rft.volume=16&rft.issue=5&rft.spage=707&rft.isbn=&rft.btitle=&rft.title=Neuro-oncology&rft.issn=1523-5866&rft_id=info:doi/10.1093%2Fneuonc%2Fnou004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-31 N1 - Date created - 2014-04-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Anticancer Drugs. 2001 Mar;12(3):193-7 [11290865] Nature. 2002 Jan 31;415(6871):526-30 [11793011] Cancer Res. 2002 Mar 1;62(5):1573-7 [11894862] J Med Genet. 2002 May;39(5):311-4 [12011145] Expert Rev Anticancer Ther. 2003 Oct;3(5):595-614 [14599084] Value Health. 2003 Sep-Oct;6(5):522-31 [14627058] Comput Med Imaging Graph. 2004 Jul;28(5):257-65 [15249071] Curr Opin Drug Discov Devel. 2004 Jul;7(4):478-86 [15338957] Cancer. 1981 Jan 1;47(1):207-14 [7459811] Neurofibromatosis. 1988;1(3):172-8 [3152465] Semin Cancer Biol. 1992 Aug;3(4):169-77 [1421161] J Pediatr. 1997 Nov;131(5):678-82 [9403645] Am J Med Genet. 1999 Mar 26;89(1):14-22 [10469432] Am J Med Genet. 1999 Mar 26;89(1):31-7 [10469434] Anticancer Drugs. 2005 Mar;16(3):317-21 [15711184] Cancer Res. 2005 Apr 1;65(7):2755-60 [15805275] Cancer Cell. 2005 Apr;7(4):297-300 [15837619] J Clin Oncol. 2006 Jan 20;24(3):507-16 [16421428] Future Oncol. 2005 Dec;1(6):719-31 [16556050] J Immunol. 2007 Feb 15;178(4):2527-34 [17277161] J Med Genet. 2007 Feb;44(2):81-8 [17105749] Neurology. 2007 Feb 27;68(9):643-7 [17215493] Pediatr Neurol. 2007 May;36(5):293-300 [17509460] BMB Rep. 2009 May 31;42(5):239-44 [19470236] Am J Med Genet C Semin Med Genet. 2009 Aug 15;151C(3):255-60 [19621444] Neurology. 2009 Oct 20;73(16):1273-9 [19841379] Transplant Proc. 2009 Dec;41(10):4285-8 [20005385] Neurology. 2011 Jan 18;76(3):265-72 [21242495] J Pediatr Orthop. 2011 Apr-May;31(3):303-11 [21415691] J Pediatr. 2012 Mar;160(3):461-7 [21996156] Am J Med Genet A. 2012 Sep;158A(9):2225-32 [22821737] Neuroscience. 2012 Oct 25;223:102-13 [22750207] Pediatr Blood Cancer. 2013 Jan;60(1):59-64 [22645095] Lancet Oncol. 2012 Dec;13(12):1218-24 [23099009] Pediatr Blood Cancer. 2013 Mar;60(3):396-401 [22961690] J Clin Oncol. 1999 Nov;17(11):3631-52 [10550163] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] Invest New Drugs. 1999;17(3):241-58 [10665477] Cell. 2001 Feb 23;104(4):593-604 [11239415] Anticancer Drugs. 2001 Mar;12(3):163-84 [11290863] Comment In: Neuro Oncol. 2014 May;16(5):617-8 [24714524] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/neuonc/nou004 ER - TY - JOUR T1 - High frequency of PTEN mutations in nevi and melanomas from xeroderma pigmentosum patients. AN - 1516401248; 24483290 AB - We examined nevi and melanomas in 10 xeroderma pigmentosum (XP) patients with defective DNA repair. The lesions had a lentiginous appearance with markedly increased numbers of melanocytes. Using laser capture microdissection, we performed DNA sequencing of 18 benign and atypical nevi and 75 melanomas (melanoma in situ and invasive melanomas). The nevi had a similar high frequency of PTEN mutations as melanomas [61% (11/18) versus 53% (39/73)]. Both had a very high proportion of UV-type mutations (occurring at adjacent pyrimidines) [91% (10/11) versus 92% (36/39)]. In contrast to melanomas in the general population, the frequency of BRAF mutations (11%, 7/61), NRAS mutations (21%, 13/62), and KIT mutations (21%, 6/28) in XP melanomas was lower than for PTEN. Phospho-S6 immunostaining indicated activation of the mTOR pathway in the atypical nevi and melanomas. Thus, the clinical and histological appearances and the molecular pathology of these UV-related XP nevi and melanomas were different from nevi and melanomas in the general population. © 2014 Published 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - Pigment cell & melanoma research AU - Masaki, Taro AU - Wang, Yun AU - DiGiovanna, John J AU - Khan, Sikandar G AU - Raffeld, Mark AU - Beltaifa, Senda AU - Hornyak, Thomas J AU - Darling, Thomas N AU - Lee, Chyi-Chia R AU - Kraemer, Kenneth H AD - Dermatology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA; Division of Dermatology, Graduate School of Medicine, Kobe University, Kobe, Japan. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 454 EP - 464 VL - 27 IS - 3 KW - DNA, Neoplasm KW - 0 KW - Membrane Proteins KW - Neoplasm Proteins KW - MTOR protein, human KW - EC 2.7.1.1 KW - TOR Serine-Threonine Kinases KW - Proto-Oncogene Proteins c-kit KW - EC 2.7.10.1 KW - BRAF protein, human KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins B-raf KW - PTEN Phosphohydrolase KW - EC 3.1.3.67 KW - PTEN protein, human KW - GTP Phosphohydrolases KW - EC 3.6.1.- KW - NRAS protein, human KW - Index Medicus KW - xeroderma pigmentosum KW - UV carcinogenesis KW - mTOR KW - nevi KW - melanoma KW - DNA repair KW - PTEN KW - Young Adult KW - Sunlight -- adverse effects KW - DNA Mutational Analysis KW - Humans KW - Neoplasms, Radiation-Induced -- genetics KW - Membrane Proteins -- genetics KW - Precancerous Conditions -- pathology KW - Proto-Oncogene Proteins B-raf -- genetics KW - Precancerous Conditions -- genetics KW - Oncogenes KW - Loss of Heterozygosity KW - GTP Phosphohydrolases -- genetics KW - Neoplasms, Radiation-Induced -- pathology KW - TOR Serine-Threonine Kinases -- physiology KW - Precancerous Conditions -- etiology KW - Adult KW - Neoplasm Proteins -- genetics KW - Ultraviolet Rays -- adverse effects KW - DNA, Neoplasm -- genetics KW - Middle Aged KW - Dermoscopy KW - Proto-Oncogene Proteins c-kit -- genetics KW - Female KW - Male KW - Nevus, Pigmented -- genetics KW - Nevus, Pigmented -- pathology KW - Melanoma -- etiology KW - Skin Neoplasms -- etiology KW - Nevus, Pigmented -- etiology KW - Xeroderma Pigmentosum -- genetics KW - Skin Neoplasms -- pathology KW - Xeroderma Pigmentosum -- complications KW - PTEN Phosphohydrolase -- genetics KW - Skin Neoplasms -- genetics KW - Melanoma -- pathology KW - Melanoma -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516401248?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pigment+cell+%26+melanoma+research&rft.atitle=High+frequency+of+PTEN+mutations+in+nevi+and+melanomas+from+xeroderma+pigmentosum+patients.&rft.au=Masaki%2C+Taro%3BWang%2C+Yun%3BDiGiovanna%2C+John+J%3BKhan%2C+Sikandar+G%3BRaffeld%2C+Mark%3BBeltaifa%2C+Senda%3BHornyak%2C+Thomas+J%3BDarling%2C+Thomas+N%3BLee%2C+Chyi-Chia+R%3BKraemer%2C+Kenneth+H&rft.aulast=Masaki&rft.aufirst=Taro&rft.date=2014-05-01&rft.volume=27&rft.issue=3&rft.spage=454&rft.isbn=&rft.btitle=&rft.title=Pigment+cell+%26+melanoma+research&rft.issn=1755-148X&rft_id=info:doi/10.1111%2Fpcmr.12226 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-18 N1 - Date created - 2014-04-14 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/pcmr.12226 ER - TY - JOUR T1 - Renal cell carcinoma: molecular biology and targeted therapy. AN - 1515647413; 24675233 AB - Renal cell carcinoma (RCC) continues to be the subject of vigorous clinical and translational investigation. Advances in systemic targeted therapies, new molecular pathways and immunotherapy approaches will be discussed. Agents targeting the vascular endothelial growth factor (VEGF) and/or the mammalian target of rapamycin (mTOR) pathways continue to be the mainstay for treating metastatic RCC (mRCC). Although enhanced target specificity has improved the toxicity profile associated with newer VEGF-pathway antagonists, durable complete responses remain the exception. Identification of novel pathways/agents, as well as the optimal sequencing and combination of existing targeted agents, remain areas of active study. In addition, emerging data from early clinical trials have reinvigorated interest in immunomodulatory agents. The therapeutic armamentarium available to genitourinary oncologists continues to grow, but much work remains to be done to fully realize the potential of pathway-specific targeted strategies and immune-based approaches for mRCC. JF - Current opinion in oncology AU - Su, Daniel AU - Stamatakis, Lambros AU - Singer, Eric A AU - Srinivasan, Ramaprasad AD - aUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland bSection of Urologic Oncology, Rutgers Cancer Institute of New Jersey and Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA. Y1 - 2014/05// PY - 2014 DA - May 2014 SP - 321 EP - 327 VL - 26 IS - 3 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Molecular Biology KW - Humans KW - Immunotherapy -- methods KW - Kidney Neoplasms -- genetics KW - Kidney Neoplasms -- drug therapy KW - Carcinoma, Renal Cell -- therapy KW - Molecular Targeted Therapy -- methods KW - Antineoplastic Agents -- therapeutic use KW - Carcinoma, Renal Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1515647413?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Renal+cell+carcinoma%3A+molecular+biology+and+targeted+therapy.&rft.au=Su%2C+Daniel%3BStamatakis%2C+Lambros%3BSinger%2C+Eric+A%3BSrinivasan%2C+Ramaprasad&rft.aulast=Su&rft.aufirst=Daniel&rft.date=2014-05-01&rft.volume=26&rft.issue=3&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=1531-703X&rft_id=info:doi/10.1097%2FCCO.0000000000000069 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-18 N1 - Date created - 2014-04-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cell Biol. 2004 Aug;24(16):7130-9 [15282312] Lancet Oncol. 2013 Feb;14(2):159-67 [23333114] J Clin Oncol. 2005 Jan 1;23(1):133-41 [15625368] N Engl J Med. 2007 Jan 11;356(2):115-24 [17215529] N Engl J Med. 2007 Jan 11;356(2):125-34 [17215530] Clin Cancer Res. 2007 Mar 15;13(6):1757-61 [17363529] N Engl J Med. 2007 May 31;356(22):2271-81 [17538086] J Immunother. 2007 Nov-Dec;30(8):825-30 [18049334] Cochrane Database Syst Rev. 2008;(2):CD006017 [18425931] Lancet. 2008 Aug 9;372(9637):449-56 [18653228] Clin Genitourin Cancer. 2009 Jan;7(1):24-7 [19213664] J Clin Oncol. 2009 Mar 20;27(9):1432-9 [19224847] Curr Cancer Drug Targets. 2009 Aug;9(5):639-51 [19508171] Nature. 2010 Jan 21;463(7279):360-3 [20054297] J Clin Oncol. 2010 Feb 20;28(6):1061-8 [20100962] J Clin Oncol. 2010 May 1;28(13):2144-50 [20368553] J Clin Oncol. 2010 May 1;28(13):2137-43 [20368558] Nat Rev Urol. 2010 May;7(5):277-85 [20448661] Target Oncol. 2010 Jun;5(2):119-29 [20680492] Cancer. 2010 Sep 15;116(18):4256-65 [20549832] Nature. 2011 Jan 27;469(7331):539-42 [21248752] Oncogene. 2011 Mar 10;30(10):1183-93 [21057538] Curr Opin Oncol. 2011 May;23(3):283-9 [21330923] Lancet. 2011 Dec 3;378(9807):1931-9 [22056247] Nat Genet. 2012 Jan;44(1):17-9 [22138691] J Clin Oncol. 2012 Feb 10;30(5):482-7 [22231040] J Clin Oncol. 2012 May 10;30(14):1678-85 [22493422] Expert Opin Ther Targets. 2012 Jun;16(6):553-72 [22530990] Cell. 2013 Feb 14;152(4):685-9 [23375745] Clin Cancer Res. 2013 Mar 1;19(5):1021-34 [23460533] Ann Oncol. 2013 Apr;24(4):1026-31 [23180114] Eur Urol. 2013 May;63(5):848-54 [23036577] Curr Opin Oncol. 2013 May;25(3):273-80 [23455028] Cancer Res. 2013 Apr 1;73(7):2044-51 [23365135] Nature. 2013 Jul 4;499(7456):43-9 [23792563] Cancer. 2013 Aug 15;119(16):2999-3006 [23696129] N Engl J Med. 2013 Aug 22;369(8):722-31 [23964934] J Clin Oncol. 2013 Oct 20;31(30):3791-9 [24019545] CA Cancer J Clin. 2014 Jan-Feb;64(1):9-29 [24399786] J Clin Oncol. 2014 Mar 10;32(8):752-9 [24297945] J Clin Oncol. 2014 Sep 1;32(25):2765-72 [25049330] N Engl J Med. 2012 Jun 28;366(26):2443-54 [22658127] N Engl J Med. 2012 Jun 28;366(26):2455-65 [22658128] J Natl Cancer Inst. 1993 Apr 21;85(8):622-32 [8468720] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/CCO.0000000000000069 ER - TY - JOUR T1 - Integrating pharmacogenetic information and clinical decision support into the electronic health record. AN - 1515643011; 24302286 AB - Pharmacogenetics (PG) examines gene variations for drug disposition, response, or toxicity. At the National Institutes of Health Clinical Center (NIH CC), a multidepartment Pharmacogenetics Testing Implementation Committee (PGTIC) was established to develop clinical decision support (CDS) algorithms for abacavir, carbamazepine, and allopurinol, medications for which human leukocyte antigen (HLA) variants predict severe hypersensitivity reactions. Providing PG CDS in the electronic health record (EHR) during order entry could prevent adverse drug events. Medical Logic Module (MLM) programming was used to implement PG CDS in our EHR. The MLM checks to see if an HLA sequence-based gene test is ordered. A message regarding test status (result present, absent, pending, or test not ordered) is displayed on the order form, and the MLM determines if the prescriber can place the order, place it but require an over-ride reason, or be blocked from placing the order. Since implementation, more than 725 medication orders have been placed for over 230 patients by 154 different prescribers for the three drugs included in our PG program. Prescribers commonly used an over-ride reason when placing the order mainly because patients had been receiving the drug without reaction before implementation of the CDS program. Successful incorporation of PG CDS into the NIH CC EHR required a coordinated, interdisciplinary effort to ensure smooth activation and a positive effect on patient care. Prescribers have adapted to using the CDS and have ordered PG testing as a direct result of the implementation. JF - Journal of the American Medical Informatics Association : JAMIA AU - Goldspiel, Barry R AU - Flegel, Willy A AU - DiPatrizio, Gary AU - Sissung, Tristan AU - Adams, Sharon D AU - Penzak, Scott R AU - Biesecker, Leslie G AU - Fleisher, Thomas A AU - Patel, Jharana J AU - Herion, David AU - Figg, William D AU - Lertora, Juan J L AU - McKeeby, Jon W AD - Pharmacy Department, National Institutes of Health Clinical Center, Bethesda, Maryland, USA. PY - 2014 SP - 522 EP - 528 VL - 21 IS - 3 KW - HLA Antigens KW - 0 KW - Index Medicus KW - Patient Safety KW - Computerized Prescriber Order Entry KW - Informatics KW - Clinical Decision Support KW - Pharmacogenetics KW - Genotype KW - HLA Antigens -- genetics KW - Systems Integration KW - Medical Order Entry Systems KW - Humans KW - Precision Medicine -- methods KW - Decision Support Systems, Clinical KW - Algorithms KW - User-Computer Interface KW - Electronic Health Records KW - Drug Therapy, Computer-Assisted UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1515643011?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Medical+Informatics+Association+%3A+JAMIA&rft.atitle=Integrating+pharmacogenetic+information+and+clinical+decision+support+into+the+electronic+health+record.&rft.au=Goldspiel%2C+Barry+R%3BFlegel%2C+Willy+A%3BDiPatrizio%2C+Gary%3BSissung%2C+Tristan%3BAdams%2C+Sharon+D%3BPenzak%2C+Scott+R%3BBiesecker%2C+Leslie+G%3BFleisher%2C+Thomas+A%3BPatel%2C+Jharana+J%3BHerion%2C+David%3BFigg%2C+William+D%3BLertora%2C+Juan+J+L%3BMcKeeby%2C+Jon+W&rft.aulast=Goldspiel&rft.aufirst=Barry&rft.date=2014-05-01&rft.volume=21&rft.issue=3&rft.spage=522&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Medical+Informatics+Association+%3A+JAMIA&rft.issn=1527-974X&rft_id=info:doi/10.1136%2Famiajnl-2013-001873 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-05 N1 - Date created - 2014-04-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Ann Intern Med. 2006 Nov 21;145(10):749-57 [17116919] J Am Med Inform Assoc. 2014 Feb;21(e1):e93-9 [23978487] N Engl J Med. 2008 Feb 7;358(6):568-79 [18256392] Ann Pharmacother. 2008 Mar;42(3):387-96 [18303141] N Engl J Med. 2010 Jul 22;363(4):301-4 [20551152] Clin Pharmacol Ther. 2011 Mar;89(3):464-7 [21270786] Clin Pharmacol Ther. 2011 Mar;89(3):387-91 [21270794] N Engl J Med. 2011 Mar 24;364(12):1126-33 [21428768] N Engl J Med. 2011 Mar 24;364(12):1134-43 [21428769] Pharmacogenomics. 2011 Dec;12(12):1741-9 [22118056] Clin Pharmacol Ther. 2012 Apr;91(4):734-8 [22378157] Clin Pharmacol Ther. 2012 Oct;92(4):467-75 [22948889] Clin Pharmacol Ther. 2012 Nov;92(5):563-6 [22990750] Nucleic Acids Res. 2013 Jan;41(Database issue):D1222-7 [23080122] Clin Pharmacol Ther. 2013 Feb;93(2):153-8 [23232549] J Am Med Inform Assoc. 2013 Mar-Apr;20(2):388-400 [22922173] Clin Pharmacol Ther. 2013 Apr;93(4):324-5 [23422873] Genet Med. 2013 Apr;15(4):258-67 [23306799] Circ Cardiovasc Genet. 2013 Aug;6(4):413-8; discussion 418 [23963161] Clin Pharmacol Ther. 2013 Sep;94(3):324-8 [23695185] Genet Med. 2013 Oct;15(10):833-41 [24009000] J Am Med Inform Assoc. 2007 Mar-Apr;14(2):141-5 [17213487] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1136/amiajnl-2013-001873 ER - TY - JOUR T1 - Cigarette smoking and postmenopausal breast cancer risk in a prospective cohort AN - 1529922224; 19814340 AB - Background: The relationship between cigarette smoking and breast cancer risk has been inconsistent, potentially due to modification by other factors or confounding. Methods: We examined smoking and breast cancer risk in a prospective cohort of 186 150 female AARP (formerly American Association of Retired Persons) members, ages 50-71 years, who joined the study in 1995-96 by responding to a questionnaire. Through 2006, 7481 breast cancers were diagnosed. Multivariable-adjusted hazard ratios (HRs) were estimated, overall and stratified by breast cancer risk factors, using Cox proportional hazards regression. Multiplicative interactions were evaluated using the likelihood ratio test. Results: Increased breast cancer risk was associated with current (HR 1.19, 95% confidence interval (CI) 1.10-1.28) and former (HR 1.07, CI 1.01-1.13) smoking. The current smoking association was stronger among women without (HR 1.24, CI 1.15-1.35) as compared to those with a family history of breast cancer (HR 0.94, CI 0.78-1.13) (P-interaction=0.03). The current smoking association was also stronger among those with later ([egs]15 years: HR 1.52, CI 1.20-1.94) as compared with earlier ([els]12 years: HR 1.14, CI 1.03-1.27; 13-14 years: HR 1.18, CI 1.05-1.32) ages at menarche (P-interaction=0.03). Conclusions: Risk was elevated in smokers, particularly in those without a family history or late menarche. Research into smoking's effects on the genome and breast development may clarify these relationships. JF - British Journal of Cancer AU - Nyante, S J AU - Gierach, G L AU - Dallal, C M AU - Freedman, N D AU - Park, Y AU - Danforth, K N AU - Hollenbeck, A R AU - Brinton, L A AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Bethesda, MD 20892, USA Y1 - 2014/04/29/ PY - 2014 DA - 2014 Apr 29 SP - 2339 EP - 2347 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 110 IS - 9 SN - 0007-0920, 0007-0920 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Health risks KW - Genetics KW - Age KW - Cigarettes KW - Post-menopause KW - Risk factors KW - Breast 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/1529922224?accountid=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=Cigarette+smoking+and+postmenopausal+breast+cancer+risk+in+a+prospective+cohort&rft.au=Nyante%2C+S+J%3BGierach%2C+G+L%3BDallal%2C+C+M%3BFreedman%2C+N+D%3BPark%2C+Y%3BDanforth%2C+K+N%3BHollenbeck%2C+A+R%3BBrinton%2C+L+A&rft.aulast=Nyante&rft.aufirst=S&rft.date=2014-04-29&rft.volume=110&rft.issue=9&rft.spage=2339&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2014.132 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Genetics; Health risks; Age; Cigarettes; Post-menopause; Risk factors; Breast cancer DO - http://dx.doi.org/10.1038/bjc.2014.132 ER - TY - JOUR T1 - Tumor microenvironment-based feed-forward regulation of NOS2 in breast cancer progression. AN - 1520340741; 24733928 AB - Inflammation is widely recognized as an inducer of cancer progression. The inflammation-associated enzyme, inducible nitric oxide synthase (NOS2), has emerged as a candidate oncogene in estrogen receptor (ER)-negative breast cancer, and its increased expression is associated with disease aggressiveness and poor survival. Although these observations implicate NOS2 as an attractive therapeutic target, the mechanisms of both NOS2 induction in tumors and nitric oxide (NO)-driven cancer progression are not fully understood. To enhance our mechanistic understanding of NOS2 induction in tumors and its role in tumor biology, we used stimulants of NOS2 expression in ER(-) and ER(+) breast cancer cells and examined downstream NO-dependent effects. Herein, we show that up-regulation of NOS2 occurs in response to hypoxia, serum withdrawal, IFN-γ, and exogenous NO, consistent with a feed-forward regulation of NO production by the tumor microenvironment in breast cancer biology. Moreover, we found that key indicators of an aggressive cancer phenotype including increased S100 calcium binding protein A8, IL-6, IL-8, and tissue inhibitor matrix metalloproteinase-1 are up-regulated by these NOS2 stimulants, whereas inhibition of NOS2 in MDA-MB-231 breast cancer cells suppressed these markers. Moreover, NO altered cellular migration and chemoresistance of MDA-MB-231 cells to Taxol. Most notably, MDA-MB-231 tumor xenographs and cell metastases from the fat pad to the brain were significantly suppressed by NOS2 inhibition in nude mice. In summary, these results link elevated NOS2 to signals from the tumor microenvironment that arise with cancer progression and show that NO production regulates chemoresistance and metastasis of breast cancer cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Heinecke, Julie L AU - Ridnour, Lisa A AU - Cheng, Robert Y S AU - Switzer, Christopher H AU - Lizardo, Michael M AU - Khanna, Chand AU - Glynn, Sharon A AU - Hussain, S Perwez AU - Young, Howard A AU - Ambs, Stefan AU - Wink, David A AD - Radiation Biology Branch, Tumor and Metastasis Biology Section, Pediatric Oncology Branch, and Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 2014/04/29/ PY - 2014 DA - 2014 Apr 29 SP - 6323 EP - 6328 VL - 111 IS - 17 KW - Biomarkers, Tumor KW - 0 KW - Culture Media, Serum-Free KW - Guanidines KW - Nitric Oxide KW - 31C4KY9ESH KW - Interferon-gamma KW - 82115-62-6 KW - NOS2 protein, human KW - EC 1.14.13.39 KW - Nitric Oxide Synthase Type II KW - pimagedine KW - SCQ4EZQ113 KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Animals KW - Humans KW - Cell Hypoxia -- drug effects KW - Interferon-gamma -- pharmacology KW - Mice KW - Cell Line, Tumor KW - Models, Biological KW - Biomarkers, Tumor -- metabolism KW - Signal Transduction -- drug effects KW - Neoplasm Metastasis KW - Cell Movement -- drug effects KW - Nitric Oxide -- pharmacology KW - Female KW - Drug Resistance, Neoplasm -- drug effects KW - Feedback, Physiological -- drug effects KW - Breast Neoplasms -- pathology KW - Disease Progression KW - Nitric Oxide Synthase Type II -- metabolism KW - Breast Neoplasms -- enzymology KW - Tumor Microenvironment -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520340741?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tumor+microenvironment-based+feed-forward+regulation+of+NOS2+in+breast+cancer+progression.&rft.au=Heinecke%2C+Julie+L%3BRidnour%2C+Lisa+A%3BCheng%2C+Robert+Y+S%3BSwitzer%2C+Christopher+H%3BLizardo%2C+Michael+M%3BKhanna%2C+Chand%3BGlynn%2C+Sharon+A%3BHussain%2C+S+Perwez%3BYoung%2C+Howard+A%3BAmbs%2C+Stefan%3BWink%2C+David+A&rft.aulast=Heinecke&rft.aufirst=Julie&rft.date=2014-04-29&rft.volume=111&rft.issue=17&rft.spage=6323&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.1401799111 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-24 N1 - Date created - 2014-04-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2000 Jul 1;60(13):3333-7 [10910033] Breast Cancer Res. 2012;14(5):R125 [22971289] Clin Cancer Res. 2000 Dec;6(12):4768-75 [11156233] Ann Surg Oncol. 2001 Mar;8(2):116-22 [11258775] Am Surg. 2001 Jul;67(7):709-13 [11450795] J Immunol. 1993 Dec 1;151(11):6329-37 [7504017] Biochem Biophys Res Commun. 1994 Jun 15;201(2):762-8 [7516158] J Exp Med. 1994 Sep 1;180(3):977-84 [7520478] J Biol Chem. 1996 Mar 8;271(10):5414-21 [8621396] Br J Pharmacol. 2005 Jun;145(3):301-12 [15778742] J Immunol. 2005 Sep 15;175(6):3846-61 [16148131] Pathol Res Pract. 2006;202(1):1-7 [16326029] Science. 2006 May 26;312(5777):1158-9 [16728625] Int J Cancer. 2006 Aug 15;119(4):861-6 [16557582] Cancer Res. 2007 Oct 1;67(19):9214-20 [17909027] Nitric Oxide. 2008 Sep;19(2):133-7 [18472017] Autophagy. 2008 Nov;4(8):1042-53 [18927491] Proc Natl Acad Sci U S A. 2008 Nov 25;105(47):18490-5 [19001271] Nat Rev Cancer. 2008 Sep;8(9):705-13 [19143055] Curr Pharm Des. 2010;16(4):421-7 [20236070] Cancer Sci. 2010 Apr;101(4):1014-23 [20151982] J Clin Invest. 2010 Nov;120(11):3843-54 [20978357] Cell. 2011 Mar 4;144(5):646-74 [21376230] Clin Cancer Res. 2011 Oct 1;17(19):6118-24 [21705455] Proc Natl Acad Sci U S A. 2012 Apr 10;109(15):5826-31 [22451906] PLoS One. 2012;7(9):e44081 [22957045] Mol Cancer Res. 2012 Sep;10(9):1203-15 [22878588] Int J Cancer. 2013 Jan 1;132(1):9-18 [22618808] EMBO J. 2013 Mar 6;32(5):688-700 [23386060] Clin Cancer Res. 2013 Mar 15;19(6):1340-6 [23271799] J Mol Med (Berl). 2013 Apr;91(4):411-29 [23515621] Int J Cancer. 2013 Jun 15;132(12):2721-9 [23055435] Cancer Res. 2013 Jun 1;73(11):3470-80 [23633491] Cancer Lett. 2013 Aug 28;337(1):49-57 [23707634] Breast Cancer Res. 2013;15(1):R2 [23294542] Cancer Res. 2000 Nov 1;60(21):6201-7 [11085546] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1401799111 ER - TY - CPAPER T1 - Role of G Proteins in regulation of energy and glucose metabolism T2 - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society AN - 1541353123; 6286982 JF - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society AU - Weinstein, Lee Y1 - 2014/04/26/ PY - 2014 DA - 2014 Apr 26 KW - Energy KW - Guanine nucleotide-binding protein KW - Glucose metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353123?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.atitle=Role+of+G+Proteins+in+regulation+of+energy+and+glucose+metabolism&rft.au=Weinstein%2C+Lee&rft.aulast=Weinstein&rft.aufirst=Lee&rft.date=2014-04-26&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/EB2014/program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Identification of a novel, highly potent D3 dopamine receptor-selective agonist T2 - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society AN - 1541353104; 6287045 JF - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society AU - Moritz, Amy Y1 - 2014/04/26/ PY - 2014 DA - 2014 Apr 26 KW - Dopamine D3 receptors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.atitle=Identification+of+a+novel%2C+highly+potent+D3+dopamine+receptor-selective+agonist&rft.au=Moritz%2C+Amy&rft.aulast=Moritz&rft.aufirst=Amy&rft.date=2014-04-26&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/EB2014/program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Peripheral CB1 receptors as emerging therapeutic targets in diabetes and obesity T2 - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society AN - 1541352996; 6287088 JF - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society AU - Kunos, George Y1 - 2014/04/26/ PY - 2014 DA - 2014 Apr 26 KW - Diabetes mellitus KW - Obesity KW - Cannabinoid CB1 receptors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541352996?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.atitle=Peripheral+CB1+receptors+as+emerging+therapeutic+targets+in+diabetes+and+obesity&rft.au=Kunos%2C+George&rft.aulast=Kunos&rft.aufirst=George&rft.date=2014-04-26&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/EB2014/program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Macrophages are required to maintain type 2-dependent inflammation, immunity, and fibrosis T2 - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society AN - 1541352940; 6287100 JF - 2014 American Society for Pharmacology and Experimental Therapeutics Annual Meeting with the Chinese Pharmacological Society AU - Barron, Luke Y1 - 2014/04/26/ PY - 2014 DA - 2014 Apr 26 KW - Macrophages KW - Fibrosis KW - Immunity KW - Inflammation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541352940?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.atitle=Macrophages+are+required+to+maintain+type+2-dependent+inflammation%2C+immunity%2C+and+fibrosis&rft.au=Barron%2C+Luke&rft.aulast=Barron&rft.aufirst=Luke&rft.date=2014-04-26&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+American+Society+for+Pharmacology+and+Experimental+Therapeutics+Annual+Meeting+with+the+Chinese+Pharmacological+Society&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/EB2014/program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - JOUR T1 - Relationship of immunologic response to antiretroviral therapy with non-AIDS defining cancer incidence AN - 1765982706; PQ0002610762 AB - The objective of this paper is to estimate the association between immunologic response to anti-retroviral therapy (ART) and non-AIDS defining cancer (NADC) incidence in HIV-infected patients. A prospective cohort including patients with at least 1 cell/[mu[l CD4[sup +] cell count and HIV-1 RNA measure after ART initiation between 1996 and 2011 in the Centers for AIDS Research Network of Integrated Clinical Systems, a collaboration of eight HIV clinics at major academic medical centres in the United States. Cox regression with inverse probability-of-exposure weights was used to calculate adjusted hazard ratios of virus-related and virus-unrelated NADC incidence. Poor CD4[sup +] cell count response was strongly associated with virus-related NADC incidence, suggesting an important role for T-cell mediated immunity in pathogenesis. Lower CD4[sup +] cell count proximal to cancer diagnosis may be a result of sub-clinical cancer. Intensified cancer screening should be considered for patients on ART with low CD4[sup +] cell counts. JF - AIDS AU - Yanik, Elizabeth L AU - Napravnik, Sonia AU - Cole, Stephen R AU - Achenbach, Chad J AU - Gopal, Satish AU - Dittmer, Dirk P AU - Olshan, Andrew F AU - Kitahata, Mari M AU - Mugavero, Michael J AU - Saag, Michael AU - Moore, Richard D AU - Mathews, W Christopher AU - Hunt, Peter AU - Eron, Joseph J AD - University of North Carolina, Chapel Hill, North Carolina, elizabeth.yanik@nih.gov Y1 - 2014/04/24/ PY - 2014 DA - 2014 Apr 24 SP - 979 EP - 987 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 IS - 7 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - antiretroviral therapy KW - cancers KW - CD4+ cell count KW - HIV infections KW - immune reconstitution KW - tumour virus infections KW - Acquired immune deficiency syndrome KW - Immunity KW - Antiretroviral agents KW - Cancer KW - USA KW - RNA KW - Human immunodeficiency virus KW - Human immunodeficiency virus 1 KW - Lymphocytes T KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765982706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Relationship+of+immunologic+response+to+antiretroviral+therapy+with+non-AIDS+defining+cancer+incidence&rft.au=Yanik%2C+Elizabeth+L%3BNapravnik%2C+Sonia%3BCole%2C+Stephen+R%3BAchenbach%2C+Chad+J%3BGopal%2C+Satish%3BDittmer%2C+Dirk+P%3BOlshan%2C+Andrew+F%3BKitahata%2C+Mari+M%3BMugavero%2C+Michael+J%3BSaag%2C+Michael%3BMoore%2C+Richard+D%3BMathews%2C+W+Christopher%3BHunt%2C+Peter%3BEron%2C+Joseph+J&rft.aulast=Yanik&rft.aufirst=Elizabeth&rft.date=2014-04-24&rft.volume=28&rft.issue=7&rft.spage=979&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000167 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Acquired immune deficiency syndrome; RNA; antiretroviral therapy; Lymphocytes T; Immunity; Cancer; Human immunodeficiency virus; Antiretroviral agents; Human immunodeficiency virus 1; USA DO - http://dx.doi.org/10.1097/QAD.0000000000000167 ER - TY - JOUR T1 - Systematic Review and Evidence Integration for Literature-Based Environmental Health Science Assessments AN - 1551644857; 20395149 AB - Background: Systematic-review methodologies provide objectivity and transparency to the process of collecting and synthesizing scientific evidence in reaching conclusions on specific research questions. There is increasing interest in applying these procedures to address environmental health questions. Objectives: The goal was to develop a systematic-review framework to address environmental health questions by extending approaches developed for clinical medicine to handle the breadth of data relevant to environmental health sciences (e.g., human, animal, and mechanistic studies). Methods: The Office of Health Assessment and Translation (OHAT) adapted guidance from authorities on systematic-review and sought advice during development of the OHAT Approach through consultation with technical experts in systematic review and human health assessments, as well as scientific advisory groups and the public. The method was refined by considering expert and public comments and through application to case studies. Results and Discussion: Here we present a seven-step framework for systematic review and evidence integration for reaching hazard identification conclusions: 1) problem formulation and protocol development, 2) search for and select studies for inclusion, 3) extract data from studies, 4) assess the quality or risk of bias of individual studies, 5) rate the confidence in the body of evidence, 6) translate the confidence ratings into levels of evidence, and 7) integrate the information from different evidence streams (human, animal, and "other relevant data" including mechanistic or in vitro studies) to develop hazard identification conclusions. Conclusion: The principles of systematic review can be successfully applied to environmental health questions to provide greater objectivity and transparency to the process of developing conclusions. Citation: Rooney AA, Boyles AL, Wolfe MS, Bucher JR, Thayer KA. 2014. Systematic review and evidence integration for literature-based environmental health science assessments. Environ Health Perspect 122:711-718; http://dx.doi.org/10.1289/ehp.1307972 JF - Environmental Health Perspectives AU - Rooney, Andrew A AU - Boyles, Abee L AU - Wolfe, Mary S AU - Bucher, John R AU - Thayer, Kristina A AD - Office of Health Assessment and Translation, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA Y1 - 2014/04/22/ PY - 2014 DA - 2014 Apr 22 SP - 711 EP - 718 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 122 IS - 7 SN - 0091-6765, 0091-6765 KW - Risk Abstracts; Environment Abstracts; Health & Safety Science Abstracts KW - Transparency KW - Risk assessment KW - Case studies KW - Reviews KW - Environmental health KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - R2 23060:Medical and environmental health KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551644857?accountid=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+Health+Perspectives&rft.atitle=Systematic+Review+and+Evidence+Integration+for+Literature-Based+Environmental+Health+Science+Assessments&rft.au=Rooney%2C+Andrew+A%3BBoyles%2C+Abee+L%3BWolfe%2C+Mary+S%3BBucher%2C+John+R%3BThayer%2C+Kristina+A&rft.aulast=Rooney&rft.aufirst=Andrew&rft.date=2014-04-22&rft.volume=122&rft.issue=7&rft.spage=711&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1307972 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Risk assessment; Transparency; Case studies; Reviews; Environmental health DO - http://dx.doi.org/10.1289/ehp.1307972 ER - TY - JOUR T1 - Integrative framework for identification of key cell identity genes uncovers determinants of ES cell identity and homeostasis. AN - 1518813283; 24711389 AB - Identification of genes associated with specific biological phenotypes is a fundamental step toward understanding the molecular basis underlying development and pathogenesis. Although RNAi-based high-throughput screens are routinely used for this task, false discovery and sensitivity remain a challenge. Here we describe a computational framework for systematic integration of published gene expression data to identify genes defining a phenotype of interest. We applied our approach to rank-order all genes based on their likelihood of determining ES cell (ESC) identity. RNAi-mediated loss-of-function experiments on top-ranked genes unearthed many novel determinants of ESC identity, thus validating the derived gene ranks to serve as a rich and valuable resource for those working to uncover novel ESC regulators. Underscoring the value of our gene ranks, functional studies of our top-hit Nucleolin (Ncl), abundant in stem and cancer cells, revealed Ncl's essential role in the maintenance of ESC homeostasis by shielding against differentiation-inducing redox imbalance-induced oxidative stress. Notably, we report a conceptually novel mechanism involving a Nucleolin-dependent Nanog-p53 bistable switch regulating the homeostatic balance between self-renewal and differentiation in ESCs. Our findings connect the dots on a previously unknown regulatory circuitry involving genes associated with traits in both ESCs and cancer and might have profound implications for understanding cell fate decisions in cancer stem cells. The proposed computational framework, by helping to prioritize and preselect candidate genes for tests using complex and expensive genetic screens, provides a powerful yet inexpensive means for identification of key cell identity genes. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Cinghu, Senthilkumar AU - Yellaboina, Sailu AU - Freudenberg, Johannes M AU - Ghosh, Swati AU - Zheng, Xiaofeng AU - Oldfield, Andrew J AU - Lackford, Brad L AU - Zaykin, Dmitri V AU - Hu, Guang AU - Jothi, Raja AD - Systems Biology Section and Stem Cell Biology Section, Laboratory of Molecular Carcinogenesis, and Biostatistics Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 2014/04/22/ PY - 2014 DA - 2014 Apr 22 SP - E1581 EP - E1590 VL - 111 IS - 16 KW - Homeodomain Proteins KW - 0 KW - Nanog Homeobox Protein KW - Nanog protein, mouse KW - Phosphoproteins KW - RNA-Binding Proteins KW - Reactive Oxygen Species KW - Tumor Suppressor Protein p53 KW - nucleolin KW - Index Medicus KW - ROS KW - RNA-binding protein KW - pluripotency KW - computational biology KW - transcription KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Phosphoproteins -- genetics KW - Reproducibility of Results KW - RNA-Binding Proteins -- metabolism KW - RNA-Binding Proteins -- genetics KW - Cell Differentiation -- genetics KW - Transcription, Genetic KW - Mice KW - Oxidative Stress -- genetics KW - Cell Proliferation KW - Tumor Suppressor Protein p53 -- metabolism KW - Pluripotent Stem Cells -- cytology KW - Homeodomain Proteins -- metabolism KW - Gene Expression Regulation KW - RNA Interference KW - Phosphoproteins -- metabolism KW - Pluripotent Stem Cells -- metabolism KW - Embryonic Stem Cells -- metabolism KW - Embryonic Stem Cells -- cytology KW - Homeostasis -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518813283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Integrative+framework+for+identification+of+key+cell+identity+genes+uncovers+determinants+of+ES+cell+identity+and+homeostasis.&rft.au=Cinghu%2C+Senthilkumar%3BYellaboina%2C+Sailu%3BFreudenberg%2C+Johannes+M%3BGhosh%2C+Swati%3BZheng%2C+Xiaofeng%3BOldfield%2C+Andrew+J%3BLackford%2C+Brad+L%3BZaykin%2C+Dmitri+V%3BHu%2C+Guang%3BJothi%2C+Raja&rft.aulast=Cinghu&rft.aufirst=Senthilkumar&rft.date=2014-04-22&rft.volume=111&rft.issue=16&rft.spage=E1581&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.1318598111 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-17 N1 - Date created - 2014-04-23 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE47872; GEO N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2009 Mar 31;106(13):5187-91 [19279218] Cell. 2008 Nov 28;135(5):852-64 [19012953] Genes Dev. 2009 Apr 1;23(7):837-48 [19339689] Nature. 2009 Apr 9;458(7239):780-3 [19194462] Cell Stem Cell. 2009 May 8;4(5):403-15 [19345177] Cell Stem Cell. 2009 May 8;4(5):377-8 [19427287] Cell. 2009 May 29;137(5):835-48 [19490893] Nature. 2009 Aug 27;460(7259):1085-6 [19713919] Genes Dev. 2009 Nov 1;23(21):2484-9 [19884255] Cell Stem Cell. 2010 Jan 8;6(1):71-9 [20036631] Nature. 2010 Feb 4;463(7281):621-6 [20054295] Trends Cell Biol. 2010 Mar;20(3):170-5 [20061153] Nature. 2010 Apr 8;464(7290):858-63 [20336070] Annu Rev Biochem. 2010;79:37-64 [20367032] EMBO J. 2010 Aug 4;29(15):2659-74 [20581802] Nucleic Acids Res. 2010 Aug;38(14):4807-20 [20385601] Nature. 2010 Sep 23;467(7314):430-5 [20720539] Nature. 2010 Nov 11;468(7321):316-20 [20953172] Cell. 2011 Mar 18;144(6):940-54 [21414485] Nat Cell Biol. 2011 May;13(5):490-6 [21540844] Nat Cell Biol. 2011 May;13(5):497-505 [21540845] Cell. 2011 Jun 10;145(6):835-50 [21663790] J Evol Biol. 2011 Aug;24(8):1836-41 [21605215] Nat Cell Biol. 2011 Aug;13(8):903-13 [21785422] Nature. 2011 Oct 27;478(7370):524-8 [21814200] J Biol Chem. 2011 Dec 16;286(50):43370-82 [22013067] Nature. 2012 Jan 19;481(7381):295-305 [22258608] PLoS Biol. 2012;10(2):e1001268 [22389628] Mol Cell. 2012 Apr 13;46(1):30-42 [22387025] Nucleic Acids Res. 2012 Apr;40(8):3364-77 [22210859] Cell Stem Cell. 2012 Aug 3;11(2):179-94 [22862944] RNA Biol. 2012 Jun;9(6):799-808 [22617883] Cell. 2012 Oct 26;151(3):576-89 [23101626] Cell Stem Cell. 2012 Dec 7;11(6):783-98 [23103054] Nature. 2013 Mar 28;495(7442):516-9 [23503660] Science. 2013 Mar 29;339(6127):1567-70 [23539597] Cell. 2013 Apr 11;153(2):389-401 [23582328] PLoS Pathog. 2013;9(6):e1003416 [23785285] Genome Biol. 2012;13(8):R71 [22909066] Oncogene. 2002 Nov 28;21(54):8320-33 [12447695] Nature. 2003 May 29;423(6939):541-5 [12774123] FEBS Lett. 2004 Aug 27;573(1-3):83-92 [15327980] J Biol Chem. 1982 Nov 25;257(22):13704-12 [6128339] Curr Biol. 1998 Jan 29;8(3):145-55 [9443911] Nat Cell Biol. 2005 Feb;7(2):165-71 [15619621] Cell. 2005 Oct 7;123(1):49-63 [16213212] Nat Med. 2005 Dec;11(12):1306-13 [16286925] Nature. 2006 Aug 3;442(7102):533-8 [16767105] Bioinformatics. 2006 Nov 15;22(22):2825-7 [16982708] Trends Cell Biol. 2007 Feb;17(2):80-6 [17157503] Nat Protoc. 2006;1(1):302-7 [17406249] Cell. 2008 Feb 22;132(4):532-6 [18295569] Cell. 2008 Feb 22;132(4):567-82 [18295576] Cell Stem Cell. 2008 Mar 6;2(3):241-51 [18371449] Free Radic Biol Med. 2008 Apr 15;44(8):1529-35 [18275858] Nat Genet. 2008 May;40(5):499-507 [18443585] Nature. 2008 May 22;453(7194):519-23 [18497825] Cell. 2008 Jun 13;133(6):1106-17 [18555785] Nat Rev Genet. 2008 Jul;9(7):554-66 [18521077] Cell. 2008 Jul 11;134(1):162-74 [18614019] Cell. 2008 Aug 8;134(3):521-33 [18692474] Nature. 2008 Sep 11;455(7210):242-5 [18690214] Nat Genet. 2008 Dec;40(12):1478-83 [18978791] Proc Natl Acad Sci U S A. 2009 Mar 31;106(13):5181-6 [19279220] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1318598111 ER - TY - JOUR T1 - Free radical metabolism of methyleugenol and related compounds. AN - 1518242114; 24564854 AB - Methyleugenol, the methyl ether of eugenol, both of which are flavorant constituents of spices, has been listed by the National Toxicology Program's Report on Carcinogens as reasonably anticipated to be a human carcinogen. This finding is based on the observation of increased incidence of malignant tumors at multiple tissue sites in experimental animals of different species. By contrast, eugenol is not listed. In this study, we show that both methyleugenol and eugenol readily undergo peroxidative metabolism in vitro to form free radicals with large hyperfine interactions of the methylene allylic hydrogen atoms. These large hyperfine splittings indicate large electron densities adjacent to those hydrogen atoms. Methyleugenol undergoes autoxidation such that the commercial product contains 10-30 mg/L hydroperoxide and is capable of activating peroxidases without the presence of added hydrogen peroxide. Additionally, the hydroperoxide is not a good substrate for catalase, which demonstrates that these antioxidant defenses will not be effective in protecting against methyleugenol exposure. JF - Chemical research in toxicology AU - Sipe, Herbert J AU - Lardinois, Olivier M AU - Mason, Ronald P AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health , P.O. Box 12233, Research Triangle Park, North Carolina 27709, United States. Y1 - 2014/04/21/ PY - 2014 DA - 2014 Apr 21 SP - 483 EP - 489 VL - 27 IS - 4 KW - Free Radicals KW - 0 KW - methyleugenol KW - 29T9VA6R7M KW - Eugenol KW - 3T8H1794QW KW - Index Medicus KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Spectrophotometry, Ultraviolet KW - Free Radicals -- metabolism KW - Eugenol -- analogs & derivatives KW - Eugenol -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518242114?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Free+radical+metabolism+of+methyleugenol+and+related+compounds.&rft.au=Sipe%2C+Herbert+J%3BLardinois%2C+Olivier+M%3BMason%2C+Ronald+P&rft.aulast=Sipe&rft.aufirst=Herbert&rft.date=2014-04-21&rft.volume=27&rft.issue=4&rft.spage=483&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=1520-5010&rft_id=info:doi/10.1021%2Ftx400256b LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-15 N1 - Date created - 2014-04-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Anticancer Res. 1998 Jan-Feb;18(1A):425-8 [9568113] J Chromatogr B Biomed Appl. 1995 Jan 20;663(2):255-62 [7735473] Chem Res Toxicol. 2006 Jan;19(1):111-6 [16411663] Toxicol In Vitro. 2011 Feb;25(1):267-85 [20828604] Food Funct. 2012 Apr;3(4):428-36 [22302122] Xenobiotica. 2012 May;42(5):429-41 [22188410] Toxicol Appl Pharmacol. 2012 May 1;260(3):271-84 [22445790] Toxicol Sci. 2012 Sep;129(1):21-34 [22610610] Carcinogenesis. 2013 May;34(5):1025-30 [23334163] Environ Health Perspect. 2000 Apr;108(4):323-8 [10753090] Anticancer Res. 2000 Jul-Aug;20(4):2519-24 [10953321] Anticancer Res. 2000 Sep-Oct;20(5A):2955-60 [11062707] In Vitr Mol Toxicol. 2000 Winter;13(4):269-80 [11319278] Food Chem Toxicol. 2002 Jul;40(7):851-70 [12065208] Environ Health Perspect. 2004 May;112(6):678-80 [15121510] J Biol Chem. 1972 May 25;247(10):3353-60 [5063682] Anal Biochem. 1972 Oct;49(2):474-8 [5082943] J Biol Chem. 1979 Sep 25;254(18):9101-6 [39073] Mol Pharmacol. 1983 Mar;23(2):461-6 [6300652] Biochem Pharmacol. 1984 Sep 15;33(18):2933-6 [6089841] J Biol Chem. 1985 Mar 10;260(5):2609-12 [2982828] Proc Natl Acad Sci U S A. 1986 Jun;83(11):3708-12 [3012530] J Biol Chem. 1989 Jan 15;264(2):1016-21 [2536013] Biochem J. 1990 Jun 1;268(2):475-80 [2163614] J Magn Reson B. 1994 Jun;104(2):105-10 [8049862] Photochem Photobiol. 1994 Sep;60(3):199-204 [7972369] J Pharmacol Exp Ther. 1995 Feb;272(2):588-96 [7853172] Mutat Res. 2005 Jul 1;574(1-2):124-38 [15914212] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/tx400256b ER - TY - JOUR T1 - Accommodating Measurements Below a Limit of Detection: A Novel Application of Cox Regression AN - 1516746342; 19545030 AB - In environmental epidemiology, measurements of exposure biomarkers often fall below the assay's limit of detection. Existing methods for handling this problem, including deletion, substitution, parametric regression, and multiple imputation, can perform poorly if the proportion of "nondetects" is high or parametric models are misspecified. We propose an approach that treats the measured analyte as the modeled outcome, implying a role reversal when the analyte is a putative cause of a health outcome. Following a scale reversal as well, our approach uses Cox regression to model the analyte, with confounder adjustment. The method makes full use of quantifiable analyte measures, while appropriately treating nondetects as censored. Under the proportional hazards assumption, the hazard ratio for a binary health outcome is interpretable as an adjusted odds ratio: the odds for the outcome at any particular analyte concentration divided by the odds given a lower concentration. Our approach is broadly applicable to cohort studies, case-control studies (frequency matched or not), and cross-sectional studies conducted to identify determinants of exposure. We illustrate the method with cross-sectional survey data to assess sex as a determinant of 2,3,7,8-tetrachlorodibenzo-p-dioxin concentration and with prospective cohort data to assess the association between 2,4,4'-trichlorobiphenyl exposure and psychomotor development. JF - American Journal of Epidemiology AU - Dinse, Gregg E AU - Jusko, Todd A AU - Ho, Lindsey A AU - Annam, Kaushik AU - Graubard, Barry I AU - Hertz-Picciotto, Irva AU - Miller, Frederick W AU - Gillespie, Brenda W AU - Weinberg, Clarice R AD - Correspondence to Dr. Clarice R. Weinberg, Mail Drop A3-03, P.O. Box 12233, Research Triangle Park, NC 27709., weinber2@niehs.nih.gov Y1 - 2014/04/15/ PY - 2014 DA - 2014 Apr 15 SP - 1018 EP - 1024 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 179 IS - 8 SN - 0002-9262, 0002-9262 KW - Health & Safety Science Abstracts KW - Bioindicators KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516746342?accountid=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=Accommodating+Measurements+Below+a+Limit+of+Detection%3A+A+Novel+Application+of+Cox+Regression&rft.au=Dinse%2C+Gregg+E%3BJusko%2C+Todd+A%3BHo%2C+Lindsey+A%3BAnnam%2C+Kaushik%3BGraubard%2C+Barry+I%3BHertz-Picciotto%2C+Irva%3BMiller%2C+Frederick+W%3BGillespie%2C+Brenda+W%3BWeinberg%2C+Clarice+R&rft.aulast=Dinse&rft.aufirst=Gregg&rft.date=2014-04-15&rft.volume=179&rft.issue=8&rft.spage=1018&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu017 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2014-06-12 N1 - SubjectsTermNotLitGenreText - Bioindicators DO - http://dx.doi.org/10.1093/aje/kwu017 ER - TY - JOUR T1 - MATILDE chemotherapy regimen for primary CNS lymphoma: results at a median follow-up of 12 years. AN - 1516722335; 24634458 AB - We report updated results at a median follow-up of 12 years of a phase II trial assessing first-line MATILDE chemotherapy and response-tailored radiotherapy in patients with primary CNS lymphomas (PCNSL). Forty-one HIV-negative patients (18-70 years; Eastern Cooperative Oncology Group performance status ≤3) with histologically confirmed PCNSL received 3 courses of MATILDE chemotherapy followed by whole-brain radiotherapy (WBRT). Chemotherapy activity was the primary endpoint. Overall response rate was 76% (95% confidence interval [CI] 63%-89%) after chemotherapy and 83% (95% CI 71%-95%) after chemotherapy ± radiotherapy. At a median follow-up of 144 months (range 47-153), 31 patients experienced an event: relapse in 24, progressive disease in 3, and toxic death in 4, with a 5-year progression-free survival of 24% ± 8%. Two patients experienced a late relapse (100 and 101 months). Nine patients are alive and disease-free, 8 of whom are alive at >10 years, with a 5-year overall survival of 30% ± 7%. At 10 years from diagnosis, no patient showed chronic hematologic and nonhematologic toxicities, with a Mini-Mental State Examination score of ≥29 in all cases but one. At a median follow-up of 12 years, MATILDE regimen followed by WBRT confirmed the previously reported survival plateau, which further proves its long-lasting efficacy with acceptable neurologic deficits. This study provides Class IV evidence that in patients with PCNSL, MATILDE chemotherapy followed by response-tailored radiotherapy increases the probability of disease remission at 12 years. JF - Neurology AU - Ferreri, Andrés J M AU - Ciceri, Fabio AU - Brandes, Alba A AU - Montanari, Mauro AU - Balzarotti, Monica AU - Spina, Michele AU - Ilariucci, Fiorella AU - Zaja, Francesco AU - Stelitano, Caterina AU - Bobbio, Flavio AU - Corazzelli, Gaetano AU - Baldini, Luca AU - Reni, Michele AD - From the Unit of Lymphoid Malignancies (A.J.M.F.), UTMO & Hematology Unit, Department of Onco-Hematology (F.C.), and Medical Oncology Unit, Department of Oncology (M.R.), San Raffaele Scientific Institute, Milan; Department of Medical Oncology (A.A.B.), Bellaria-Maggiore Hospital, Azienda Unità Sanitaria Locale, Bologna; Division of Hematology (M.M.), Ospedale di Ancona; Department of Medical Oncology and Hematology (M.B.), Istituto Clinico Humanitas, Rozzano; Division of Medical Oncology A (M.S.), National Cancer Institute, Aviano; Division of Hematology (F.I.), Ospedale di Reggio Emilia; Division of Hematology (F.Z.), Ospedale di Udine; Division of Hematology (C.S.), Ospedale di Reggio Calabria; Division of Hematology (F.B.), Ospedale Maggiore di Novara; Division of Hematology (G.C.), Istituto Nazionale dei Tumori Pascale di Napoli; and the Division of Hematology (L.B.), Ospedale Maggiore di Milano, Italy. Y1 - 2014/04/15/ PY - 2014 DA - 2014 Apr 15 SP - 1370 EP - 1373 VL - 82 IS - 15 KW - Cytarabine KW - 04079A1RDZ KW - Thiotepa KW - 905Z5W3GKH KW - Methotrexate KW - YL5FZ2Y5U1 KW - Idarubicin KW - ZRP63D75JW KW - Abridged Index Medicus KW - Index Medicus KW - Disease-Free Survival KW - Combined Modality Therapy KW - Humans KW - Cytarabine -- administration & dosage KW - Idarubicin -- administration & dosage KW - Idarubicin -- therapeutic use KW - Cytarabine -- therapeutic use KW - Thiotepa -- therapeutic use KW - Treatment Outcome KW - Methotrexate -- therapeutic use KW - Thiotepa -- administration & dosage KW - Follow-Up Studies KW - Methotrexate -- administration & dosage KW - Female KW - Male KW - Remission Induction KW - Central Nervous System Neoplasms -- radiotherapy KW - Central Nervous System Neoplasms -- drug therapy KW - Lymphoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Lymphoma -- radiotherapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516722335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurology&rft.atitle=MATILDE+chemotherapy+regimen+for+primary+CNS+lymphoma%3A+results+at+a+median+follow-up+of+12+years.&rft.au=Ferreri%2C+Andr%C3%A9s+J+M%3BCiceri%2C+Fabio%3BBrandes%2C+Alba+A%3BMontanari%2C+Mauro%3BBalzarotti%2C+Monica%3BSpina%2C+Michele%3BIlariucci%2C+Fiorella%3BZaja%2C+Francesco%3BStelitano%2C+Caterina%3BBobbio%2C+Flavio%3BCorazzelli%2C+Gaetano%3BBaldini%2C+Luca%3BReni%2C+Michele&rft.aulast=Ferreri&rft.aufirst=Andr%C3%A9s+J&rft.date=2014-04-15&rft.volume=82&rft.issue=15&rft.spage=1370&rft.isbn=&rft.btitle=&rft.title=Neurology&rft.issn=1526-632X&rft_id=info:doi/10.1212%2FWNL.0000000000000314 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-09 N1 - Date created - 2014-04-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: Neurology. 2014 Apr 15;82(15):1373 [24634452] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1212/WNL.0000000000000314 ER - TY - CPAPER T1 - How to approach networking T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541355152; 6287661 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Wiest, Jonathan Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Networking UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541355152?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=How+to+approach+networking&rft.au=Wiest%2C+Jonathan&rft.aulast=Wiest&rft.aufirst=Jonathan&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Funding opportunities and resources from the NCI's Physical Sciences in Oncology Initiative T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541355125; 6287739 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Hanlon, Sean Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Financing KW - Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541355125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Funding+opportunities+and+resources+from+the+NCI%27s+Physical+Sciences+in+Oncology+Initiative&rft.au=Hanlon%2C+Sean&rft.aulast=Hanlon&rft.aufirst=Sean&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - NCI-supported tobacco research priorities T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541355117; 6287672 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Croyle, Robert Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Tobacco KW - Priorities UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541355117?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=NCI-supported+tobacco+research+priorities&rft.au=Croyle%2C+Robert&rft.aulast=Croyle&rft.aufirst=Robert&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - How to Write a CV T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541355107; 6287604 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Wiest, Jonathan Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541355107?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=How+to+Write+a+CV&rft.au=Wiest%2C+Jonathan&rft.aulast=Wiest&rft.aufirst=Jonathan&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - T cell biology: From the bench to the bedside T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541355033; 6287179 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Mackall, Crystal Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Lymphocytes T KW - Cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541355033?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=T+cell+biology%3A+From+the+bench+to+the+bedside&rft.au=Mackall%2C+Crystal&rft.aulast=Mackall&rft.aufirst=Crystal&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - NCI Genomics Data Commons T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354959; 6287477 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Zenklusen, Jean Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Data processing KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354959?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=NCI+Genomics+Data+Commons&rft.au=Zenklusen%2C+Jean&rft.aulast=Zenklusen&rft.aufirst=Jean&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - CPTAC: Proteomic resources for cancer research T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354890; 6287741 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Kinsinger, Christopher Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - proteomics KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354890?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=CPTAC%3A+Proteomic+resources+for+cancer+research&rft.au=Kinsinger%2C+Christopher&rft.aulast=Kinsinger&rft.aufirst=Christopher&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Cell-based therapies, cytokines T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354848; 6287206 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Mackall, Crystal Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Therapy KW - Cytokines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354848?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Cell-based+therapies%2C+cytokines&rft.au=Mackall%2C+Crystal&rft.aulast=Mackall&rft.aufirst=Crystal&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - The NCI Cancer Genomics Cloud Pilots T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354815; 6287478 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Davidsen, Tanja Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Clouds KW - Pilots KW - genomics KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354815?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=The+NCI+Cancer+Genomics+Cloud+Pilots&rft.au=Davidsen%2C+Tanja&rft.aulast=Davidsen&rft.aufirst=Tanja&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Developing novel therapies for rare tumors T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354805; 6287574 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Kummar, Shivaani Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Therapy KW - Tumors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354805?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Developing+novel+therapies+for+rare+tumors&rft.au=Kummar%2C+Shivaani&rft.aulast=Kummar&rft.aufirst=Shivaani&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Why Cancer Research Needs You T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354800; 6287895 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Springfield, Sanya Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354800?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Why+Cancer+Research+Needs+You&rft.au=Springfield%2C+Sanya&rft.aulast=Springfield&rft.aufirst=Sanya&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - The role of the tumor microenvironment in mantle cell lymphoma T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354743; 6287626 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Wiestner, Adrian Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - mantle cell lymphoma KW - Microenvironments KW - Tumors KW - Lymphoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354743?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=The+role+of+the+tumor+microenvironment+in+mantle+cell+lymphoma&rft.au=Wiestner%2C+Adrian&rft.aulast=Wiestner&rft.aufirst=Adrian&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Systemic influence of the gut microbiota on inflammation and immunity: Modulation of the response to antitumor therapy T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354681; 6287236 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Trinchieri, Giorgio Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Digestive tract KW - Therapy KW - Immunity KW - Inflammation KW - Antitumor activity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354681?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Systemic+influence+of+the+gut+microbiota+on+inflammation+and+immunity%3A+Modulation+of+the+response+to+antitumor+therapy&rft.au=Trinchieri%2C+Giorgio&rft.aulast=Trinchieri&rft.aufirst=Giorgio&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Targeting the Genetic and Metabolic Basis of Cancer T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354665; 6287588 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Linehan, W Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Targeting+the+Genetic+and+Metabolic+Basis+of+Cancer&rft.au=Linehan%2C+W&rft.aulast=Linehan&rft.aufirst=W&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Ongoing and planned genomicbased trials T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354540; 6287326 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Doroshow, James Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354540?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Ongoing+and+planned+genomicbased+trials&rft.au=Doroshow%2C+James&rft.aulast=Doroshow&rft.aufirst=James&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - NCI's Alliance for Nanotechnology in Cancer Program and resources for cancer nanotechnology research T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354526; 6287740 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Morris, Stephanie Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Cancer KW - nanotechnology KW - Nanotechnology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354526?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=NCI%27s+Alliance+for+Nanotechnology+in+Cancer+Program+and+resources+for+cancer+nanotechnology+research&rft.au=Morris%2C+Stephanie&rft.aulast=Morris&rft.aufirst=Stephanie&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Research Funding for New Investigators and Fellowship Opportunities: Postdoctoral Level T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354458; 6287867 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Marino, Pamela Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Financing KW - Fellowships UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354458?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Research+Funding+for+New+Investigators+and+Fellowship+Opportunities%3A+Postdoctoral+Level&rft.au=Marino%2C+Pamela&rft.aulast=Marino&rft.aufirst=Pamela&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Development of effective therapies for neurofibromatosis type 1-related tumors T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354439; 6287575 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Widemann, Brigitte Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Therapy KW - Tumors KW - Neurofibromatosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354439?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Development+of+effective+therapies+for+neurofibromatosis+type+1-related+tumors&rft.au=Widemann%2C+Brigitte&rft.aulast=Widemann&rft.aufirst=Brigitte&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Integrating model systems into rare tumor research T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354434; 6287576 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Reilly, Karlyne Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Tumors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354434?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Integrating+model+systems+into+rare+tumor+research&rft.au=Reilly%2C+Karlyne&rft.aulast=Reilly&rft.aufirst=Karlyne&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Value of collecting normal tissue T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354395; 6287333 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Figueroa, Jonine Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354395?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Value+of+collecting+normal+tissue&rft.au=Figueroa%2C+Jonine&rft.aulast=Figueroa&rft.aufirst=Jonine&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Overview of the Innovation Molecular Analysis Technologies (IMAT) Program T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354372; 6287737 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Dickherber, Anthony Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Reviews KW - Technology KW - Innovations UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354372?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Overview+of+the+Innovation+Molecular+Analysis+Technologies+%28IMAT%29+Program&rft.au=Dickherber%2C+Anthony&rft.aulast=Dickherber&rft.aufirst=Anthony&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - The Cancer Genome Atlas (TCGA): A primer on accessing the data T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354338; 6287392 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Zenklusen, Jean Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Genomes KW - Data processing KW - Atlases KW - Primers KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354338?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=The+Cancer+Genome+Atlas+%28TCGA%29%3A+A+primer+on+accessing+the+data&rft.au=Zenklusen%2C+Jean&rft.aulast=Zenklusen&rft.aufirst=Jean&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Recombinant Immunotoxins: From Conception to Clinical Reality in Mesothelioma and Leukemia T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354297; 6287585 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Pastan, Ira Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Recombinants KW - Leukemia KW - mesothelioma KW - Mesothelioma KW - Immunotoxins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Recombinant+Immunotoxins%3A+From+Conception+to+Clinical+Reality+in+Mesothelioma+and+Leukemia&rft.au=Pastan%2C+Ira&rft.aulast=Pastan&rft.aufirst=Ira&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Grantsmanship: Junior Faculty T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354274; 6287860 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Ogunbiyi, Peter Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354274?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Grantsmanship%3A+Junior+Faculty&rft.au=Ogunbiyi%2C+Peter&rft.aulast=Ogunbiyi&rft.aufirst=Peter&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - The curative potential of T cell transfer therapy for patients with cancer T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354244; 6287593 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Rosenberg, Steven Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Lymphocytes T KW - Therapy KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354244?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=The+curative+potential+of+T+cell+transfer+therapy+for+patients+with+cancer&rft.au=Rosenberg%2C+Steven&rft.aulast=Rosenberg&rft.aufirst=Steven&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - What's happening in the NCI Office of Cancer Genomics T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354238; 6287738 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Guidry Auvil, Jaime Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - genomics KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354238?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=What%27s+happening+in+the+NCI+Office+of+Cancer+Genomics&rft.au=Guidry+Auvil%2C+Jaime&rft.aulast=Guidry+Auvil&rft.aufirst=Jaime&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - NCI's Provocative Questions Initiative: Program review and evaluation T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354225; 6287834 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Greenspan, Emily Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=NCI%27s+Provocative+Questions+Initiative%3A+Program+review+and+evaluation&rft.au=Greenspan%2C+Emily&rft.aulast=Greenspan&rft.aufirst=Emily&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Mechanisms that maintain genome stability T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354191; 6287434 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Nussenzweig, Andre Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Genomes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354191?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Mechanisms+that+maintain+genome+stability&rft.au=Nussenzweig%2C+Andre&rft.aulast=Nussenzweig&rft.aufirst=Andre&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - New lymphoma therapies based on functional and structural genomics T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541354153; 6287420 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Staudt, Louis Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Structure-function relationships KW - Therapy KW - genomics KW - Lymphoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541354153?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=New+lymphoma+therapies+based+on+functional+and+structural+genomics&rft.au=Staudt%2C+Louis&rft.aulast=Staudt&rft.aufirst=Louis&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - TCGA initiative data overview T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353997; 6287951 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Zenklusen, Jean Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Data processing KW - Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353997?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=TCGA+initiative+data+overview&rft.au=Zenklusen%2C+Jean&rft.aulast=Zenklusen&rft.aufirst=Jean&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Translating genomics into theranostics for patients with pediatric cancers T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353880; 6287961 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Khan, Javed Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Pediatrics KW - genomics KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353880?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Translating+genomics+into+theranostics+for+patients+with+pediatric+cancers&rft.au=Khan%2C+Javed&rft.aulast=Khan&rft.aufirst=Javed&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Future directions for the discovery and characterization of the spectrum of cancer susceptibility variants T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353853; 6287969 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Chanock, Stephen Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353853?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Future+directions+for+the+discovery+and+characterization+of+the+spectrum+of+cancer+susceptibility+variants&rft.au=Chanock%2C+Stephen&rft.aulast=Chanock&rft.aufirst=Stephen&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Accessing TARGET genomics data T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353737; 6287950 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Davidsen, Tanja Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Data processing KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353737?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Accessing+TARGET+genomics+data&rft.au=Davidsen%2C+Tanja&rft.aulast=Davidsen&rft.aufirst=Tanja&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Cell therapy targeting unique cancer mutations T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353637; 6288054 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Rosenberg, Steven Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Therapy KW - Mutation KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353637?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Cell+therapy+targeting+unique+cancer+mutations&rft.au=Rosenberg%2C+Steven&rft.aulast=Rosenberg&rft.aufirst=Steven&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Development of novel combination targeted therapies for pediatric sarcomas T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353512; 6288165 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Helman, Lee Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Pediatrics KW - Therapy KW - Sarcoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353512?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Development+of+novel+combination+targeted+therapies+for+pediatric+sarcomas&rft.au=Helman%2C+Lee&rft.aulast=Helman&rft.aufirst=Lee&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Integration of Cancer Epidemiology and Biomarkers in Precision Cancer Medicine T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353314; 6288035 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Harris, Curtis Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Bioindicators KW - Integration KW - Epidemiology KW - Biomarkers KW - biomarkers KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353314?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Integration+of+Cancer+Epidemiology+and+Biomarkers+in+Precision+Cancer+Medicine&rft.au=Harris%2C+Curtis&rft.aulast=Harris&rft.aufirst=Curtis&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Translational control and tumor stem cell radio response T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353309; 6288184 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Tofilon, Philip Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Translation KW - Stem cells KW - Radio KW - Tumors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353309?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Translational+control+and+tumor+stem+cell+radio+response&rft.au=Tofilon%2C+Philip&rft.aulast=Tofilon&rft.aufirst=Philip&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Building highly effective antitumor T cells T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353253; 6288001 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Restifo, Nicholas Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Lymphocytes T KW - Antitumor activity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353253?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Building+highly+effective+antitumor+T+cells&rft.au=Restifo%2C+Nicholas&rft.aulast=Restifo&rft.aufirst=Nicholas&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Chimeric Antigen Receptor-Based Immunotherapy for Pediatric Cancer: Progress and Challenges T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353228; 6288137 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Mackall, Crystal Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Antigens KW - Pediatrics KW - Immunotherapy KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353228?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Chimeric+Antigen+Receptor-Based+Immunotherapy+for+Pediatric+Cancer%3A+Progress+and+Challenges&rft.au=Mackall%2C+Crystal&rft.aulast=Mackall&rft.aufirst=Crystal&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Racial disparities and genetics of prostate cancer T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353225; 6288155 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Cook, Michael Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Genetics KW - Prostate cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Racial+disparities+and+genetics+of+prostate+cancer&rft.au=Cook%2C+Michael&rft.aulast=Cook&rft.aufirst=Michael&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - CPAPER T1 - Establishing standards such that cross-platform comparisons and validations can be undertaken to validate variants T2 - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AN - 1541353196; 6288030 JF - 105th Annual Meeting of the American Association for Cancer Research (AACR 2014) AU - Williams, Mickey Y1 - 2014/04/05/ PY - 2014 DA - 2014 Apr 05 KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541353196?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.atitle=Establishing+standards+such+that+cross-platform+comparisons+and+validations+can+be+undertaken+to+validate+variants&rft.au=Williams%2C+Mickey&rft.aulast=Williams&rft.aufirst=Mickey&rft.date=2014-04-05&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=105th+Annual+Meeting+of+the+American+Association+for+Cancer+Research+%28AACR+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aacr.org/home/scientists/meetings--workshops/aacr-annual-meeting-2014/program.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-27 N1 - Last updated - 2014-06-30 ER - TY - JOUR T1 - Cooking Methods and Esophageal Squamous Cell Carcinoma in High-Risk Areas of Iran AN - 1524403555; 19629836 AB - Cooking methods have been implicated in the etiology of gastrointestinal cancers, reflecting exposure to potential carcinogens as results of cooking. We used a validated food frequency questionnaire and a pretested cooking method questionnaire in 3 groups: 40 esophageal squamous cell carcinoma (ESCC) cases from a high-risk area in northeast of Iran, 40 healthy subjects from the same high-risk area, and 40 healthy subjects from a low-risk area in Southern Iran. We compared the frequency of boiling, grilling, and frying, and the frying score among these 3 groups. We also calculated "frying index" by multiplying the frequency of each fried food item by its frying score. Mean frying to boiling ratios were 18.2:1, 12.8:1, and 2.6:1 for cases, high-risk controls, and low-risk controls, respectively (P < 0.01). Reuse of cooking oil for frying was reported in 37.5% of the ESCC cases, 25% of high-risk controls, and 7.5% of low-risk controls (P < 0.001). Frying index was higher in the high-risk than in the low-risk controls (P < 0.001) and in cases than in the high-risk controls (P < 0.05) after adjusting for smoking, opium use, rural residence, education, and ethnicity. High-temperature cooking and frying may be associated with increased risk of ESCC in high-risk areas. JF - Nutrition and Cancer AU - Hakami, Roya AU - Etemadi, Arash AU - Kamangar, Farin AU - Pourshams, Akram AU - Mohtadinia, Javad AU - Firoozi, Mehdi Saberi AU - Birkett, Nicholas AU - Boffetta, Paolo AU - Dawsey, Sanford M AU - Malekzadeh, Reza AD - Digestive Disease Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran, arash.etemadi@nih.gov Y1 - 2014/04/03/ PY - 2014 DA - 2014 Apr 03 SP - 500 EP - 505 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 66 IS - 3 SN - 0163-5581, 0163-5581 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Iran KW - Health risks KW - Smoking KW - Education KW - Etiology KW - Cooking KW - Carcinogens KW - Cancer KW - Ethnic groups KW - Rural areas 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/1524403555?accountid=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=Cooking+Methods+and+Esophageal+Squamous+Cell+Carcinoma+in+High-Risk+Areas+of+Iran&rft.au=Hakami%2C+Roya%3BEtemadi%2C+Arash%3BKamangar%2C+Farin%3BPourshams%2C+Akram%3BMohtadinia%2C+Javad%3BFiroozi%2C+Mehdi+Saberi%3BBirkett%2C+Nicholas%3BBoffetta%2C+Paolo%3BDawsey%2C+Sanford+M%3BMalekzadeh%2C+Reza&rft.aulast=Hakami&rft.aufirst=Roya&rft.date=2014-04-03&rft.volume=66&rft.issue=3&rft.spage=500&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+Cancer&rft.issn=01635581&rft_id=info:doi/10.1080%2F01635581.2013.779384 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Smoking; Health risks; Etiology; Education; Cooking; Carcinogens; Ethnic groups; Cancer; Rural areas; Iran DO - http://dx.doi.org/10.1080/01635581.2013.779384 ER - TY - JOUR T1 - Human metabolic correlates of body mass index AN - 1709172176; 19348156 AB - A high body mass index (BMI) is a major risk factor for several chronic diseases, but the biology underlying these associations is not well-understood. Dyslipidemia, inflammation, and elevated levels of growth factors and sex steroid hormones explain some of the increased disease risk, but other metabolic factors not yet identified may also play a role. In order to discover novel metabolic biomarkers of BMI, we used non-targeted metabolomics to assay 317 metabolites in blood samples from 947 participants and examined the cross-sectional associations between metabolite levels and BMI. Participants were from three studies in the United States and China. Height, weight, and potential confounders were ascertained by questionnaire (US studies) or direct measurement (Chinese study). Metabolite levels were measured using liquid-phase chromatography and gas chromatography coupled with mass spectrometry. We evaluated study-specific associations using linear regression, adjusted for age, gender, and smoking, and we estimated combined associations using random effects meta-analysis. The meta-analysis revealed 37 metabolites significantly associated with BMI, including 19 lipids, 12 amino acids, and 6 others, at the Bonferroni significance threshold (P 0.05). In total, 110 metabolites were associated with BMI at the P < 0.05 level. These findings establish a baseline for the BMI metabolome, and suggest new targets for researchers attempting to clarify mechanistic links between BMI and disease risk. JF - Metabolomics AU - Moore, Steven C AU - Matthews, Charles E AU - Sampson, Joshua N AU - Stolzenberg-Solomon, Rachael Z AU - Zheng, Wei AU - Cai, Qiuyin AU - Tan, Yu Ting AU - Chow, Wong-Ho AU - Ji, Bu-Tian AU - Liu, Da Ke AU - Xiao, Qian AU - Boca, Simina M AU - Leitzmann, Michael F AU - Yang, Gong AU - Xiang, Yong Bing AU - Sinha, Rashmi AU - Shu, Xiao Ou AU - Cross, Amanda J AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, 9609 Medical Center Drive, Rockville, MD, 20850, USA, moorest@mail.nih.gov Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 259 EP - 269 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 10 IS - 2 SN - 1573-3882, 1573-3882 KW - Biotechnology and Bioengineering Abstracts KW - Inventories KW - Amino acids KW - Lipids KW - Metabolites KW - Steroid hormones KW - biomarkers KW - Mass spectroscopy KW - Inflammation KW - Smoking KW - Histidine KW - Reviews KW - Risk factors KW - Oxidation KW - Dyslipidemia KW - Fatty acids KW - Neurotransmitters KW - Body mass index KW - metabolomics KW - Sex KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709172176?accountid=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=Metabolomics&rft.atitle=Human+metabolic+correlates+of+body+mass+index&rft.au=Moore%2C+Steven+C%3BMatthews%2C+Charles+E%3BSampson%2C+Joshua+N%3BStolzenberg-Solomon%2C+Rachael+Z%3BZheng%2C+Wei%3BCai%2C+Qiuyin%3BTan%2C+Yu+Ting%3BChow%2C+Wong-Ho%3BJi%2C+Bu-Tian%3BLiu%2C+Da+Ke%3BXiao%2C+Qian%3BBoca%2C+Simina+M%3BLeitzmann%2C+Michael+F%3BYang%2C+Gong%3BXiang%2C+Yong+Bing%3BSinha%2C+Rashmi%3BShu%2C+Xiao+Ou%3BCross%2C+Amanda+J&rft.aulast=Moore&rft.aufirst=Steven&rft.date=2014-04-01&rft.volume=10&rft.issue=2&rft.spage=259&rft.isbn=&rft.btitle=&rft.title=Metabolomics&rft.issn=15733882&rft_id=info:doi/10.1007%2Fs11306-013-0574-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 41 N1 - Last updated - 2015-09-03 N1 - SubjectsTermNotLitGenreText - Inventories; Amino acids; Lipids; Metabolites; Steroid hormones; biomarkers; Mass spectroscopy; Inflammation; Smoking; Risk factors; Reviews; Histidine; Dyslipidemia; Oxidation; Fatty acids; Neurotransmitters; Body mass index; metabolomics; Sex DO - http://dx.doi.org/10.1007/s11306-013-0574-1 ER - TY - JOUR T1 - Targeting the Splicing of mRNA in Autoimmune Diseases: BAFF Inhibition in Sjogren's Syndrome as a Proof of Concept AN - 1673390604; PQ0001372852 AB - BAFF (B-cell-activating factor of the tumor necrosis factor family), a pivotal cytokine for B-cell activation, is overexpressed by salivary gland (SG) epithelial cells in primary Sjogren's syndrome (pSS). Delta BAFF, a physiological inhibitor of BAFF, is a minor alternative splice variant of BAFF. A U7 RNA was reengineered to deliver antisense sequences targeting BAFF splice regions. A major decrease of BAFF messenger RNA (mRNA) and protein secretion, concomitantly with the increase of Delta BAFF mRNA, was observed in vitro. In vivo, SG retrograd instillation of nonobese diabetic mice by the modified U7 cloned into an adeno-associated virus vector significantly decreased BAFF protein expression and lymphocytic infiltrates and improved salivary flow. This study offers a rationale for localized therapeutic BAFF inhibition in pSS and represents a proof of concept of the interest of exon skipping in autoimmune diseases. JF - Molecular Therapy AU - Roescher, N AU - Vosters, J L AU - Alsaleh, G AU - Dreyfus, P AU - Jacques, S AU - Chiocchia, G AU - Sibilia, J AU - Tak, P P AU - Chiorini, J A AU - Mariette, X AU - Gottenberg, Jacques-Eric AD - Division of Clinical Immunology and Rheumatology, Academic Medical Center, Amsterdam, The Netherlands; Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA, jacques-eric.gottenberg@chru-strasbourg.fr Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 821 EP - 827 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 22 IS - 4 SN - 1525-0016, 1525-0016 KW - Immunology Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Epithelial cells KW - Lymphocytes B KW - Tumor necrosis factor KW - Autoimmune diseases KW - Salivary gland KW - Exon skipping KW - Adeno-associated virus KW - Alternative splicing KW - mRNA KW - Diabetes mellitus KW - Expression vectors KW - Sjogren's syndrome KW - Antisense KW - Cytokines KW - BLyS protein KW - W 30905:Medical Applications KW - F 06960:Molecular Immunology KW - N 14830:RNA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673390604?accountid=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=Targeting+the+Splicing+of+mRNA+in+Autoimmune+Diseases%3A+BAFF+Inhibition+in+Sjogren%27s+Syndrome+as+a+Proof+of+Concept&rft.au=Roescher%2C+N%3BVosters%2C+J+L%3BAlsaleh%2C+G%3BDreyfus%2C+P%3BJacques%2C+S%3BChiocchia%2C+G%3BSibilia%2C+J%3BTak%2C+P+P%3BChiorini%2C+J+A%3BMariette%2C+X%3BGottenberg%2C+Jacques-Eric&rft.aulast=Roescher&rft.aufirst=N&rft.date=2014-04-01&rft.volume=22&rft.issue=4&rft.spage=821&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2013.275 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Epithelial cells; Lymphocytes B; Tumor necrosis factor; Autoimmune diseases; Salivary gland; Exon skipping; mRNA; Alternative splicing; Sjogren's syndrome; Expression vectors; Diabetes mellitus; Antisense; Cytokines; BLyS protein; Adeno-associated virus DO - http://dx.doi.org/10.1038/mt.2013.275 ER - TY - JOUR T1 - Rational development of radiopharmaceuticals for HIV-1 AN - 1668264864; 20136170 AB - The global battle against HIV-1 would benefit from a sensitive and specific radiopharmaceutical to localize HIV-infected cells. Ideally, this probe would be able to identify latently infected host cells containing replication competent HIV sequences. Clinical and research applications would include assessment of reservoirs, informing clinical management by facilitating assessment of burden of infection in different compartments, monitoring disease progression and monitoring response to therapy. A "rational" development approach could facilitate efficient identification of an appropriate targeted radiopharmaceutical. Rational development starts with understanding characteristics of the disease that can be effectively targeted and then engineering radiopharmaceuticals to hone in on an appropriate target, which in the case of HIV-1 (HIV) might be an HIV-specific product on or in the host cell, a differentially expressed gene product, an integrated DNA sequence specific enzymatic activity, part of the inflammatory response, or a combination of these. This is different from the current approach that starts with a radiopharmaceutical for a target associated with a disease, mostly from autopsy studies, without a strong rationale for the potential to impact patient care. At present, no targeted therapies are available for HIV latency, although a number of approaches are under study. Here we discuss requirements for a radiopharmaceutical useful in strategies targeting persistently infected cells. The radiopharmaceutical for HIV should be developed based on HIV biology, studied in an animal model and then in humans, and ultimately used in clinical and research settings. JF - Nuclear Medicine and Biology AU - Lau, Chuen-Yen AU - Maldarelli, Frank AU - Eckelman, William C AU - Neumann, Ronald D AD - National Institutes of Health, lauc@mail.nih.gov Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 299 EP - 308 PB - Elsevier B.V., Box 882 New York NY 10159 United States VL - 41 IS - 4 SN - 0969-8051, 0969-8051 KW - Biotechnology and Bioengineering Abstracts KW - Human Immunodeficiency Virus KW - Radiopharmaceutical KW - Infectious disease imaging KW - Autopsy KW - Latent infection KW - Replication KW - Nucleotide sequence KW - Animal models KW - Probes KW - Infection KW - Inflammation KW - Human immunodeficiency virus KW - Human immunodeficiency virus 1 KW - Radioisotopes KW - Pharmaceuticals KW - Nuclear medicine KW - Enzymatic activity KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668264864?accountid=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=Nuclear+Medicine+and+Biology&rft.atitle=Rational+development+of+radiopharmaceuticals+for+HIV-1&rft.au=Lau%2C+Chuen-Yen%3BMaldarelli%2C+Frank%3BEckelman%2C+William+C%3BNeumann%2C+Ronald+D&rft.aulast=Lau&rft.aufirst=Chuen-Yen&rft.date=2014-04-01&rft.volume=41&rft.issue=4&rft.spage=299&rft.isbn=&rft.btitle=&rft.title=Nuclear+Medicine+and+Biology&rft.issn=09698051&rft_id=info:doi/10.1016%2Fj.nucmedbio.2014.01.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Latent infection; Autopsy; Replication; Nucleotide sequence; Probes; Animal models; Radioisotopes; Nuclear medicine; Pharmaceuticals; Enzymatic activity; Infection; Inflammation; Human immunodeficiency virus; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1016/j.nucmedbio.2014.01.005 ER - TY - JOUR T1 - Ebola virus vaccines: an overview of current approaches AN - 1668264148; PQ0001123777 AB - Ebola hemorrhagic fever is one of the most fatal viral diseases worldwide affecting humans and nonhuman primates. Although infections only occur frequently in Central Africa, the virus has the potential to spread globally and is classified as a category A pathogen that could be misused as a bioterrorism agent. As of today there is no vaccine or treatment licensed to counteract Ebola virus infections. DNA, subunit and several viral vector approaches, replicating and non-replicating, have been tested as potential vaccine platforms and their protective efficacy has been evaluated in nonhuman primate models for Ebola virus infections, which closely resemble disease progression in humans. Though these vaccine platforms seem to confer protection through different mechanisms, several of them are efficacious against lethal disease in nonhuman primates attesting that vaccination against Ebola virus infections is feasible. JF - Expert Review of Vaccines AU - Marzi, Andrea AU - Feldmann, Heinz AD - Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, Montana 59840, MT, USA Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 521 EP - 531 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 13 IS - 4 SN - 1476-0584, 1476-0584 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - animal model KW - Ebola virus KW - filovirus KW - prophylaxis KW - vaccine KW - bioterrorism KW - Disasters KW - Animal models KW - Pathogens KW - Bioterrorism KW - Infection KW - Primates KW - Viral diseases KW - Reviews KW - DNA KW - Africa KW - Hemorrhagic fever KW - Vaccines KW - H 4000:Food and Drugs KW - V 22400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668264148?accountid=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=Expert+Review+of+Vaccines&rft.atitle=Ebola+virus+vaccines%3A+an+overview+of+current+approaches&rft.au=Marzi%2C+Andrea%3BFeldmann%2C+Heinz&rft.aulast=Marzi&rft.aufirst=Andrea&rft.date=2014-04-01&rft.volume=13&rft.issue=4&rft.spage=521&rft.isbn=&rft.btitle=&rft.title=Expert+Review+of+Vaccines&rft.issn=14760584&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 77 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - bioterrorism; Reviews; Animal models; Hemorrhagic fever; Pathogens; Vaccines; Infection; Viral diseases; DNA; Disasters; Bioterrorism; Primates; Ebola virus; Africa ER - TY - JOUR T1 - Transient Increase of Interferon-Stimulated Genes and No Clinical Benefit by Chloroquine Treatment During Acute Simian Immunodeficiency Virus Infection of Macaques AN - 1635021473; 21057628 AB - Simian immunodeficiency virus (SIV) infection leads to AIDS in experimentally infected Rhesus macaques similarly to HIV-infected humans. In contrast, SIV infection of natural hosts is characterized by a down-regulation of innate acute responses to the vims within a few weeks of infection and results in limited pathology. Chloroquine (CQ) has been used in the treatment or prevention of malaria AIDS has recently been shown to cause a decrease of immune activation and CD4 cell loss in HIV-induced individuals treated with antiretroviral therapy. Here, we treated Rhesus macaques with CQ during the acute phase of SIV sub(mac251) infection with the intent to decrease viral-induced immune activation and possibly limit disease progression. Contrary to what was expected, CQ treatment resulted in a temporary increased expression of interferon (IFN)-stimulating genes and it worsened the recovery of CD4 super(+) T cells in the blood. Our findings confirm recent results observed in asymptomatic HIV-infected patients and suggest that CQ does not provide an obvious benefit in the absence of antiretroviral therapy. JF - AIDS Research and Human Retroviruses AU - Vaccari, Monica AU - Fenizia, Claudio AU - Ma, Zhong-Min AU - Hryniewicz, Anna AU - Boasso, Adriano AU - Doster, Melvin N AU - Miller, Christopher J AU - Lindegardh, Niklas AU - Tarning, Joel AU - Landay, Alan L AU - Shearer, Gene M AU - Franchini, Genoveffa AD - Animal Models and Retroviral Vaccines Section, NCI, NIH, Bethesda, Maryland Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 355 EP - 362 PB - Mary Ann Liebert, Inc., 140 Huguenot Street New Rochelle NY 10801 United States VL - 30 IS - 4 SN - 0889-2229, 0889-2229 KW - Genetics Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts; Virology & AIDS Abstracts KW - Acquired immune deficiency syndrome KW - Human diseases KW - Pathology KW - antiretroviral therapy KW - Disease control KW - Therapy KW - Chloroquine KW - Malaria KW - Hosts KW - Infection KW - Swine influenza virus KW - Public health KW - Blood KW - Interferon KW - CD4 antigen KW - Retrovirus KW - Genes KW - Human immunodeficiency virus KW - Lymphocytes T KW - Macaca mulatta KW - Immune response KW - Simian immunodeficiency virus KW - V 22360:AIDS and HIV KW - Q1 08484:Species interactions: parasites and diseases KW - G 07730:Development & Cell Cycle 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/1635021473?accountid=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=AIDS+Research+and+Human+Retroviruses&rft.atitle=Transient+Increase+of+Interferon-Stimulated+Genes+and+No+Clinical+Benefit+by+Chloroquine+Treatment+During+Acute+Simian+Immunodeficiency+Virus+Infection+of+Macaques&rft.au=Vaccari%2C+Monica%3BFenizia%2C+Claudio%3BMa%2C+Zhong-Min%3BHryniewicz%2C+Anna%3BBoasso%2C+Adriano%3BDoster%2C+Melvin+N%3BMiller%2C+Christopher+J%3BLindegardh%2C+Niklas%3BTarning%2C+Joel%3BLanday%2C+Alan+L%3BShearer%2C+Gene+M%3BFranchini%2C+Genoveffa&rft.aulast=Vaccari&rft.aufirst=Monica&rft.date=2014-04-01&rft.volume=30&rft.issue=4&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/10.1089%2Faid.2013.0218 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Human diseases; Genes; Pathology; Therapy; Disease control; Malaria; Hosts; Public health; Interferon; Blood; CD4 antigen; Acquired immune deficiency syndrome; antiretroviral therapy; Lymphocytes T; Chloroquine; Immune response; Infection; Retrovirus; Human immunodeficiency virus; Macaca mulatta; Swine influenza virus; Simian immunodeficiency virus DO - http://dx.doi.org/10.1089/aid.2013.0218 ER - TY - JOUR T1 - Impact of Socio-Economic Status in Meeting the Needs of People with Mental Illness; Human Rights Perspective AN - 1559003765; 201407068 AB - The present descriptive study investigated the impact of socio-economic status in meeting the human rights needs among randomly selected recovered psychiatric patients (n = 100) at a tertiary care center. Data was collected through face to face interview, using structured Needs Assessment Questionnaire. The findings revealed that the participants from below poverty line were deprived of physical needs such as 'electricity facilities' (X 2 = 6.821, p < .009) 'safe drinking water' (X 2 = 13.506, p < .004) and purchasing medications (X 2 = 9.958, p < .019). Conversely, participants from above poverty line were dissatisfied in emotional needs dimension i.e. 'commenting on physical appearance (X 2 = 8.337, p < .040), afraid of family members (X 2 = 17.809, p < .000). Thus, there is an urgent need to implement mental illness awareness campaigns and government should take active steps for providing employment, disability pension, free housing, free treatment and free transportation service for people with mental illness to attend hospital or rehabilitation centres. Adapted from the source document. JF - Community Mental Health Journal AU - Vijayalakshmi, Poreddi AU - Ramachandra, Ramachandra AU - Reddemma, Konduru AU - Math, Suresh Bada AD - Department of Nursing, College of Nursing, National Institute of Mental Health and Neuro Sciences, Deemed University, Bangalore, 560 029, India pvijayalakshmireddy@gmail.com Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 245 EP - 250 PB - Springer, Dordrecht The Netherlands VL - 50 IS - 3 SN - 0010-3853, 0010-3853 KW - Consciousness KW - Physically Handicapped KW - Purchasing KW - Poverty KW - Socioeconomic Status KW - Disadvantaged KW - Water Supply KW - Mental Illness KW - Human Rights KW - article KW - 6142: mental & emotional health problems UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1559003765?accountid=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=Community+Mental+Health+Journal&rft.atitle=Impact+of+Socio-Economic+Status+in+Meeting+the+Needs+of+People+with+Mental+Illness%3B+Human+Rights+Perspective&rft.au=Vijayalakshmi%2C+Poreddi%3BRamachandra%2C+Ramachandra%3BReddemma%2C+Konduru%3BMath%2C+Suresh+Bada&rft.aulast=Vijayalakshmi&rft.aufirst=Poreddi&rft.date=2014-04-01&rft.volume=50&rft.issue=3&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Community+Mental+Health+Journal&rft.issn=00103853&rft_id=info:doi/10.1007%2Fs10597-012-9577-z LA - English DB - Social Services Abstracts N1 - Date revised - 2014-09-01 N1 - Number of references - 41 N1 - Last updated - 2016-09-28 N1 - CODEN - CMHJAY N1 - SubjectsTermNotLitGenreText - Mental Illness; Socioeconomic Status; Human Rights; Poverty; Purchasing; Physically Handicapped; Water Supply; Consciousness; Disadvantaged DO - http://dx.doi.org/10.1007/s10597-012-9577-z ER - TY - JOUR T1 - Vocal coordination and vocal imitation: A role for mirror neurons? AN - 1558998570; 201413406 AB - Some birds and mammals have vocal communication systems in which coordination between individuals is important. Examples would include duetting or antiphonal calling in some birds and mammals, rapid exchanges of the same vocalization, and vocal exchanges between paired individuals and other nearby pairs. Mirror neurons may play a role in such systems but become functional only after experience. Adapted from the source document JF - Behavioral and Brain Sciences AU - Newman, John D AD - Laboratory of Comparative Ethology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health (NIH), Poolesville, MD 20837. jn1g@nih.gov Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 211 EP - 212 VL - 37 IS - 2 SN - 0140-525X, 0140-525X KW - Imitation (34600) KW - Animal Communication (03150) KW - Mirror Neurons (54280) KW - Communication (13600) KW - Birds (08980) KW - Drama (19750) KW - article KW - 6410: language-pathological and normal; language and speech pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1558998570?accountid=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=Behavioral+and+Brain+Sciences&rft.atitle=Vocal+coordination+and+vocal+imitation%3A+A+role+for+mirror+neurons%3F&rft.au=Newman%2C+John+D&rft.aulast=Newman&rft.aufirst=John&rft.date=2014-04-01&rft.volume=37&rft.issue=2&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Behavioral+and+Brain+Sciences&rft.issn=0140525X&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2014-09-01 N1 - Last updated - 2016-09-27 N1 - CODEN - BBSCDH N1 - SubjectsTermNotLitGenreText - Mirror Neurons (54280); Birds (08980); Animal Communication (03150); Drama (19750); Imitation (34600); Communication (13600) ER - TY - JOUR T1 - Identification of Volatile Organic Compounds Produced by Bacteria Using HS-SPME-GC-MS AN - 1551618775; 20177086 AB - The analysis of volatile organic compounds (VOCs) as a tool for bacterial identification is reported. Head space solid-phase microextraction (HSSPME) coupled to gas chromatography-mass spectrometry (GC-MS) was applied to the analysis of bacterial VOCs with the aim of determining the impact of experimental parameters on the generated VOC profiles. The effect of culture medium, SPME fiber type and GC column were fully evaluated with the Gram-negative bacteria Escherichia coli and Klebsiella pneumoniae and the Gram-positive species Staphylococcus aureus. Multivariate analysis, including cluster analysis and principal component analysis, was applied to VOC data to determine whether the parameters under investigation significantly affected bacterial VOC profiles. Culture medium, and to a lesser extent, SPME fiber type, were found to significantly alter detected bacterial VOC profiles. The detected VOCs varied little with the polarity of the GC column. The results indicate that the generated bacterial VOC profiles need careful evaluation if they are to be used for clinical diagnostics. The whole process is limited by the need to grow the bacteria in broth (18 h) before extraction and analysis (63 min). JF - Journal of Chromatographic Science AU - Tait, Emma AU - Perry, John D AU - Stanforth, Stephen P AU - Dean, John R AD - Department of Applied Sciences, Northumbria University, Ellison Building, Newcastle upon Tyne, NEI 8ST, UK, john.dean@unn.ac.uk Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 363 EP - 373 PB - Preston Publications, Inc., 6600 W. Touhy Ave. Niles IL 60714 United States VL - 52 IS - 4 SN - 0021-9665, 0021-9665 KW - Microbiology Abstracts B: Bacteriology KW - Data processing KW - Head KW - Mass spectroscopy KW - Fibers KW - Gas chromatography KW - Multivariate analysis KW - Principal components analysis KW - Gram-negative bacteria KW - Headspace KW - Escherichia coli KW - volatile organic compounds KW - Polarity KW - Staphylococcus aureus KW - Solid phase methods KW - Klebsiella pneumoniae KW - J 02320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551618775?accountid=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+Chromatographic+Science&rft.atitle=Identification+of+Volatile+Organic+Compounds+Produced+by+Bacteria+Using+HS-SPME-GC-MS&rft.au=Tait%2C+Emma%3BPerry%2C+John+D%3BStanforth%2C+Stephen+P%3BDean%2C+John+R&rft.aulast=Tait&rft.aufirst=Emma&rft.date=2014-04-01&rft.volume=52&rft.issue=4&rft.spage=363&rft.isbn=&rft.btitle=&rft.title=Journal+of+Chromatographic+Science&rft.issn=00219665&rft_id=info:doi/10.1093%2Fchromsci%2Fbmt042 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Fibers; Data processing; Head; Multivariate analysis; Gas chromatography; Gram-negative bacteria; Principal components analysis; Headspace; volatile organic compounds; Polarity; Solid phase methods; Mass spectroscopy; Escherichia coli; Staphylococcus aureus; Klebsiella pneumoniae DO - http://dx.doi.org/10.1093/chromsci/bmt042 ER - TY - JOUR T1 - Genetics and personal responsibility for health AN - 1550999669; 201430519 AB - Advances in genetic medicine may have implications for how we should think about personal responsibility for health, because they may show how it is possible to exert some control over risk factors that were previously thought as beyond the individual's control. Although we cannot control the genes that we are born with, we can often make decisions concerning genetic testing, disease prevention, and treatment. One might argue, therefore, that individuals should be treated as morally responsible for taking effective action in response to genetic risks factors, since genetically based health risks are similar to other health risks. While this argument makes sense as an abstract, philosophical position, it is not a useful guide to public policy. Given these concerns, there is little society can or should do to encourage individuals to address their genetic risk factors, other than praising those who make prudent choices. Adapted from the source document. JF - New Genetics and Society AU - Resnik, David B AD - National Institute of Environmental Health Sciences, National Institutes of Health, Box 12233, Mail Drop CU 03, Research Triangle Park, NC 27709, USA Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 113 EP - 125 PB - Routledge/Taylor & Francis, Abingdon UK VL - 33 IS - 2 SN - 1463-6778, 1463-6778 KW - Genetic Testing KW - Risk KW - Genetics KW - Prevention KW - Responsibility KW - Choices KW - Health Behavior KW - Health KW - Medical Decision Making KW - article KW - 1864: demography and human biology; genetic engineering/reproductive biotechnology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1550999669?accountid=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=New+Genetics+and+Society&rft.atitle=Genetics+and+personal+responsibility+for+health&rft.au=Resnik%2C+David+B&rft.aulast=Resnik&rft.aufirst=David&rft.date=2014-04-01&rft.volume=33&rft.issue=2&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=New+Genetics+and+Society&rft.issn=14636778&rft_id=info:doi/10.1080%2F14636778.2014.905195 LA - English DB - Sociological Abstracts N1 - Date revised - 2014-08-01 N1 - Last updated - 2016-09-28 N1 - SubjectsTermNotLitGenreText - Genetics; Health; Risk; Responsibility; Medical Decision Making; Health Behavior; Prevention; Genetic Testing; Choices DO - http://dx.doi.org/10.1080/14636778.2014.905195 ER - TY - JOUR T1 - Cancer stem cells: a systems biology view of their role in prognosis and therapy AN - 1544017127; 20150164 AB - Evidence has accumulated that characterizes highly tumorigenic cancer cells residing in heterogeneous populations. The accepted term for such a subpopulation is cancer stem cells (CSCs). While many questions still remain about their precise role in the origin, progression, and drug resistance of tumors, it is clear they exist. In this review, a current understanding of the nature of CSC, their potential usefulness in prognosis, and the need to target them will be discussed. In particular, separate studies now suggest that the CSC is plastic in its phenotype, toggling between tumorigenic and nontumorigenic states depending on both intrinsic and extrinsic conditions. Because of this, a static view of gene and protein levels defined by correlations may not be sufficient to either predict disease progression or aid in the discovery and development of drugs to molecular targets leading to cures. Quantitative dynamic modeling, a bottom up systems biology approach whereby signal transduction pathways are described by differential equations, may offer a novel means to overcome the challenges of oncology today. In conclusion, the complexity of CSCs can be captured in mathematical models that may be useful for selecting molecular targets, defining drug action, and predicting sensitivity or resistance pathways for improved patient outcomes. JF - Anti-Cancer Drugs AU - Merlins, Susan D AD - Screening Technologies Branch, Developmental Therapeutics Program, Division of Cancer Diagnosis and Treatment, National Cancer Institute at Frederick, PO Box B, Bldg. 315, Room 6, Frederick, Maryland, USA, smertins@mail.nih.gov Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 353 EP - 367 PB - Rapid Science Publishers, The Old Malthouse Oxford OX1 1LD United Kingdom VL - 25 IS - 4 SN - 0959-4973, 0959-4973 KW - Biotechnology and Bioengineering Abstracts; Oncogenes & Growth Factors Abstracts KW - cancer stem cells KW - dynamic modeling KW - plasticity KW - prognosis KW - signal transduction pathways KW - systems biology KW - therapeutics KW - Stem cells KW - Mathematical models KW - Drug resistance KW - Prognosis KW - Drug development KW - Oncology KW - Tumors KW - Plastics KW - Cancer KW - Signal transduction KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544017127?accountid=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=Anti-Cancer+Drugs&rft.atitle=Cancer+stem+cells%3A+a+systems+biology+view+of+their+role+in+prognosis+and+therapy&rft.au=Merlins%2C+Susan+D&rft.aulast=Merlins&rft.aufirst=Susan&rft.date=2014-04-01&rft.volume=25&rft.issue=4&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Anti-Cancer+Drugs&rft.issn=09594973&rft_id=info:doi/10.1097%2FCAD.0000000000000075 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-07-01 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Stem cells; Mathematical models; Drug resistance; Prognosis; Oncology; Drug development; Plastics; Tumors; Cancer; Signal transduction DO - http://dx.doi.org/10.1097/CAD.0000000000000075 ER - TY - JOUR T1 - Exploiting sensitization windows of opportunity in hyper and hypo-fractionated radiation therapy. AN - 1540117966; 24688774 AB - In contrast to the conventional radiotherapy/chemoradiotherapy paradigms used in the treatment of majority of cancer types, this review will describe two areas of radiobiology, hyperfractionated and hypofractionated radiation therapy, for cancer treatment focusing on application of novel concepts underlying these treatment modalities. The initial part of the review discusses the phenomenon of hyper-radiation sensitivity (HRS) at lower doses (0.1 to 0.6 Gy), describing the underlying mechanisms and how this could enhance the effects of chemotherapy, particularly, in hyperfractionated settings. The second part examines the radiobiological/physiological mechanisms underlying the effects of high-dose hypofractionated radiation therapy that can be exploited for tumor cure. These include abscopal/bystander effects, activation of immune system, endothelial cell death and effect of hypoxia with re-oxygenation. These biological properties along with targeted dose delivery and distribution to reduce normal tissue toxicity may make high-dose hypofractionation more effective than conventional radiation therapy for treatment of advanced cancers. The novel radiation physics based methods that take into consideration the tumor volume to be irradiated and normal tissue avoidance/tolerance can further improve treatment outcome and post-treatment quality of life. In conclusion, there is enough evidence to further explore novel avenues to exploit biological mechanisms from hyper-fractionation by enhancing the efficacy of chemotherapy and hypo-fractionated radiation therapy that could enhance tumor control and use imaging and technological advances to reduce toxicity. JF - Journal of thoracic disease AU - Prasanna, Anish AU - Ahmed, Mansoor M AU - Mohiuddin, Mohammed AU - Coleman, C Norman AD - 1 Radiation Research Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Rockville, MD, USA ; 2 Oncology Centre, King Faisal Specialist Hospital and Research Centre, Riyadh, Kingdom of Saudi Arabia. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 287 EP - 302 VL - 6 IS - 4 SN - 2072-1439, 2072-1439 KW - hyperfractionation KW - spatially fractionated GRID radiotherapy (SFGRT) KW - lattice KW - hyper-radiation sensitivity (HRS) KW - stereotactic ablative radiotherapy (SABR) KW - chemopotentiation KW - stereotactic radiosurgery (SRS) KW - induced radiation resistance (IRR) KW - Low Doses Fractionated Radiation Therapy (LDFRT) KW - stereotactic ablative radiosurgery (SARS) KW - stereotactic body radiation therapy (SBRT) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1540117966?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+thoracic+disease&rft.atitle=Exploiting+sensitization+windows+of+opportunity+in+hyper+and+hypo-fractionated+radiation+therapy.&rft.au=Prasanna%2C+Anish%3BAhmed%2C+Mansoor+M%3BMohiuddin%2C+Mohammed%3BColeman%2C+C+Norman&rft.aulast=Prasanna&rft.aufirst=Anish&rft.date=2014-04-01&rft.volume=6&rft.issue=4&rft.spage=287&rft.isbn=&rft.btitle=&rft.title=Journal+of+thoracic+disease&rft.issn=20721439&rft_id=info:doi/10.3978%2Fj.issn.2072-1439.2014.01.14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-24 N1 - Date created - 2014-04-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3978/j.issn.2072-1439.2014.01.14 ER - TY - JOUR T1 - Plasmodium genetic loci linked to host cytokine and chemokine responses AN - 1529957668; 19859602 AB - Both host and parasite factors contribute to disease severity of malaria infection; however, the molecular mechanisms responsible for the disease and the host-parasite interactions involved remain largely unresolved. To investigate the effects of parasite factors on host immune responses and pathogenesis, we measured levels of plasma cytokines/chemokines (CCs) and growth rates in mice infected with two Plasmodium yoelii strains having different virulence phenotypes and in progeny from a genetic cross of the two parasites. Quantitative trait loci (QTL) analysis linked levels of many CCs, particularly IL-1 beta , IP-10, IFN- gamma , MCP-1 and MIG, and early parasite growth rate to loci on multiple parasite chromosomes, including chromosomes 7, 9, 10, 12 and 13. Comparison of the genome sequences spanning the mapped loci revealed various candidate genes. The loci on chromosomes 7 and 13 had significant (P<0.005) additive effects on IL-1 beta , IL-5 and IP-10 responses, and the chromosome 9 and 12 loci had significant (P=0.017) interaction. Infection of knockout mice showed critical roles of MCP-1 and IL-10 in parasitemia control and host mortality. These results provide important information for a better understanding of malaria pathogenesis and can be used to examine the role of these factors in human malaria infection. JF - Genes and Immunity AU - Pattaradilokrat, S AU - Li, J AU - Wu, J AU - Qi, Y AU - Eastman, R T AU - Zilversmit, M AU - Nair, S C AU - Huaman, M C AU - Quinones, M AU - Jiang, H AU - Li, N AU - Zhu, J AU - Zhao, K AU - Kaneko, O AU - Long, C A AU - Su, X-z AD - 1] Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA [2] Department of Biology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 145 EP - 152 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 15 IS - 3 SN - 1466-4879, 1466-4879 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Genetics Abstracts; Immunology Abstracts KW - Genomes KW - gamma -Interferon KW - Molecular modelling KW - Parasites KW - Chemokines KW - Human diseases KW - Interleukin 5 KW - Interleukin 1 KW - Malaria KW - Hosts KW - Infection KW - Phenotypes KW - Interleukin 10 KW - chromosome 7 KW - Public health KW - Virulence KW - chromosome 9 KW - Chromosomes KW - IP-10 protein KW - Cytokines KW - Plasmodium yoelii KW - Host-parasite interactions KW - Growth rate KW - Mortality KW - Quantitative trait loci KW - Monocyte chemoattractant protein 1 KW - parasitemia KW - Immune response KW - Genetic crosses KW - Mortality causes KW - K 03410:Animal Diseases KW - G 07720:Immunogenetics KW - Q1 08485:Species interactions: pests and control KW - Q5 08524:Public health, medicines, dangerous organisms KW - F 06950:Immunogenetics, MHC, HLA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1529957668?accountid=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=Genes+and+Immunity&rft.atitle=Plasmodium+genetic+loci+linked+to+host+cytokine+and+chemokine+responses&rft.au=Pattaradilokrat%2C+S%3BLi%2C+J%3BWu%2C+J%3BQi%2C+Y%3BEastman%2C+R+T%3BZilversmit%2C+M%3BNair%2C+S+C%3BHuaman%2C+M+C%3BQuinones%2C+M%3BJiang%2C+H%3BLi%2C+N%3BZhu%2C+J%3BZhao%2C+K%3BKaneko%2C+O%3BLong%2C+C+A%3BSu%2C+X-z&rft.aulast=Pattaradilokrat&rft.aufirst=S&rft.date=2014-04-01&rft.volume=15&rft.issue=3&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=Genes+and+Immunity&rft.issn=14664879&rft_id=info:doi/10.1038%2Fgene.2013.74 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Growth rate; Parasites; Human diseases; Chromosomes; Malaria; Hosts; Phenotypes; Mortality causes; Public health; Genomes; Molecular modelling; Quantitative trait loci; gamma -Interferon; Mortality; Chemokines; Interleukin 5; Monocyte chemoattractant protein 1; Interleukin 1; Infection; Interleukin 10; chromosome 7; chromosome 9; Virulence; parasitemia; IP-10 protein; Cytokines; Immune response; Genetic crosses; Host-parasite interactions; Plasmodium yoelii DO - http://dx.doi.org/10.1038/gene.2013.74 ER - TY - JOUR T1 - Genetics of low spinal muscular atrophy carrier frequency in sub-Saharan Africa AN - 1529945116; 19812897 AB - Objective Spinal muscular atrophy (SMA) is one of the most common severe hereditary diseases of infancy and early childhood in North America, Europe, and Asia. SMA is usually caused by deletions of the survival motor neuron 1 (SMN1) gene. A closely related gene, SMN2, modifies the disease severity. SMA carriers have only 1 copy of SMN1 and are relatively common (1 in 30-50) in populations of European and Asian descent. SMN copy numbers and SMA carrier frequencies have not been reliably estimated in Malians and other sub-Saharan Africans. Methods We used a quantitative polymerase chain reaction assay to determine SMN1 and SMN2 copy numbers in 628 Malians, 120 Nigerians, and 120 Kenyans. We also explored possible mechanisms for SMN1 and SMN2 copy number differences in Malians, and investigated their effects on SMN mRNA and protein levels. Results The SMA carrier frequency in Malians is 1 in 209, lower than in Eurasians. Malians and other sub-Saharan Africans are more likely to have greater than or equal to 3 copies of SMN1 than Eurasians, and more likely to lack SMN2 than Europeans. There was no evidence of gene conversion, gene locus duplication, or natural selection from malaria resistance to account for the higher SMN1 copy numbers in Malians. High SMN1 copy numbers were not associated with increased SMN mRNA or protein levels in human cell lines. Interpretation SMA carrier frequencies are much lower in sub-Saharan Africans than in Eurasians. This finding is important to consider in SMA genetic counseling in individuals with black African ancestry. Ann Neurol 2014; 75:525-532 JF - Annals of Neurology AU - Sangare, Modibo AU - Hendrickson, Brant AU - Sango, Hammadoun Ali AU - Chen, Kelian AU - Nofziger, Jonathan AU - Amara, Abdelbasset AU - Dutra, Amalia AU - Schindler, Alice B AU - Guindo, Aldiouma AU - Traore, Mahamadou AU - Harmison, George AU - Pak, Evgenia AU - Yaro, Fatoumata N'Go AU - Bricceno, Katherine AU - Grunseich, Christopher AU - Chen, Guibin AU - Boehm, Manfred AU - Zukosky, Kristen AU - Bocoum, Nouhoum AU - Meilleur, Katherine G AU - Daou, Fatoumata AU - Bagayogo, Koumba AU - Coulibaly, Yaya Ibrahim AU - Diakite, Mahamadou AU - Fay, Michael P AU - Lee, Hee-Suk AU - Saad, Ali AU - Gribaa, Moez AU - Singleton, Andrew B AU - Maiga, Youssoufa AU - Auh, Sungyoung AU - Landoure, Guida AU - Fairhurst, Rick M AU - Burnett, Barrington G AU - Scholl, Thomas AU - Fischbeck, Kenneth H AD - Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 525 EP - 532 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 75 IS - 4 SN - 0364-5134, 0364-5134 KW - Genetics Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; CSA Neurosciences Abstracts KW - Cell survival KW - Human diseases KW - Nucleotide sequence KW - Malaria KW - Natural selection KW - Public health KW - Gene deletion KW - ANE, Europe KW - Polymerase chain reaction KW - spinal muscular atrophy KW - Asia KW - North America KW - SMN protein KW - Hereditary diseases KW - Children KW - Gene conversion KW - mRNA KW - copy number KW - Motor neurons KW - Neurons KW - Africa KW - Q1 08443:Population genetics KW - G 07730:Development & Cell Cycle 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/1529945116?accountid=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=Annals+of+Neurology&rft.atitle=Genetics+of+low+spinal+muscular+atrophy+carrier+frequency+in+sub-Saharan+Africa&rft.au=Sangare%2C+Modibo%3BHendrickson%2C+Brant%3BSango%2C+Hammadoun+Ali%3BChen%2C+Kelian%3BNofziger%2C+Jonathan%3BAmara%2C+Abdelbasset%3BDutra%2C+Amalia%3BSchindler%2C+Alice+B%3BGuindo%2C+Aldiouma%3BTraore%2C+Mahamadou%3BHarmison%2C+George%3BPak%2C+Evgenia%3BYaro%2C+Fatoumata+N%27Go%3BBricceno%2C+Katherine%3BGrunseich%2C+Christopher%3BChen%2C+Guibin%3BBoehm%2C+Manfred%3BZukosky%2C+Kristen%3BBocoum%2C+Nouhoum%3BMeilleur%2C+Katherine+G%3BDaou%2C+Fatoumata%3BBagayogo%2C+Koumba%3BCoulibaly%2C+Yaya+Ibrahim%3BDiakite%2C+Mahamadou%3BFay%2C+Michael+P%3BLee%2C+Hee-Suk%3BSaad%2C+Ali%3BGribaa%2C+Moez%3BSingleton%2C+Andrew+B%3BMaiga%2C+Youssoufa%3BAuh%2C+Sungyoung%3BLandoure%2C+Guida%3BFairhurst%2C+Rick+M%3BBurnett%2C+Barrington+G%3BScholl%2C+Thomas%3BFischbeck%2C+Kenneth+H&rft.aulast=Sangare&rft.aufirst=Modibo&rft.date=2014-04-01&rft.volume=75&rft.issue=4&rft.spage=525&rft.isbn=&rft.btitle=&rft.title=Annals+of+Neurology&rft.issn=03645134&rft_id=info:doi/10.1002%2Fana.24114 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Human diseases; Nucleotide sequence; Neurons; Polymerase chain reaction; Malaria; Natural selection; Public health; Cell survival; SMN protein; Hereditary diseases; Children; copy number; mRNA; Gene conversion; Motor neurons; Gene deletion; spinal muscular atrophy; North America; ANE, Europe; Africa; Asia DO - http://dx.doi.org/10.1002/ana.24114 ER - TY - JOUR T1 - Vaccination with tumor cells expressing IL-15 and IL-15R alpha inhibits murine breast and prostate cancer AN - 1524404496; 19750152 AB - A number of antitumor vaccines have recently shown promise in upregulating immune responses against tumor antigens and improving patient survival. In this study, we examine the effectiveness of vaccination using interleukin (IL)-15-expressing tumor cells and also examine their ability to upregulate immune responses to tumor antigens. We demonstrated that the coexpression of IL-15 with its receptor, IL-15R alpha , increased the cell-surface expression and secretion of IL-15. We show that a gene transfer approach using recombinant adenovirus to express IL-15 and IL-15R alpha in murine TRAMP-C2 prostate or TS/A breast tumors induced antitumor immune responses. From this, we developed a vaccine platform, consisting of TRAMP-C2 prostate cancer cells or TS/A breast cancer cells coexpressing IL-15 and IL-15R alpha that inhibited tumor formation when mice were challenged with tumor. Inhibition of tumor growth led to improved survival when compared with animals receiving cells expressing IL-15 alone or unmodified tumor cells. Animals vaccinated with tumor cells coexpressing IL-15 and IL-15R alpha showed greater tumor infiltration with CD8 super(+) T and natural killer (NK) cells, as well as increased antitumor CD8 super(+) T-cell responses. Vaccination with IL-15/IL-15R alpha -modified TS/A breast cancer cells provided a survival advantage to mice challenged with unrelated murine TUBO breast cancer cells, indicating the potential for allogeneic IL-15/IL-15R alpha -expressing vaccines. JF - Gene Therapy AU - Morris, J C AU - Ramlogan-Steel, C A AU - Yu, P AU - Black, B A AU - Mannan, P AU - Allison, J P AU - Waldmann, T A AU - Steel, J C AD - 1] Division of Hematology/Oncology, Department of Internal Medicine, University of Cincinnati, Cincinnati, OH, USA [2] Metabolism Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 393 EP - 401 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 21 IS - 4 SN - 0969-7128, 0969-7128 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Cell survival KW - Gene therapy KW - Adenovirus KW - Natural killer cells KW - CD8 antigen KW - Tumors KW - Tumor cells KW - Metastases KW - Prostate cancer KW - Interleukin 15 KW - Antigen (tumor-associated) KW - Lymphocytes T KW - Breast cancer KW - Immune response KW - Vaccines KW - Antitumor activity KW - G 07720:Immunogenetics KW - W 30905:Medical Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524404496?accountid=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=Vaccination+with+tumor+cells+expressing+IL-15+and+IL-15R+alpha+inhibits+murine+breast+and+prostate+cancer&rft.au=Morris%2C+J+C%3BRamlogan-Steel%2C+C+A%3BYu%2C+P%3BBlack%2C+B+A%3BMannan%2C+P%3BAllison%2C+J+P%3BWaldmann%2C+T+A%3BSteel%2C+J+C&rft.aulast=Morris&rft.aufirst=J&rft.date=2014-04-01&rft.volume=21&rft.issue=4&rft.spage=393&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2014.10 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-05-29 N1 - SubjectsTermNotLitGenreText - Cell survival; Gene therapy; Natural killer cells; Tumors; CD8 antigen; Tumor cells; Metastases; Prostate cancer; Interleukin 15; Antigen (tumor-associated); Lymphocytes T; Breast cancer; Vaccines; Immune response; Antitumor activity; Adenovirus DO - http://dx.doi.org/10.1038/gt.2014.10 ER - TY - JOUR T1 - Personality traits and vulnerability or resilience to substance use disorders. AN - 1522680053; 24612993 AB - Clear evidence supports a genetic basis for substance use disorders (SUD). Yet, the search to identify individual gene contributions to SUD has been unsuccessful. Here, we argue for the study of endophenotypes within the frame of individual differences, and identify three high-order personality traits that are tied to specific brain systems and genes, and that offer a tractable approach to studying SUD. These personality traits, and the genes that moderate them, interact dynamically with the environment and with the drugs themselves to determine ultimately an individual's vulnerability or resilience to developing SUD. Published by Elsevier Ltd. JF - Trends in cognitive sciences AU - Belcher, Annabelle M AU - Volkow, Nora D AU - Moeller, F Gerard AU - Ferré, Sergi AD - National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA. ; National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD 20892, USA. ; Departments of Psychiatry and Pharmacology and Toxicology, Virginia Commonwealth University School of Medicine, Richmond, VA 23219, USA. ; National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA. Electronic address: sferre@intra.nida.nih.gov. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 211 EP - 217 VL - 18 IS - 4 KW - Index Medicus KW - Humans KW - Endophenotypes KW - Personality KW - Substance-Related Disorders -- psychology KW - Substance-Related Disorders -- genetics KW - Individuality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1522680053?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cognitive+sciences&rft.atitle=Personality+traits+and+vulnerability+or+resilience+to+substance+use+disorders.&rft.au=Belcher%2C+Annabelle+M%3BVolkow%2C+Nora+D%3BMoeller%2C+F+Gerard%3BFerr%C3%A9%2C+Sergi&rft.aulast=Belcher&rft.aufirst=Annabelle&rft.date=2014-04-01&rft.volume=18&rft.issue=4&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Trends+in+cognitive+sciences&rft.issn=1879-307X&rft_id=info:doi/10.1016%2Fj.tics.2014.01.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-17 N1 - Date created - 2014-04-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Psychiatry. 2010 Jul;167(7):748-51 [20595427] Psychiatry Res. 2010 Jul 30;178(2):299-304 [20478631] Psychol Bull. 2010 Sep;136(5):768-821 [20804236] Neuron. 2011 Feb 24;69(4):680-94 [21338879] J Neurosci. 2011 Mar 30;31(13):4805-10 [21451018] Drug Alcohol Depend. 2011 May 1;115(1-2):120-30 [21145178] Annu Rev Neurosci. 2011;34:441-66 [21469956] Mol Psychiatry. 2011 Aug;16(8):818-25 [21483434] Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15037-42 [21402948] Neuroimage. 2012 Feb 1;59(3):2860-70 [21979383] Nat Neurosci. 2012 Feb;15(2):181-9 [22281715] Science. 2012 Feb 3;335(6068):601-4 [22301321] Neuroreport. 2012 Mar 7;23(4):251-4 [22257904] Nat Neurosci. 2012 Mar;15(3):358-66 [22267164] J Neurosci. 2012 May 2;32(18):6170-6 [22553023] Mol Psychiatry. 2012 Jun;17(6):650-62 [21844870] J Neurosci. 2012 May 23;32(21):7316-24 [22623677] Am J Psychiatry. 2012 Sep;169(9):926-36 [22952072] Nat Rev Neurosci. 2004 Jun;5(6):483-94 [15152198] J Pers Soc Psychol. 2000 Dec;79(6):1057-67 [11138754] Alcohol. 2000 Nov;22(3):139-46 [11163121] Behav Brain Sci. 1999 Jun;22(3):491-517; discussion 518-69 [11301519] Dev Psychol. 2001 May;37(3):283-97 [11370906] Am J Psychiatry. 2001 Nov;158(11):1783-93 [11691682] Science. 2002 Jul 19;297(5580):400-3 [12130784] Am J Psychiatry. 2003 Apr;160(4):636-45 [12668349] Science. 2003 Jul 18;301(5631):386-9 [12869766] Am J Med Genet B Neuropsychiatr Genet. 2003 Aug 15;121B(1):44-9 [12898574] Curr Opin Neurobiol. 2013 Feb;23(1):57-61 [22878161] Hum Genet. 2013 Mar;132(3):347-58 [23203481] Nat Rev Genet. 2013 Aug;14(8):549-58 [23835440] Pharmacol Ther. 2013 Dec;140(3):267-79 [23872493] Neuropharmacology. 2014 Jan;76 Pt B:498-509 [23851257] Pharmacogenomics J. 2014 Feb;14(1):70-6 [23358500] Neuron. 2012 Nov 8;76(3):470-85 [23141060] J Pers Soc Psychol. 1988 Jun;54(6):1031-9 [3397862] J Pers Soc Psychol. 1994 Sep;67(3):485-98 [7965602] J Pers Soc Psychol. 1994 Nov;67(5):898-909 [7983581] J Pers Soc Psychol. 1995 May;68(5):901-16 [7776186] J Pers. 1996 Sep;64(3):577-91 [8776880] Comput Biomed Res. 1996 Jun;29(3):162-73 [8812068] Science. 1996 Nov 29;274(5292):1527-31 [8929413] Nature. 1997 Apr 24;386(6627):830-3 [9126741] Pharmacogenetics. 1997 Dec;7(6):479-84 [9429233] Mol Psychiatry. 1998 May;3(3):256-60 [9672901] J Pers. 1999 Feb;67(1):39-65 [10030020] Biol Psychiatry. 1999 Jul 15;46(2):151-60 [10418689] Exp Neurol. 1999 Jul;158(1):214-20 [10448434] Arch Gen Psychiatry. 1999 Oct;56(10):921-6 [10530634] Trends Cogn Sci. 2004 Apr;8(4):170-7 [15050513] Biol Psychiatry. 2005 Feb 1;57(3):210-9 [15691521] Nat Neurosci. 2005 Jun;8(6):828-34 [15880108] Mol Psychiatry. 2005 Jul;10(7):686-98 [15809660] Brain Res Cogn Brain Res. 2005 Dec;25(3):851-61 [16289773] Trends Genet. 2006 Jun;22(6):306-13 [16697071] Arch Gen Psychiatry. 2006 Sep;63(9):999-1008 [16953002] Am J Psychiatry. 2007 Apr;164(4):622-9 [17403976] J Neurosci. 2007 Apr 4;27(14):3743-52 [17409238] Am J Psychiatry. 2007 Oct;164(10):1476-88 [17898336] Am J Med Genet B Neuropsychiatr Genet. 2008 Jan 5;147B(1):27-32 [17525955] Nat Genet. 2008 May;40(5):489-90 [18443579] BMC Psychiatry. 2008;8:22 [18405382] J Psychopharmacol. 2008 Mar;22(2 Suppl):12-9 [18477617] Philos Trans R Soc Lond B Biol Sci. 2008 Oct 12;363(1507):3125-35 [18640910] Philos Trans R Soc Lond B Biol Sci. 2008 Oct 12;363(1507):3223-32 [18640923] Mov Disord. 2008;23 Suppl 3:S548-59 [18781672] PLoS One. 2008;3(10):e3461 [18941515] Neuropharmacology. 2009;56 Suppl 1:3-8 [18617195] J Child Psychol Psychiatry. 2009 Jun;50(6):657-68 [19175806] J Neurosci. 2009 Sep 16;29(37):11614-8 [19759308] Neuroimage. 2010 Jan 1;49(1):963-70 [19683585] J Neurosci. 2009 Nov 25;29(47):14734-40 [19940168] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.tics.2014.01.010 ER - TY - JOUR T1 - A systematic review comparing cisplatin and carboplatin plus paclitaxel-based chemotherapy for recurrent or metastatic cervical cancer. AN - 1521913393; 24486604 AB - The prognosis of advanced/recurrent cervical cancer patients is generally poor with 1-year survival ranging between 15 and 20%. Cisplatin (CDDP) based treatments are considered the most effective regimens; unfortunately toxicity is an issue in a population in which the treatment remains palliative in the finality. Carboplatin (CBDCA), with its more favorable non toxicity profile and the convenience of outpatient administration, may be a suitable alternative to CDDP in combination regimens. We performed a systematic review of the literature comparing CDDP and CBDCA based chemotherapy for advanced cervical cancer (recurrent, persistent or metastatic disease). Only studies that met the following criteria were considered for the present review: 1) patients treated with CDDP/paclitaxel or CBDCA/paclitaxel combinations as first line chemotherapy for metastatic disease; 2) one or more of the following data available: overall response rate (RR), progression free survival (PFS) or time to progression (TTP), overall survival (OS); 3) single-arm retrospective or prospective study; and 4) at least 20 patients enrolled. 17 eligible studies comprehensive of 1181 patients were included in the final analysis. The objective RR was 48.5% for CBDCA and 49.3% for CDDP-based chemotherapy. Median PFS for CDDP and CBDCA-based treatments was 6.9months and 5months respectively (p=0.03); the corresponding figures for median OS were 12.87 and 10months respectively (p=0.17). Our study indicates that CBDCA may represent an attractive and valid alternative to the more toxic and equally effective CDDP in the treatment of advanced or recurrent cervical cancer. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Gynecologic oncology AU - Lorusso, Domenica AU - Petrelli, Fausto AU - Coinu, Andrea AU - Raspagliesi, Francesco AU - Barni, Sandro AD - Gynecologic Oncology Unit, Fodazione IRCCS National Cancer Institute, Via Venezian 1, 20133 Milan, Italy. ; Medical Oncology Unit, Oncology Department, Azienda Ospedaliera Treviglio, Piazzale Ospedale 1, 24047 Treviglio, BG, Italy. Electronic address: faupe@libero.it. ; Medical Oncology Unit, Oncology Department, Azienda Ospedaliera Treviglio, Piazzale Ospedale 1, 24047 Treviglio, BG, Italy. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 117 EP - 123 VL - 133 IS - 1 KW - Carboplatin KW - BG3F62OND5 KW - Paclitaxel KW - P88XT4IS4D KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Chemotherapy KW - Advanced cervical cancer KW - Paclitaxel -- administration & dosage KW - Disease-Free Survival KW - Humans KW - Treatment Outcome KW - Carboplatin -- administration & dosage KW - Female KW - Cisplatin -- administration & dosage KW - Uterine Cervical Neoplasms -- drug therapy KW - Neoplasm Recurrence, Local -- drug therapy KW - Neoplasm Metastasis -- drug therapy KW - Carcinoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521913393?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gynecologic+oncology&rft.atitle=A+systematic+review+comparing+cisplatin+and+carboplatin+plus+paclitaxel-based+chemotherapy+for+recurrent+or+metastatic+cervical+cancer.&rft.au=Lorusso%2C+Domenica%3BPetrelli%2C+Fausto%3BCoinu%2C+Andrea%3BRaspagliesi%2C+Francesco%3BBarni%2C+Sandro&rft.aulast=Lorusso&rft.aufirst=Domenica&rft.date=2014-04-01&rft.volume=133&rft.issue=1&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Gynecologic+oncology&rft.issn=1095-6859&rft_id=info:doi/10.1016%2Fj.ygyno.2014.01.042 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-05-13 N1 - Date created - 2014-03-31 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ygyno.2014.01.042 ER - TY - JOUR T1 - New antituberculosis drugs, regimens, and adjunct therapies: needs, advances, and future prospects. AN - 1521324288; 24670627 AB - About 1·3 million people died of tuberculosis in 2012, despite availability of effective drug treatment. Barriers to improvements in outcomes include long treatment duration (resulting in poor patient adherence and loss of patients to follow-up), complex regimens that involve expensive and toxic drugs, toxic effects when given with antiretroviral therapy, and multidrug resistance. After 50 years of no antituberculosis drug development, a promising pipeline is emerging through the repurposing of old drugs, re-engineering of existing antibacterial compounds, and discovery of new compounds. A range of novel antituberculosis drugs are in preclinical development, several phase 2 and 3 trials are underway, and use of adjunct therapies is being explored for drug-sensitive and drug-resistant tuberculosis. Historical advances include approval of two new drugs, delamanid and bedaquiline. Combinations of new and existing drugs are being assessed to shorten the duration of therapy and to treat multidrug-resistant tuberculosis. There has also been progress in development of new antituberculosis drugs that are active against dormant or persister populations of Mycobacterium tuberculosis. In this Review, we discuss recent advances in antituberculosis drug discovery and development, clinical trial designs, laboratory methods, and adjunct host-directed therapies, and we provide an update of phase 3 trials of various fluoroquinolones (RIFAQUIN, NIRT, OFLOTUB, and REMoxTB). We also emphasise the need to engage the community in design, implementation, and uptake of research, to increase international cooperation between drug developers and health-care providers adopting new regimens. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - The Lancet. Infectious diseases AU - Zumla, Alimuddin I AU - Gillespie, Stephen H AU - Hoelscher, Michael AU - Philips, Patrick P J AU - Cole, Stewart T AU - Abubakar, Ibrahim AU - McHugh, Timothy D AU - Schito, Marco AU - Maeurer, Markus AU - Nunn, Andrew J AD - Centre for Clinical Microbiology, Division of Infection and Immunity, University College London, London, UK; University College London Hospitals NHS Foundation Trust, London, UK. Electronic address: a.zumla@ucl.ac.uk. ; School of Medicine, University of St Andrews, St Andrews, UK. ; Department for Infectious Diseases and Tropical Medicine, University of Munich, Munich, Germany; German Centre for Infection Research, Munich, Germany. ; Medical Research Council Clinical Trials Unit at University College London, London, UK. ; Global Health Institute, Ecole Polytechnique Fédérale de Lausanne, EPFLSV/GHI/UPCOL, Lausanne, Switzerland. ; Centre for Clinical Microbiology, Division of Infection and Immunity, University College London, London, UK. ; Henry M Jackson Foundation-Division of AIDS, TB Clinical Research Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; Centre for Allogeneic Stem Cell Transplantation, Therapeutic Immunology Division, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 327 EP - 340 VL - 14 IS - 4 KW - Antitubercular Agents KW - 0 KW - Biomarkers KW - Index Medicus KW - Drug Therapy, Combination KW - Medication Adherence KW - Immunotherapy KW - Humans KW - Research Design KW - Drug Discovery KW - Clinical Trials as Topic KW - Antitubercular Agents -- adverse effects KW - Tuberculosis, Pulmonary -- therapy KW - Tuberculosis, Multidrug-Resistant -- drug therapy KW - Antitubercular Agents -- therapeutic use KW - Tuberculosis, Pulmonary -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521324288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Infectious+diseases&rft.atitle=New+antituberculosis+drugs%2C+regimens%2C+and+adjunct+therapies%3A+needs%2C+advances%2C+and+future+prospects.&rft.au=Zumla%2C+Alimuddin+I%3BGillespie%2C+Stephen+H%3BHoelscher%2C+Michael%3BPhilips%2C+Patrick+P+J%3BCole%2C+Stewart+T%3BAbubakar%2C+Ibrahim%3BMcHugh%2C+Timothy+D%3BSchito%2C+Marco%3BMaeurer%2C+Markus%3BNunn%2C+Andrew+J&rft.aulast=Zumla&rft.aufirst=Alimuddin&rft.date=2014-04-01&rft.volume=14&rft.issue=4&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Infectious+diseases&rft.issn=1474-4457&rft_id=info:doi/10.1016%2FS1473-3099%2813%2970328-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-09 N1 - Date created - 2014-03-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: Lancet Infect Dis. 2014 Sep;14(9):795-6 [25164192] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/S1473-3099(13)70328-1 ER - TY - JOUR T1 - Adiabatic inversion pulses for myocardial T1 mapping AN - 1520377711; 19634666 AB - Purpose To evaluate the error in T1 estimates using inversion-recovery-based T1 mapping due to imperfect inversion and to perform a systematic study of adiabatic inversion pulse designs in order to maximize inversion efficiency for values of transverse relaxation (T2) in the myocardium subject to a peak power constraint. Methods The inversion factor for hyperbolic secant and tangent/hyperbolic tangent adiabatic full passage waveforms was calculated using Bloch equations. A brute-force search was conducted for design parameters: pulse duration, frequency range, shape parameters, and peak amplitude. A design was selected that maximized the inversion factor over a specified range of amplitude and off-resonance and validated using phantom measurements. Empirical correction for imperfect inversion was performed. Results The tangent/hyperbolic tangent adiabatic pulse was found to outperform hyperbolic secant designs and achieve an inversion factor of 0.96 within plus or minus 150 Hz over 25% amplitude range with 14.7 mu T peak amplitude. T1 mapping errors of the selected design due to imperfect inversion was 4% and could be corrected to <1%. Conclusions Nonideal inversion leads to significant errors in inversion-recovery-based T1 mapping. The inversion efficiency of adiabatic pulses is sensitive to transverse relaxation. The tangent/hyperbolic tangent design achieved the best performance subject to the peak amplitude constraint. Magn Reson Med 71:1428-1434, 2014. copyright 2013 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Kellman, Peter AU - Herzka, Daniel A AU - Hansen, Michael Schacht AD - National Institutes of Health, Department of Health and Human Services, National Heart, Lung and Blood Institute, Bethesda, Maryland, USA. Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 1428 EP - 1434 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 71 IS - 4 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Mathematical models KW - Inversion KW - Adiabatic KW - N.M.R. KW - Mapping KW - Myocardium KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520377711?accountid=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=Adiabatic+inversion+pulses+for+myocardial+T1+mapping&rft.au=Kellman%2C+Peter%3BHerzka%2C+Daniel+A%3BHansen%2C+Michael+Schacht&rft.aulast=Kellman&rft.aufirst=Peter&rft.date=2014-04-01&rft.volume=71&rft.issue=4&rft.spage=1428&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24793 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2014-05-02 N1 - SubjectsTermNotLitGenreText - Mathematical models; Inversion; Adiabatic; N.M.R.; Mapping; Myocardium DO - http://dx.doi.org/10.1002/mrm.24793 ER - TY - JOUR T1 - Prediction of cartilage compressive modulus using multiexponential analysis of T sub(2) relaxation data and support vector regression AN - 1520377622; 19634775 AB - Evaluation of mechanical characteristics of cartilage by magnetic resonance imaging would provide a noninvasive measure of tissue quality both for tissue engineering and when monitoring clinical response to therapeutic interventions for cartilage degradation. We use results from multiexponential transverse relaxation analysis to predict equilibrium and dynamic stiffness of control and degraded bovine nasal cartilage, a biochemical model for articular cartilage. Sulfated glycosaminoglycan concentration/wet weight (ww) and equilibrium and dynamic stiffness decreased with degradation from 103.6 plus or minus 37.0 mu g/mg ww, 1.71 plus or minus 1.10 MPa and 15.3 plus or minus 6.7 MPa in controls to 8.25 plus or minus 2.4 mu g/mg ww, 0.015 plus or minus 0.006 MPa and 0.89 plus or minus 0.25MPa, respectively, in severely degraded explants. Magnetic resonance measurements were performed on cartilage explants at 4 degree C in a 9.4 T wide-bore NMR spectrometer using a Carr-Purcell-Meiboom-Gill sequence. Multiexponential T sub(2) analysis revealed four water compartments with T sub(2) values of approximately 0.14, 3, 40 and 150 ms, with corresponding weight fractions of approximately 3, 2, 4 and 91%. Correlations between weight fractions and stiffness based on conventional univariate and multiple linear regressions exhibited a maximum r super(2) of 0.65, while those based on support vector regression (SVR) had a maximum r super(2) value of 0.90. These results indicate that (i) compartment weight fractions derived from multiexponential analysis reflect cartilage stiffness and (ii) SVR-based multivariate regression exhibits greatly improved accuracy in predicting mechanical properties as compared with conventional regression. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. We performed multiexponential transverse relaxation analysis on bovine nasal cartilage, and detected four water compartments with weight fractions of approximately 3, 2, 4 and 91%. Correlations between weight fractions and mechanical stiffness based on conventional univariate and multivariate linear regressions exhibited a maximum r super(2) = 0.65, while those based on support vector regression had a maximum r super(2) = 0.90. This indicates that support vector regression analysis using underlying tissue component fractions as input parameters may be useful for the noninvasive determination of cartilage mechanical quality. JF - NMR in Biomedicine AU - Irrechukwu, Onyi N AU - Thaer, Sarah Von AU - Frank, Eliot H AU - Lin, Ping-Chang AU - Reiter, David A AU - Grodzinsky, Alan J AU - Spencer, Richard G AD - National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 468 EP - 477 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 27 IS - 4 SN - 0952-3480, 0952-3480 KW - Calcium & Calcified Tissue Abstracts; Biotechnology and Bioengineering Abstracts KW - biomechanical stiffness KW - multiexponential T sub(2) relaxation KW - cartilage KW - water compartments KW - Data processing KW - Cartilage KW - Magnetic resonance imaging KW - Therapeutic applications KW - Tissue engineering KW - Models KW - Glycosaminoglycans KW - Regression analysis KW - N.M.R. KW - Cartilage (articular) KW - Explants KW - Mechanical properties 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/1520377622?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NMR+in+Biomedicine&rft.atitle=Prediction+of+cartilage+compressive+modulus+using+multiexponential+analysis+of+T+sub%282%29+relaxation+data+and+support+vector+regression&rft.au=Irrechukwu%2C+Onyi+N%3BThaer%2C+Sarah+Von%3BFrank%2C+Eliot+H%3BLin%2C+Ping-Chang%3BReiter%2C+David+A%3BGrodzinsky%2C+Alan+J%3BSpencer%2C+Richard+G&rft.aulast=Irrechukwu&rft.aufirst=Onyi&rft.date=2014-04-01&rft.volume=27&rft.issue=4&rft.spage=468&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.3083 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Glycosaminoglycans; Data processing; Cartilage; Magnetic resonance imaging; Regression analysis; Therapeutic applications; N.M.R.; Tissue engineering; Cartilage (articular); Explants; Models; Mechanical properties DO - http://dx.doi.org/10.1002/nbm.3083 ER - TY - JOUR T1 - Subsite Awareness in Neuropathology Evaluation of National Toxicology Program (NTP) Studies: A Review of Select Neuroanatomical Structures with Their Functional Significance in Rodents AN - 1520377510; 19503700 AB - This review article is designed to serve as an introductory guide in neuroanatomy for toxicologic pathologists evaluating general toxicity studies. The article provides an overview of approximately 50 neuroanatomical subsites and their functional significance across 7 transverse sections of the brain. Also reviewed are 3 sections of the spinal cord, cranial and peripheral nerves (trigeminal and sciatic, respectively), and intestinal autonomic ganglia. The review is limited to the evaluation of hematoxylin and eosin-stained tissue sections, as light microscopic evaluation of these sections is an integral part of the first-tier toxicity screening of environmental chemicals, drugs, and other agents. Prominent neuroanatomical sites associated with major neurological disorders are noted. This guide, when used in conjunction with detailed neuroanatomic atlases, may aid in an understanding of the significance of functional neuroanatomy, thereby improving the characterization of neurotoxicity in general toxicity and safety evaluation studies. JF - Toxicologic Pathology AU - Rao, Deepa B AU - Little, Peter B AU - Sills, Robert C AD - Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, USA, sills@niehs.nih.gov PY - 2014 SP - 487 EP - 509 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 42 IS - 3 SN - 0192-6233, 0192-6233 KW - CSA Neurosciences Abstracts; Toxicology Abstracts KW - neuropathology KW - neuroanatomy KW - NTP KW - brain KW - spinal cord KW - nerve KW - functional neuroanatomy. KW - Neurological diseases KW - Spinal cord KW - Brain KW - Functional anatomy KW - Anatomy KW - Skull KW - Atlases KW - Reviews KW - Neurotoxicity KW - Intestine KW - Autonomic ganglia KW - Drugs KW - Peripheral nerves KW - Neuropathology KW - Brain architecture KW - N3 11027:Neurology & neuropathology KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520377510?accountid=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=Subsite+Awareness+in+Neuropathology+Evaluation+of+National+Toxicology+Program+%28NTP%29+Studies%3A+A+Review+of+Select+Neuroanatomical+Structures+with+Their+Functional+Significance+in+Rodents&rft.au=Rao%2C+Deepa+B%3BLittle%2C+Peter+B%3BSills%2C+Robert+C&rft.aulast=Rao&rft.aufirst=Deepa&rft.date=2014-04-01&rft.volume=42&rft.issue=3&rft.spage=487&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313501893 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Number of references - 144 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Neurological diseases; Spinal cord; Brain; Functional anatomy; Anatomy; Atlases; Skull; Reviews; Neurotoxicity; Intestine; Drugs; Autonomic ganglia; Neuropathology; Peripheral nerves; Brain architecture DO - http://dx.doi.org/10.1177/0192623313501893 ER - TY - JOUR T1 - N,N-Dimethyl-p-toluidine, a Component in Dental Materials, Causes Hematologic Toxic and Carcinogenic Responses in Rodent Model Systems AN - 1520375681; 19503691 AB - Because of the potential for exposure to N,N-dimethyl-p-toluidine (DMPT) in medical devices and the lack of toxicity and carcinogenicity information available in the literature, the National Toxicology Program conducted toxicity and carcinogenicity studies of DMPT in male and female F344/N rats and B6C3F1/N mice. In these studies, a treatment-related macrocytic regenerative anemia characterized by increased levels of methemoglobin and Heinz body formation developed within a few weeks of DMPT exposure in rats and mice. DMPT induced nasal cavity, splenic, and liver toxicity in rats and mice at 3 months and 2 years. DMPT carcinogenic effects were seen in the liver of male and female rats and mice, the nasal cavity of male and female rats, and the lung and forestomach of female mice. In rodents, DMPT is distributed to many of the sites where toxic and carcinogenic effects occurred. DMPT-induced oxidative damage at these target sites may be one mechanism for the treatment-related lesions. Methemoglobinemia, as seen in these DMPT studies, is caused by oxidation of the heme moiety, and this end point served as an early alert for other target organ toxicities and carcinogenic responses that followed with longer term exposure. JF - Toxicologic Pathology AU - Dunnick, June K AU - Brix, A AU - Sanders, J M AU - Travlos, G S AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, dunnickj@niehs.nih.gov Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 603 EP - 615 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 42 IS - 3 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - N,N-dimethyl-p-toluidine KW - carcinogenic effects KW - hematologic toxicity. KW - Methemoglobinemia KW - Heme KW - Carcinogenicity KW - Lung KW - Oxidation KW - Liver KW - Anemia KW - Spleen KW - Nose KW - Toxicity KW - Methemoglobin KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520375681?accountid=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=N%2CN-Dimethyl-p-toluidine%2C+a+Component+in+Dental+Materials%2C+Causes+Hematologic+Toxic+and+Carcinogenic+Responses+in+Rodent+Model+Systems&rft.au=Dunnick%2C+June+K%3BBrix%2C+A%3BSanders%2C+J+M%3BTravlos%2C+G+S&rft.aulast=Dunnick&rft.aufirst=June&rft.date=2014-04-01&rft.volume=42&rft.issue=3&rft.spage=603&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313489604 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Number of references - 52 N1 - Last updated - 2014-10-15 N1 - SubjectsTermNotLitGenreText - Methemoglobinemia; Heme; Lung; Carcinogenicity; Oxidation; Anemia; Liver; Spleen; Nose; Toxicity; Methemoglobin DO - http://dx.doi.org/10.1177/0192623313489604 ER - TY - JOUR T1 - Mutation Spectra of Kras and Tp53 in Urethral and Lung Neoplasms in B6C3F1 Mice Treated with 3,3',4,4'-Tetrachloroazobenzene AN - 1520375580; 19503692 AB - 3,3',4,4'-tetrachloroazobenzene (TCAB) is a contaminant formed during manufacture of various herbicide compounds. A recent National Toxicology Program study showed B6C3F1 mice exposed to TCAB developed a treatment-related increase in lung carcinomas in the high-dose group, and urethral carcinomas, an extremely rare lesion in rodents, in all dose groups. As the potential for environmental exposure to TCAB is widespread, and the mechanisms of urethral carcinogenesis are unknown, TCAB-induced urethral and pulmonary tumors were evaluated for alterations in critical human cancer genes, Kras and Tp53. Uroplakin III, CK20, and CK7 immunohistochemistry was performed to confirm the urothelial origin of urethral tumors. TCAB-induced urethral carcinomas harbored transforming point mutations in K-ras (38%) and Tp53 (63%), and 71% displayed nuclear TP53 expression, consistent with formation of mutant protein. Transition mutations accounted for 88% of Tp53 mutations in urethral carcinomas, suggesting that TCAB or its metabolites target guanine or cytosine bases and that these mutations are involved in urethral carcinogenesis. Pulmonary carcinomas in TCAB-exposed animals harbored similar rates of Tp53 (55%) and Kras (36%) mutations as urethral carcinomas, suggesting that TCAB may induce mutations at multiple sites by a common mechanism. In conclusion, TCAB is carcinogenic at multiple sites in male and female B6C3F1 mice through mechanisms involving Tp53 and Kras mutation. JF - Toxicologic Pathology AU - Bhusari, Sachin AU - Malarkey, David E AU - Hong, Hue-Hua AU - Wang, Yu AU - Masinde, Tiwanda AU - Nolan, Michael AU - Hooth, Michelle J AU - Lea, Isabel A AU - Vasconcelos, Daphne AU - Sills, Robert C AU - Hoenerhoff, Mark J AD - Cellular and Molecular Pathology Branch, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, hoenerhm@niehs.nih.gov Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 555 EP - 564 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 42 IS - 3 SN - 0192-6233, 0192-6233 KW - Genetics Abstracts; Toxicology Abstracts KW - environmental toxicology KW - agricultural products KW - animal models KW - carcinogenesis KW - genotoxins/nongenotoxins KW - mechanisms of toxicity KW - molecular pathology. KW - Lung carcinoma KW - Point mutation KW - Herbicides KW - Metabolites KW - Tumors KW - Cancer KW - Carcinoma KW - p53 protein KW - Cytosine KW - K-Ras protein KW - Guanine KW - Carcinogenesis KW - Contaminants KW - Immunohistochemistry KW - G 07720:Immunogenetics KW - X 24330:Agrochemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520375580?accountid=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=Mutation+Spectra+of+Kras+and+Tp53+in+Urethral+and+Lung+Neoplasms+in+B6C3F1+Mice+Treated+with+3%2C3%27%2C4%2C4%27-Tetrachloroazobenzene&rft.au=Bhusari%2C+Sachin%3BMalarkey%2C+David+E%3BHong%2C+Hue-Hua%3BWang%2C+Yu%3BMasinde%2C+Tiwanda%3BNolan%2C+Michael%3BHooth%2C+Michelle+J%3BLea%2C+Isabel+A%3BVasconcelos%2C+Daphne%3BSills%2C+Robert+C%3BHoenerhoff%2C+Mark+J&rft.aulast=Bhusari&rft.aufirst=Sachin&rft.date=2014-04-01&rft.volume=42&rft.issue=3&rft.spage=555&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313491169 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Number of references - 43 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Lung carcinoma; Point mutation; Metabolites; Herbicides; Tumors; Cancer; p53 protein; Carcinoma; K-Ras protein; Cytosine; Guanine; Carcinogenesis; Contaminants; Immunohistochemistry DO - http://dx.doi.org/10.1177/0192623313491169 ER - TY - JOUR T1 - The Problem of Helicobacter pylori Resistance to Antibiotics: A Systematic Review in Latin America AN - 1520363818; 19633621 AB - OBJECTIVES: Latin America has a high prevalence of Helicobacter pylori infection and associated diseases, including gastric cancer. Antibiotic therapy can eradicate the bacterial infection and decrease associated morbidity and mortality. To tailor recommendations for optimal treatments, we summarized published literature and calculated region- and country-specific prevalences of antibiotic resistance. METHODS: Searches of PubMed and regional databases for observational studies evaluating H. pylori antibiotic resistance yielded a total of 59 independent studies (56 in adults, 2 in children, and 1 in both groups) published up to October 2013 regarding H. pylori isolates collected between 1988 and 2011. Study-specific prevalences of primary resistance to commonly prescribed antibiotics were summarized using random-effects models. Between-study heterogeneity was assessed by meta-regression. As a sensitivity analysis, we extended our research to studies of patients with prior H. pylori-eradication therapy. RESULTS: Summary prevalences of antimicrobial primary resistance among adults varied by antibiotic, including 12% for clarithromycin (n=35 studies), 53% for metronidazole (n=34), 4% for amoxicillin (n=28), 6% for tetracycline (n=20), 3% for furazolidone (n=6), 15% for fluoroquinolones (n=5), and 8% for dual clarithromycin and metronidazole (n=10). Resistance prevalence varied significantly by country, but not by year of sample collection. Analyses including studies of patients with prior therapy yielded similar estimates. Pediatric reports were too few to be summarized by meta-analysis. CONCLUSIONS: Resistance to first-line anti-H. pylori antibiotics is high in Latin American populations. In some countries, the empirical use of clarithromycin without susceptibility testing may not be appropriate. These findings stress the need for appropriate surveillance programs, improved antimicrobial regulations, and increased public awareness. JF - American Journal of Gastroenterology AU - Camargo, M Constanza AU - Garcia, Apolinaria AU - Riquelme, Arnoldo AU - Otero, William AU - Camargo, Claudia A AU - Hernandez-Garcia, Tomas AU - Candia, Roberto AU - Bruce, Michael G AU - Rabkin, Charles S AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 485 EP - 495 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 109 IS - 4 SN - 0002-9270, 0002-9270 KW - Microbiology Abstracts B: Bacteriology KW - Helicobacter pylori KW - Mortality KW - Metronidazole KW - Amoxicillin KW - Fluoroquinolones KW - Pediatrics KW - Antibiotics KW - Children KW - Tetracyclines KW - Infection KW - Morbidity KW - Antimicrobial agents KW - Models KW - Clarithromycin KW - Databases KW - Furazolidone KW - Reviews KW - Gastric cancer KW - Antibiotic resistance KW - J 02310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520363818?accountid=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+Gastroenterology&rft.atitle=The+Problem+of+Helicobacter+pylori+Resistance+to+Antibiotics%3A+A+Systematic+Review+in+Latin+America&rft.au=Camargo%2C+M+Constanza%3BGarcia%2C+Apolinaria%3BRiquelme%2C+Arnoldo%3BOtero%2C+William%3BCamargo%2C+Claudia+A%3BHernandez-Garcia%2C+Tomas%3BCandia%2C+Roberto%3BBruce%2C+Michael+G%3BRabkin%2C+Charles+S&rft.aulast=Camargo&rft.aufirst=M&rft.date=2014-04-01&rft.volume=109&rft.issue=4&rft.spage=485&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Gastroenterology&rft.issn=00029270&rft_id=info:doi/10.1038%2Fajg.2014.24 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Metronidazole; Mortality; Amoxicillin; Fluoroquinolones; Pediatrics; Antibiotics; Infection; Tetracyclines; Children; Morbidity; Models; Antimicrobial agents; Databases; Clarithromycin; Furazolidone; Reviews; Gastric cancer; Antibiotic resistance; Helicobacter pylori DO - http://dx.doi.org/10.1038/ajg.2014.24 ER - TY - JOUR T1 - Targeting the mTOR pathway in hepatocellular carcinoma: current state and future trends. AN - 1519836056; 24308993 AB - Mechanistic target of rapamycin (mTOR) regulates cell growth, metabolism and aging in response to nutrients, cellular energy stage and growth factors. mTOR is frequently up-regulated in cancer including hepatocellular carcinoma (HCC) and is associated with bad prognosis, poorly differentiated tumors, and earlier recurrence. Blocking mTOR with rapamycin and first generation mTOR inhibitors, called rapalogs, has shown promising reduction of HCC tumor growth in preclinical models. Currently, rapamycin/rapalogs are used in several clinical trials for the treatment of advanced HCC, and as adjuvant therapy in HCC patients after liver transplantation and TACE. A second generation of mTOR pathway inhibitors has been developed recently and is being tested in various clinical trials of solid cancers, and has been used in preclinical HCC models. The results of series of clinical trials using mTOR inhibitors in HCC treatment will emerge in the near future. Published by Elsevier B.V. JF - Journal of hepatology AU - Matter, Matthias S AU - Decaens, Thomas AU - Andersen, Jesper B AU - Thorgeirsson, Snorri S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD, USA. ; Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD, USA. Electronic address: snorri_thorgeirsson@nih.gov. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 855 EP - 865 VL - 60 IS - 4 KW - TOR Serine-Threonine Kinases KW - EC 2.7.1.1 KW - Sirolimus KW - W36ZG6FT64 KW - Index Medicus KW - Rapalogs KW - mTOR KW - Second generation mTOR inhibitors KW - Rapamycin KW - HCC KW - Animals KW - Liver Neoplasms, Experimental -- metabolism KW - Humans KW - Sirolimus -- pharmacology KW - Signal Transduction -- drug effects KW - Liver Neoplasms, Experimental -- therapy KW - Clinical Trials as Topic KW - Chemoembolization, Therapeutic KW - Liver Neoplasms, Experimental -- prevention & control KW - Models, Biological KW - Liver Transplantation KW - Liver Neoplasms -- metabolism KW - Carcinoma, Hepatocellular -- metabolism KW - TOR Serine-Threonine Kinases -- antagonists & inhibitors KW - Liver Neoplasms -- therapy KW - Carcinoma, Hepatocellular -- drug therapy KW - Liver Neoplasms -- drug therapy KW - Carcinoma, Hepatocellular -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1519836056?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Targeting+the+mTOR+pathway+in+hepatocellular+carcinoma%3A+current+state+and+future+trends.&rft.au=Matter%2C+Matthias+S%3BDecaens%2C+Thomas%3BAndersen%2C+Jesper+B%3BThorgeirsson%2C+Snorri+S&rft.aulast=Matter&rft.aufirst=Matthias&rft.date=2014-04-01&rft.volume=60&rft.issue=4&rft.spage=855&rft.isbn=&rft.btitle=&rft.title=Journal+of+hepatology&rft.issn=1600-0641&rft_id=info:doi/10.1016%2Fj.jhep.2013.11.031 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2014-03-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Liver Int. 2013 May;33(5):780-93 [23489999] Gastroenterology. 2013 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AN - 1516760278; 19446493 AB - Chlamydia trachomatis is an obligate intracellular pathogen that replicates in a vacuole termed the inclusion. Many of the interactions of chlamydiae with the host cell are dependent upon bacterial protein synthesis and presumably exposure of these proteins to the cytosol. Because of the dearth of genetic tools for chlamydiae, previous studies examining secreted proteins required the use of heterologous bacterial systems. Recent advances in genetic manipulation of chlamydia now allow for transformation of the bacteria with plasmids. We describe here a shuttle vector system, pBOMB4, that permits expression of recombinant proteins under constitutive or conditional promoter control. We show that the inclusion membrane protein IncD is secreted in a type III-dependent manner from Yersinia pseudotuberculosis and also secreted from C. trachomatis in infected cells where it localizes appropriately to the inclusion membrane. IncD truncated of the first 30 amino acids containing the secretion signal is no longer secreted and is retained by the bacteria. Cytosolic exposure of secreted proteins can be confirmed by using CyaA, GSK, or microinjection assays. A protein predicted to be retained within the bacteria, NrdB is indeed localized to the chlamydia. In addition, we have shown that the chlamydial effector protein, CPAF, which is secreted into the host cell cytosol by a Sec-dependent pathway, also accesses the cytosol when expressed from this system. These assays should prove useful to assess the secretion of other chlamydial proteins that are potentially exposed to the cytosol of the host cell. JF - Journal of Bacteriology AU - Bauler, Laura D AU - Hackstadt, Ted Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 1325 EP - 1334 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 196 IS - 7 SN - 0021-9193, 0021-9193 KW - Microbiology Abstracts B: Bacteriology KW - Transformation KW - Protein biosynthesis KW - Amino acids KW - Secretion KW - Chlamydia trachomatis KW - Yersinia pseudotuberculosis KW - Membrane proteins KW - shuttle vectors KW - Pathogens KW - Plasmids KW - Microinjection KW - Promoters KW - secretion signals KW - Vacuoles KW - Cytosol KW - Pseudotuberculosis KW - J 02310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516760278?accountid=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=Expression+and+Targeting+of+Secreted+Proteins+from+Chlamydia+trachomatis&rft.au=Bauler%2C+Laura+D%3BHackstadt%2C+Ted&rft.aulast=Bauler&rft.aufirst=Laura&rft.date=2014-04-01&rft.volume=196&rft.issue=7&rft.spage=1325&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.01290-13 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Number of references - 78 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Transformation; Amino acids; Protein biosynthesis; Secretion; Pathogens; shuttle vectors; Membrane proteins; Microinjection; Plasmids; Promoters; secretion signals; Vacuoles; Cytosol; Pseudotuberculosis; Yersinia pseudotuberculosis; Chlamydia trachomatis DO - http://dx.doi.org/10.1128/JB.01290-13 ER - TY - JOUR T1 - Perfluoroalkyl Substances During Pregnancy and Validated Preeclampsia Among Nulliparous Women in the Norwegian Mother and Child Cohort Study AN - 1516754492; 19531753 AB - Perfluoroalkyl substances (PFAS) are persistent and ubiquitous environmental contaminants, and human exposure to these substances may be related to preeclampsia, a common pregnancy complication. Previous studies have found serum concentrations of PFAS to be positively associated with pregnancy-induced hypertension and preeclampsia in a population with high levels of exposure to perfluorooctanoate. Whether this association exists among pregnant women with background levels of PFAS exposure is unknown. Using data from the Norwegian Mother and Child Cohort Study conducted by the Norwegian Institute of Public Health, we carried out a study of nulliparous pregnant women enrolled in 2003-2007 (466 cases, 510 noncases) to estimate associations between PFAS concentrations and an independently validated diagnosis of preeclampsia. We measured levels of 9 PFAS in maternal plasma extracted midpregnancy; statistical analyses were restricted to 7 PFAS that were quantifiable in more than 50% of samples. In proportional hazards models adjusted for maternal age, prepregnancy body mass index (weight (kg)/height (m) super(2)), educational level, and smoking status, we observed no strongly positive associations between PFAS levels and preeclampsia. We found an inverse association between preeclampsia and the highest quartile of perfluoroundecanoic acid concentration relative to the lowest quartile (hazard ratio = 0.55, 95% confidence interval: 0.38, 0.81). Overall, our findings do not support an increased risk of preeclampsia among nulliparous Norwegian women with background levels of PFAS exposure. JF - American Journal of Epidemiology AU - Starling, Anne P AU - Engel, Stephanie M AU - Richardson, David B AU - Baird, Donna D AU - Haug, Line S AU - Stuebe, Alison M AU - Klungsoeyr, Kari AU - Harmon, Quaker AU - Becher, Georg AU - Thomsen, Cathrine AU - Sabaredzovic, Azemira AU - Eggesboe, Merete AU - Hoppin, Jane A AU - Travlos, Gregory S AU - Wilson, Ralph E AU - Trogstad, Lill I AU - Magnus, Per AU - Longnecker, Matthew P AD - Correspondence to Dr. Matthew P. Longnecker, NIEHS, Epidemiology Branch, Mail Drop A3-05, P.O. Box 12233, Research Triangle Park, NC 27709-2233., longnec1@niehs.nih.gov Y1 - 2014/04/01/ PY - 2014 DA - 2014 Apr 01 SP - 824 EP - 833 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 179 IS - 7 SN - 0002-9262, 0002-9262 KW - Risk Abstracts KW - Smoking KW - Age KW - Complications KW - Body mass KW - Females KW - Norway KW - Pregnancy KW - Hypertension KW - Public health KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516754492?accountid=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=Perfluoroalkyl+Substances+During+Pregnancy+and+Validated+Preeclampsia+Among+Nulliparous+Women+in+the+Norwegian+Mother+and+Child+Cohort+Study&rft.au=Starling%2C+Anne+P%3BEngel%2C+Stephanie+M%3BRichardson%2C+David+B%3BBaird%2C+Donna+D%3BHaug%2C+Line+S%3BStuebe%2C+Alison+M%3BKlungsoeyr%2C+Kari%3BHarmon%2C+Quaker%3BBecher%2C+Georg%3BThomsen%2C+Cathrine%3BSabaredzovic%2C+Azemira%3BEggesboe%2C+Merete%3BHoppin%2C+Jane+A%3BTravlos%2C+Gregory+S%3BWilson%2C+Ralph+E%3BTrogstad%2C+Lill+I%3BMagnus%2C+Per%3BLongnecker%2C+Matthew+P&rft.aulast=Starling&rft.aufirst=Anne&rft.date=2014-04-01&rft.volume=179&rft.issue=7&rft.spage=824&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwt432 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2014-05-15 N1 - SubjectsTermNotLitGenreText - Smoking; Age; Complications; Body mass; Females; Public health; Hypertension; Pregnancy; Norway DO - http://dx.doi.org/10.1093/aje/kwt432 ER - TY - JOUR T1 - Genetic assessment of environmental features that influence deer dispersal: implications for prion-infected populations AN - 1516749053; 19508046 AB - The landscape can influence host dispersal and density, which in turn, affect infectious disease transmission, spread, and persistence. Understanding how the landscape influences wildlife dispersal and pathogen epidemiology can enhance the efficacy of disease management in natural populations. We applied landscape genetics to examine relationships among landscape variables, dispersal of white-tailed deer hosts and transmission/spread of chronic wasting disease (CWD), a fatal prion encephalopathy. Our focus was on quantifying movements and population structure of host deer in infected areas as a means of predicting the spread of this pathology and promoting its adaptive management. We analyzed microsatellite genotypes of CWD-infected and uninfected deer from two disease foci (Southern Wisconsin, Northern Illinois). We quantified gene flow and population structure using F sub(ST), assignment tests, and spatial autocorrelation analyses. Gene flow estimates were then contrasted against a suite of landscape variables that potentially mediate deer dispersal. Forest fragmentation and grassland connectivity promoted deer movements while rivers, agricultural fields and large urbanized areas impeded movement. Landscape variables, deer dispersal, and disease transmission covaried significantly and positively in our analyses. Habitats with elevated host gene flow supported the concept of dispersal-mediated CWD transmission by reflecting a concomitant, rapid CWD expansion. Large, interrelated social groups isolated by movement barriers overlapped disease foci, suggesting that philopatry exacerbated CWD transmission. Our results promote adaptive management of CWD by predicting patterns of its spread and identifying habitats at risk for invasion. Further, our landscape genetics approach underscores the significance of topography and host behavior in wildlife disease transmission. JF - Population Ecology AU - Kelly, Amy C AU - Mateus-Pinilla, Nohra E AU - Brown, William AU - Ruiz, Marilyn O AU - Douglas, Marlis R AU - Douglas, Michael E AU - Shelton, Paul AU - Beissel, Tom AU - Novakofski, Jan AD - Department of Animal Sciences, University of Illinois, 1503 S. Maryland Dr., Urbana, IL, 61801, USA, kellyac@mail.nih.gov Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 327 EP - 340 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 56 IS - 2 SN - 1438-3896, 1438-3896 KW - Genetics Abstracts; Virology & AIDS Abstracts; Ecology Abstracts KW - Forests KW - Genotypes KW - Habitat fragmentation KW - Population ecology KW - Disease transmission KW - Transmissible spongiform encephalopathy KW - Infectious diseases KW - Gene flow KW - Prion protein KW - Encephalopathy KW - Topography KW - Rivers KW - Data processing KW - Wildlife KW - Landscape KW - Microsatellites KW - Pathogens KW - Habitat KW - Chronic wasting disease KW - Philopatry KW - Grasslands KW - Epidemiology KW - Population structure KW - Dispersal KW - D 04040:Ecosystem and Ecology Studies KW - G 07750:Ecological & Population Genetics KW - V 22380:Prions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516749053?accountid=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=Population+Ecology&rft.atitle=Genetic+assessment+of+environmental+features+that+influence+deer+dispersal%3A+implications+for+prion-infected+populations&rft.au=Kelly%2C+Amy+C%3BMateus-Pinilla%2C+Nohra+E%3BBrown%2C+William%3BRuiz%2C+Marilyn+O%3BDouglas%2C+Marlis+R%3BDouglas%2C+Michael+E%3BShelton%2C+Paul%3BBeissel%2C+Tom%3BNovakofski%2C+Jan&rft.aulast=Kelly&rft.aufirst=Amy&rft.date=2014-04-01&rft.volume=56&rft.issue=2&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=Population+Ecology&rft.issn=14383896&rft_id=info:doi/10.1007%2Fs10144-013-0427-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Number of references - 83 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Rivers; Data processing; Landscape; Wildlife; Microsatellites; Forests; Pathogens; Genotypes; Habitat; Philopatry; Chronic wasting disease; Habitat fragmentation; Disease transmission; Population ecology; Transmissible spongiform encephalopathy; Grasslands; Infectious diseases; Epidemiology; Gene flow; Prion protein; Population structure; Dispersal; Encephalopathy; Topography DO - http://dx.doi.org/10.1007/s10144-013-0427-9 ER - TY - JOUR T1 - Immune-related conditions and subsequent risk of brain cancer in a cohort of 4.5 million male US veterans AN - 1516746449; 19543137 AB - Background: Case-control studies have reported an inverse association between self-reported history of allergy and risk of glioma, but cohort data are limited. Our objectives were to evaluate the associations of major groups of medically diagnosed immune-related conditions (allergy/atopy, autoimmune disease, diabetes, infectious/inflammatory disease) and to explore associations with specific conditions in relation to subsequent diagnosis of brain cancer in a large cohort study. Methods: We used hospital discharge records for a cohort of 4.5 million male US veterans, of whom 4383 developed primary brain cancer. Rate ratios (RRs) and 95% confidence intervals (CIs) were calculated using time-dependent Poisson regression. Results: We found a significant trend of decreasing RRs for brain cancer with longer duration of allergy/atopy (P=0.02), but not for other conditions studied. Rate ratios of brain cancer for allergy/atopy and diabetes with duration of 10 or more years were 0.60 (95% CI: 0.43, 0.83) and 0.75 (95% CI: 0.62, 0.93), respectively. Several associations with specific conditions were found, but these did not withstand correction for multiple comparisons. Conclusions: This study lends some support to an inverse association between allergy/atopy and diabetes of long duration and brain cancer risk, but prospective studies with biological samples are needed to uncover the underlying biological mechanisms. JF - British Journal of Cancer AU - Cahoon, E K AU - Inskip, P D AU - Gridley, G AU - Brenner, A V AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20850, USA Y1 - 2014/04/01/ PY - 2014 DA - 2014 Apr 01 SP - 1825 EP - 1833 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 110 IS - 7 SN - 0007-0920, 0007-0920 KW - Immunology Abstracts; Risk Abstracts KW - Historical account KW - Data processing KW - Males KW - Autoimmune diseases KW - Brain KW - Allergies KW - Cancer KW - Diabetes mellitus KW - Brain tumors KW - Health risks KW - USA KW - Hypersensitivity KW - Atopy KW - Inflammatory diseases KW - Glioma KW - Hospitals 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/1516746449?accountid=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=Immune-related+conditions+and+subsequent+risk+of+brain+cancer+in+a+cohort+of+4.5+million+male+US+veterans&rft.au=Cahoon%2C+E+K%3BInskip%2C+P+D%3BGridley%2C+G%3BBrenner%2C+A+V&rft.aulast=Cahoon&rft.aufirst=E&rft.date=2014-04-01&rft.volume=110&rft.issue=7&rft.spage=1825&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2014.97 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2014-07-24 N1 - SubjectsTermNotLitGenreText - Brain tumors; Diabetes mellitus; Hypersensitivity; Data processing; Inflammatory diseases; Atopy; Autoimmune diseases; Brain; Glioma; Hospitals; Historical account; Health risks; Males; Allergies; Cancer; USA DO - http://dx.doi.org/10.1038/bjc.2014.97 ER - TY - JOUR T1 - Population-based absolute risk estimation with survey data AN - 1516740133; 19506182 AB - Absolute risk is the probability that a cause-specific event occurs in a given time interval in the presence of competing events. We present methods to estimate population-based absolute risk from a complex survey cohort that can accommodate multiple exposure-specific competing risks. The hazard function for each event type consists of an individualized relative risk multiplied by a baseline hazard function, which is modeled nonparametrically or parametrically with a piecewise exponential model. An influence method is used to derive a Taylor-linearized variance estimate for the absolute risk estimates. We introduce novel measures of the cause-specific influences that can guide modeling choices for the competing event components of the model. To illustrate our methodology, we build and validate cause-specific absolute risk models for cardiovascular and cancer deaths using data from the National Health and Nutrition Examination Survey. Our applications demonstrate the usefulness of survey-based risk prediction models for predicting health outcomes and quantifying the potential impact of disease prevention programs at the population level. JF - Lifetime Data Analysis AU - Kovalchik, Stephanie A AU - Pfeiffer, Ruth M AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Bethesda, MD, 20892-9702, USA, pfeiffer@mail.nih.gov Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 252 EP - 275 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 20 IS - 2 SN - 1380-7870, 1380-7870 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Health risks KW - Mortality KW - Prevention KW - Prediction models KW - Population levels KW - Nutrition 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/1516740133?accountid=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=Lifetime+Data+Analysis&rft.atitle=Population-based+absolute+risk+estimation+with+survey+data&rft.au=Kovalchik%2C+Stephanie+A%3BPfeiffer%2C+Ruth+M&rft.aulast=Kovalchik&rft.aufirst=Stephanie&rft.date=2014-04-01&rft.volume=20&rft.issue=2&rft.spage=252&rft.isbn=&rft.btitle=&rft.title=Lifetime+Data+Analysis&rft.issn=13807870&rft_id=info:doi/10.1007%2Fs10985-013-9258-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Number of references - 36 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Mortality; Health risks; Prevention; Prediction models; Population levels; Nutrition; Cancer DO - http://dx.doi.org/10.1007/s10985-013-9258-4 ER - TY - JOUR T1 - PARP1-TDP1 coupling for the repair of topoisomerase I-induced DNA damage. AN - 1516722995; 24493735 AB - Poly(ADP-ribose) polymerases (PARP) attach poly(ADP-ribose) (PAR) chains to various proteins including themselves and chromatin. Topoisomerase I (Top1) regulates DNA supercoiling and is the target of camptothecin and indenoisoquinoline anticancer drugs, as it forms Top1 cleavage complexes (Top1cc) that are trapped by the drugs. Endogenous and carcinogenic DNA lesions can also trap Top1cc. Tyrosyl-DNA phosphodiesterase 1 (TDP1), a key repair enzyme for trapped Top1cc, hydrolyzes the phosphodiester bond between the DNA 3'-end and the Top1 tyrosyl moiety. Alternative repair pathways for Top1cc involve endonuclease cleavage. However, it is unknown what determines the choice between TDP1 and the endonuclease repair pathways. Here we show that PARP1 plays a critical role in this process. By generating TDP1 and PARP1 double-knockout lymphoma chicken DT40 cells, we demonstrate that TDP1 and PARP1 are epistatic for the repair of Top1cc. The N-terminal domain of TDP1 directly binds the C-terminal domain of PARP1, and TDP1 is PARylated by PARP1. PARylation stabilizes TDP1 together with SUMOylation of TDP1. TDP1 PARylation enhances its recruitment to DNA damage sites without interfering with TDP1 catalytic activity. TDP1-PARP1 complexes, in turn recruit X-ray repair cross-complementing protein 1 (XRCC1). This work identifies PARP1 as a key component driving the repair of trapped Top1cc by TDP1. JF - Nucleic acids research AU - Das, Benu Brata AU - Huang, Shar-yin N AU - Murai, Junko AU - Rehman, Ishita AU - Amé, Jean-Christophe AU - Sengupta, Souvik AU - Das, Subhendu K AU - Majumdar, Papiya AU - Zhang, Hongliang AU - Biard, Denis AU - Majumder, Hemanta K AU - Schreiber, Valérie AU - Pommier, Yves AD - Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4255, USA, Laboratory of Molecular Biology, Indian Association for the Cultivation of Science, Jadavpur, Kolkata 700032, India, Biotechnology and Cell Signaling, UMR7242 CNRS, Université de Strasbourg, Laboratory of Excellence Medalis, ESBS, Blvd Sébastien Brant, CS 10413, 67412 Illkirch, France, CEA-DSV-iMETI-SEPIA, BP6, 92265 Fontenay-aux-Roses cedex, France and Laboratory of Molecular Parasitology, Indian Institute of Chemical Biology, Kolkata 700032, India. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 4435 EP - 4449 VL - 42 IS - 7 KW - DNA-Binding Proteins KW - 0 KW - X-ray repair cross complementing protein 1 KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - Phosphoric Diester Hydrolases KW - EC 3.1.4.- KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - Index Medicus KW - Animals KW - Humans KW - Cell Line, Tumor KW - Sumoylation KW - Protein Interaction Domains and Motifs KW - Epistasis, Genetic KW - DNA Topoisomerases, Type I -- metabolism KW - Phosphoric Diester Hydrolases -- genetics KW - Poly(ADP-ribose) Polymerases -- genetics KW - DNA Repair KW - Poly(ADP-ribose) Polymerases -- chemistry KW - DNA Damage KW - Phosphoric Diester Hydrolases -- metabolism KW - Poly(ADP-ribose) Polymerases -- metabolism KW - Phosphoric Diester Hydrolases -- chemistry KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516722995?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=PARP1-TDP1+coupling+for+the+repair+of+topoisomerase+I-induced+DNA+damage.&rft.au=Das%2C+Benu+Brata%3BHuang%2C+Shar-yin+N%3BMurai%2C+Junko%3BRehman%2C+Ishita%3BAm%C3%A9%2C+Jean-Christophe%3BSengupta%2C+Souvik%3BDas%2C+Subhendu+K%3BMajumdar%2C+Papiya%3BZhang%2C+Hongliang%3BBiard%2C+Denis%3BMajumder%2C+Hemanta+K%3BSchreiber%2C+Val%C3%A9rie%3BPommier%2C+Yves&rft.aulast=Das&rft.aufirst=Benu&rft.date=2014-04-01&rft.volume=42&rft.issue=7&rft.spage=4435&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgku088 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-08 N1 - Date created - 2014-04-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cell. 2009 Jan 16;33(1):117-23 [19150433] Annu Rev Biochem. 2009;78:31-54 [19489720] EMBO Rep. 2009 Aug;10(8):887-93 [19557000] EMBO J. 2009 Dec 2;28(23):3667-80 [19851285] PLoS Genet. 2010 Jan;6(1):e1000828 [20107609] Cell Cycle. 2010 Feb 1;9(3):588-595 [20009512] Nat Rev Cancer. 2010 Apr;10(4):293-301 [20200537] Trends Biochem Sci. 2010 Apr;35(4):208-19 [20106667] Nucleic Acids Res. 2010 Apr;38(7):2444-52 [20097655] Mol Cell. 2010 Sep 10;39(5):736-49 [20832725] Mol Microbiol. 2010 Oct;78(1):119-37 [20659295] PLoS One. 2010;5(10):e15387 [21060845] Proc Natl Acad Sci U S A. 2010 Nov 16;107(46):19790-5 [21041670] EMBO Mol Med. 2011 Feb;3(2):78-88 [21246735] Nucleic Acids Res. 2011 May;39(9):3607-20 [21227924] Biochem J. 2011 Jun 15;436(3):559-66 [21463258] J Cell Biol. 2011 Nov 28;195(5):739-49 [22123861] J Biol Chem. 2011 Dec 30;286(52):44945-51 [22039049] J Biol Chem. 2012 Feb 3;287(6):4198-210 [22158865] Genes Dev. 2012 Mar 1;26(5):417-32 [22391446] Nat Commun. 2012;3:733 [22415824] Nat Struct Mol Biol. 2012 Apr;19(4):417-23 [22388737] J Biol Chem. 2012 Apr 13;287(16):12848-57 [22375014] Biochem Pharmacol. 2012 Jul 15;84(2):137-46 [22469522] Cancer Res. 2012 Nov 1;72(21):5588-99 [23118055] ACS Chem Biol. 2013 Jan 18;8(1):82-95 [23259582] Nat Struct Mol Biol. 2013 Mar;20(3):347-54 [23396353] Nucleic Acids Res. 2013 Sep;41(16):7793-803 [23775789] Nucleic Acids Res. 2014 Mar;42(5):3089-103 [24335147] Ann N Y Acad Sci. 2000;922:1-10 [11193884] Br J Cancer. 2001 Jan 5;84(1):106-12 [11139322] Genes Cells. 2001 Aug;6(8):677-87 [11532027] Proc Natl Acad Sci U S A. 2001 Oct 9;98(21):12009-14 [11572945] Annu Rev Biochem. 2001;70:369-413 [11395412] Nat Genet. 2002 Oct;32(2):267-72 [12244316] Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13669-74 [12368472] DNA Repair (Amst). 2003 Oct 7;2(10):1087-100 [13679147] Nucleic Acids Res. 2003 Oct 1;31(19):5526-33 [14500814] J Biol Chem. 2004 Feb 13;279(7):5244-8 [14699148] EMBO J. 2004 Jul 7;23(13):2674-83 [15201865] Cancer Commun. 1989;1(6):389-94 [2562007] J Cell Sci Suppl. 1995;19:73-7 [8655650] J Biol Chem. 1999 Jun 18;274(25):17860-8 [10364231] Science. 1999 Oct 15;286(5439):552-5 [10521354] J Cell Sci. 2005 Jan 1;118(Pt 1):211-22 [15615785] Nature. 2005 Mar 3;434(7029):108-13 [15744309] J Biol Chem. 2005 Apr 22;280(16):16335-44 [15711017] Cancer Res. 2005 May 1;65(9):3894-902 [15867389] J Biol Chem. 2005 Oct 28;280(43):36518-28 [16141202] Mol Biol Cell. 2006 Jan;17(1):1-13 [16267266] EMBO J. 2006 Mar 22;25(6):1305-14 [16498404] Nucleic Acids Res. 2006;34(6):1685-91 [16556909] Nat Rev Mol Cell Biol. 2006 Jul;7(7):517-28 [16829982] Prog Nucleic Acid Res Mol Biol. 2006;81:179-229 [16891172] J Biol Chem. 2006 Oct 13;281(41):30814-23 [16905549] DNA Repair (Amst). 2006 Dec 9;5(12):1489-94 [16935573] Nucleic Acids Res. 2006;34(21):6170-82 [17088286] Neuroscience. 2007 Apr 14;145(4):1260-6 [17045754] BMC Mol Biol. 2007;8:81 [17880707] EMBO J. 2007 Nov 14;26(22):4720-31 [17914460] EMBO J. 2007 Nov 14;26(22):4732-43 [17948061] Nature. 2007 Nov 22;450(7169):509-14 [17965729] Nucleic Acids Res. 2007;35(22):7665-75 [17982172] Biochem Biophys Res Commun. 2008 May 9;369(3):982-8 [18054777] Anticancer Agents Med Chem. 2008 May;8(4):381-9 [18473723] Nat Rev Genet. 2008 Aug;9(8):619-31 [18626472] Nucleic Acids Res. 2008 Aug;36(13):4454-64 [18603595] J Cell Biol. 2008 Dec 29;183(7):1203-12 [19103807] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/nar/gku088 ER - TY - JOUR T1 - A quantitative high-resolution genetic profile rapidly identifies sequence determinants of hepatitis C viral fitness and drug sensitivity. AN - 1515643204; 24722365 AB - Widely used chemical genetic screens have greatly facilitated the identification of many antiviral agents. However, the regions of interaction and inhibitory mechanisms of many therapeutic candidates have yet to be elucidated. Previous chemical screens identified Daclatasvir (BMS-790052) as a potent nonstructural protein 5A (NS5A) inhibitor for Hepatitis C virus (HCV) infection with an unclear inhibitory mechanism. Here we have developed a quantitative high-resolution genetic (qHRG) approach to systematically map the drug-protein interactions between Daclatasvir and NS5A and profile genetic barriers to Daclatasvir resistance. We implemented saturation mutagenesis in combination with next-generation sequencing technology to systematically quantify the effect of every possible amino acid substitution in the drug-targeted region (domain IA of NS5A) on replication fitness and sensitivity to Daclatasvir. This enabled determination of the residues governing drug-protein interactions. The relative fitness and drug sensitivity profiles also provide a comprehensive reference of the genetic barriers for all possible single amino acid changes during viral evolution, which we utilized to predict clinical outcomes using mathematical models. We envision that this high-resolution profiling methodology will be useful for next-generation drug development to select drugs with higher fitness costs to resistance, and also for informing the rational use of drugs based on viral variant spectra from patients. JF - PLoS pathogens AU - Qi, Hangfei AU - Olson, C Anders AU - Wu, Nicholas C AU - Ke, Ruian AU - Loverdo, Claude AU - Chu, Virginia AU - Truong, Shawna AU - Remenyi, Roland AU - Chen, Zugen AU - Du, Yushen AU - Su, Sheng-Yao AU - Al-Mawsawi, Laith Q AU - Wu, Ting-Ting AU - Chen, Shu-Hua AU - Lin, Chung-Yen AU - Zhong, Weidong AU - Lloyd-Smith, James O AU - Sun, Ren AD - Department of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America. ; The Molecular Biology Institute, University of California Los Angeles, Los Angeles, California, United States of America. ; Department of Ecology and Evolutionary Biology, University of California Los Angeles, Los Angeles, California, United States of America. ; Department of Molecular, Cell and Developmental Biology, University of California Los Angeles, Los Angeles, California, United States of America. ; Department of Human Genetics, University of California Los Angeles, Los Angeles, California, United States of America. ; Institute of Information Science, Academia Sinica, Taipei, Taiwan; Institute of Biomedical Informatics, National Yang-Ming University, Taipei, Taiwan. ; Institute of Information Science, Academia Sinica, Taipei, Taiwan. ; Department of Infectious Diseases, Novartis Institutes for BioMedical Research, Emeryville, California, United States of America. ; Department of Ecology and Evolutionary Biology, University of California Los Angeles, Los Angeles, California, United States of America; Fogarty International Center, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Molecular and Medical Pharmacology, University of California Los Angeles, Los Angeles, California, United States of America; The Molecular Biology Institute, University of California Los Angeles, Los Angeles, California, United States of America; School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 1 VL - 10 IS - 4 KW - BMS-790052 KW - 0 KW - Imidazoles KW - NS-5 protein, hepatitis C virus KW - Viral Nonstructural Proteins KW - Index Medicus KW - Viral Nonstructural Proteins -- genetics KW - Humans KW - Viral Nonstructural Proteins -- metabolism KW - Cell Line KW - Hepacivirus -- physiology KW - Gene Expression Profiling KW - Virus Replication -- genetics KW - Hepatitis C -- drug therapy KW - Imidazoles -- pharmacology KW - Virus Replication -- drug effects KW - Genetic Fitness KW - Drug Resistance, Viral -- genetics KW - Hepatitis C -- metabolism KW - Hepatitis C -- genetics KW - Hepatitis C -- pathology KW - Drug Resistance, Viral -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1515643204?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+pathogens&rft.atitle=A+quantitative+high-resolution+genetic+profile+rapidly+identifies+sequence+determinants+of+hepatitis+C+viral+fitness+and+drug+sensitivity.&rft.au=Qi%2C+Hangfei%3BOlson%2C+C+Anders%3BWu%2C+Nicholas+C%3BKe%2C+Ruian%3BLoverdo%2C+Claude%3BChu%2C+Virginia%3BTruong%2C+Shawna%3BRemenyi%2C+Roland%3BChen%2C+Zugen%3BDu%2C+Yushen%3BSu%2C+Sheng-Yao%3BAl-Mawsawi%2C+Laith+Q%3BWu%2C+Ting-Ting%3BChen%2C+Shu-Hua%3BLin%2C+Chung-Yen%3BZhong%2C+Weidong%3BLloyd-Smith%2C+James+O%3BSun%2C+Ren&rft.aulast=Qi&rft.aufirst=Hangfei&rft.date=2014-04-01&rft.volume=10&rft.issue=4&rft.spage=e1004064&rft.isbn=&rft.btitle=&rft.title=PLoS+pathogens&rft.issn=1553-7374&rft_id=info:doi/10.1371%2Fjournal.ppat.1004064 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-10 N1 - Date created - 2014-04-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cell Host Microbe. 2011 Jan 20;9(1):32-45 [21238945] J Virol. 2010 Dec;84(24):12480-91 [20926572] N Engl J Med. 2011 Mar 31;364(13):1195-206 [21449783] J Biol Chem. 2011 Apr 1;286(13):11290-8 [21297162] Virology. 2011 May 25;414(1):10-8 [21513964] Proc Natl Acad Sci U S A. 2011 Jun 21;108(25):10290-5 [21646519] N Engl J Med. 2011 Jun 23;364(25):2405-16 [21696307] J Virol. 2011 Sep;85(17):8870-83 [21697487] PLoS One. 2011;6(10):e26300 [22022594] Hepatology. 2011 Dec;54(6):1924-35 [21809362] Hepatology. 2011 Dec;54(6):1956-65 [21837752] N Engl J Med. 2012 Jan 19;366(3):216-24 [22256805] Antimicrob Agents Chemother. 2012 Mar;56(3):1588-90 [22203595] Antimicrob Agents Chemother. 2012 Mar;56(3):1350-8 [22214777] Curr Opin Virol. 2011 Dec;1(6):599-606 [22440917] Lancet Infect Dis. 2012 Sep;12(9):671-7 [22714001] PLoS Pathog. 2012;8(8):e1002881 [22927817] Rev Med Virol. 2012 Nov;22(6):392-411 [22936636] Virus Res. 2012 Dec;170(1-2):1-14 [23009750] J Virol. 2013 Jan;87(2):1193-9 [23152521] Proc Natl Acad Sci U S A. 2013 Mar 5;110(10):3991-6 [23431163] PLoS Comput Biol. 2013;9(3):e1002959 [23516348] Antimicrob Agents Chemother. 2013 May;57(5):2054-65 [23403428] PLoS Pathog. 2013 May;9(5):e1003359 [23675303] J Mol Biol. 2013 Jun 26;425(12):2100-32 [23507311] Hepatology. 2013 Jul;58(1):428-38 [23467911] Nat Med. 2013 Jul;19(7):837-49 [23836234] Nat Rev Drug Discov. 2013 Aug;12(8):595-610 [23807378] J Antimicrob Chemother. 2014 Mar;69(3):724-7 [24169581] FASEB J. 2000 Feb;14(2):231-41 [10657980] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):6967-73 [10860958] Virus Res. 2000 Sep 25;69(2):109-17 [11018280] Science. 2000 Dec 8;290(5498):1972-4 [11110665] J Biol Chem. 2002 Mar 8;277(10):8130-9 [11744739] J Virol. 2003 May;77(10):6055-61 [12719597] Res Microbiol. 2004 Jun;155(5):360-9 [15207868] J Biol Chem. 2004 Sep 24;279(39):40835-43 [15247283] Science. 1998 Oct 2;282(5386):103-7 [9756471] Science. 1999 Jul 2;285(5424):110-3 [10390360] Nature. 2005 May 19;435(7040):374-9 [15902263] Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9294-9 [15939869] Nat Med. 2005 Jul;11(7):791-6 [15951748] Science. 2005 Jul 22;309(5734):623-6 [15947137] Nature. 2005 Aug 18;436(7053):967-72 [16107837] J Biol Chem. 2005 Oct 28;280(43):36417-28 [16126720] J Virol. 2007 Jun;81(12):6682-9 [17428867] J Virol. 2007 Aug;81(16):8374-83 [17537845] J Virol. 2007 Sep;81(17):8853-67 [17522203] Hepatology. 2009 Apr;49(4):1335-74 [19330875] J Virol. 2009 May;83(9):4395-403 [19244328] Proc Natl Acad Sci U S A. 2009 May 5;106(18):7577-82 [19376974] J Virol. 2010 Jan;84(1):482-91 [19812153] Nature. 2010 May 6;465(7294):96-100 [20410884] Sci Transl Med. 2010 May 5;2(30):30ra32 [20445200] Antimicrob Agents Chemother. 2010 Sep;54(9):3641-50 [20585111] J Virol. 2010 Sep;84(18):9267-77 [20592076] Nat Methods. 2010 Sep;7(9):741-6 [20711194] Gastroenterology. 2011 Mar;140(3):1032-42 [21111742] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.ppat.1004064 ER - TY - JOUR T1 - Activation of peroxisome proliferator-activated receptor-β/δ (PPAR-β/δ) inhibits human breast cancer cell line tumorigenicity. AN - 1514432594; 24464939 AB - The effect of activation and overexpression of the nuclear receptor PPAR-β/δ in human MDA-MB-231 (estrogen receptor-negative; ER(-)) and MCF7 (estrogen-receptor-positive; ER(+)) breast cancer cell lines was examined. Target gene induction by ligand activation of PPAR-β/δ was increased by overexpression of PPAR-β/δ compared with controls. Overexpression of PPAR-β/δ caused a decrease in cell proliferation in MCF7 and MDA-MB-231 cells compared with controls, whereas ligand activation of PPAR-β/δ further inhibited proliferation of MCF7 but not MDA-MB-231 cells. Overexpression and/or ligand activation of PPAR-β/δ in MDA-MB-231 or MCF7 cells had no effect on experimental apoptosis. Decreased clonogenicity was observed in both MDA-MB-231 and MCF7 overexpressing PPAR-β/δ in response to ligand activation of PPAR-β/δ as compared with controls. Ectopic xenografts developed from MDA-MB-231 and MCF7 cells overexpressing PPAR-β/δ were significantly smaller, and ligand activation of PPAR-β/δ caused an even greater reduction in tumor volume as compared with controls. Interestingly, the decrease in MDA-MB-231 tumor size after overexpressing PPAR-β/δ and ligand activation of PPAR-β/δ correlated with increased necrosis. These data show that ligand activation and/or overexpression of PPAR-β/δ in two human breast cancer cell lines inhibits relative breast cancer tumorigenicity and provide further support for the development of ligands for PPAR-β/δ to specifically inhibit breast carcinogenesis. These new cell-based models will be invaluable tools for delineating the role of PPAR-β/δ in breast cancer and evaluating the effects of PPAR-β/δ agonists. JF - Molecular cancer therapeutics AU - Yao, Pei-Li AU - Morales, Jose L AU - Zhu, Bokai AU - Kang, Boo-Hyon AU - Gonzalez, Frank J AU - Peters, Jeffrey M AD - Authors' Affiliations: Department of Veterinary and Biomedical Sciences and The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania; and Non-clinical Research Institute, Chemon, Jeil-Ri, Yangji-Myeon, Cheoin-Gu, Yongin-Si, Gyeonggi-Do, Korea; and Laboratory of Metabolism, National Cancer Institute, Bethesda, Maryland. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 1008 EP - 1017 VL - 13 IS - 4 KW - ANGPTL4 protein, human KW - 0 KW - Angiopoietins KW - PPAR delta KW - PPAR-beta KW - Index Medicus KW - Gene Expression Regulation, Neoplastic KW - Animals KW - Apoptosis -- genetics KW - Humans KW - MCF-7 Cells KW - Mice, Nude KW - Mice KW - Mammary Neoplasms, Experimental KW - Cell Line, Tumor KW - Cell Proliferation KW - Female KW - PPAR-beta -- metabolism KW - Breast Neoplasms -- pathology KW - Angiopoietins -- genetics KW - Breast Neoplasms -- metabolism KW - PPAR delta -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514432594?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+cancer+therapeutics&rft.atitle=Activation+of+peroxisome+proliferator-activated+receptor-%CE%B2%2F%CE%B4+%28PPAR-%CE%B2%2F%CE%B4%29+inhibits+human+breast+cancer+cell+line+tumorigenicity.&rft.au=Yao%2C+Pei-Li%3BMorales%2C+Jose+L%3BZhu%2C+Bokai%3BKang%2C+Boo-Hyon%3BGonzalez%2C+Frank+J%3BPeters%2C+Jeffrey+M&rft.aulast=Yao&rft.aufirst=Pei-Li&rft.date=2014-04-01&rft.volume=13&rft.issue=4&rft.spage=1008&rft.isbn=&rft.btitle=&rft.title=Molecular+cancer+therapeutics&rft.issn=1538-8514&rft_id=info:doi/10.1158%2F1535-7163.MCT-13-0836 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-09 N1 - Date created - 2014-04-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2005 May 1;65(9):3950-7 [15867396] Proc Soc Exp Biol Med. 1999 Jun;221(2):87-8 [10352117] Biochem Biophys Res Commun. 2006 Feb 10;340(2):656-60 [16378595] Curr Opin Cell Biol. 2007 Dec;19(6):697-704 [18035529] Toxicology. 2008 Jan 14;243(1-2):236-43 [18054822] Curr Opin Investig Drugs. 2008 May;9(5):463-9 [18465655] Biochem Biophys Res Commun. 2008 Jul 4;371(3):456-61 [18442472] Proc Natl Acad Sci U S A. 2008 May 27;105(21):7546-51 [18495924] Clin Sci (Lond). 2008 Aug;115(4):107-27 [18616431] Mol Pharmacol. 2008 Nov;74(5):1429-42 [18687807] Mol Pharmacol. 2008 Nov;74(5):1269-77 [18701617] Prostaglandins Other Lipid Mediat. 2009 Apr;88(3-4):97-100 [19101649] Breast Cancer Res. 2009;11(1):R7 [19187537] Biochim Biophys Acta. 2009 Dec;1796(2):230-41 [19505534] Cancer Lett. 2010 Feb 28;288(2):219-25 [19660859] Curr Opin Lipidol. 2010 Jun;21(3):186-91 [20480546] Mol Pharmacol. 2010 Sep;78(3):419-30 [20516370] Nat Biotechnol. 2010 Dec;28(12):1248-50 [21139605] Cell Signal. 2011 Dec;23(12):2039-50 [21843636] Mol Carcinog. 2011 Nov;50(11):884-900 [21400612] Cancer Metastasis Rev. 2011 Dec;30(3-4):619-40 [22037942] Nat Rev Cancer. 2012 Mar;12(3):181-95 [22318237] BMC Genomics. 2012;13:665 [23176727] Biochemistry. 2013 Jun 18;52(24):4193-203 [23713684] Cancer Res. 2013 Jul 15;73(14):4349-61 [23811944] Nature. 2000 Aug 17;406(6797):747-52 [10963602] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74 [11553815] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8418-23 [12829800] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15924-9 [14676330] Cancer Res. 2004 May 1;64(9):3162-70 [15126355] Blood. 1998 Nov 15;92(10):3780-92 [9808572] Atherosclerosis. 2005 Jul;181(1):29-37 [15939051] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1535-7163.MCT-13-0836 ER - TY - JOUR T1 - LGR5 positivity defines stem-like cells in colorectal cancer. AN - 1514432490; 24282287 AB - Like normal colorectal epithelium, colorectal carcinomas (CRCs) are organized hierarchically and include populations of cells with stem-like properties. Leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5) is associated with these stem cells in normal colorectal epithelium; however, the precise function of LGR5 in CRC remains largely unknown. Here, we analyzed the functional and molecular consequences of short hairpin RNA-mediated silencing of LGR5 in CRC cell lines SW480 and HT-29. Additionally, we exposed Lgr5-EGFP-IRES-CreERT2 mice to azoxymethane/dextrane sodium sulfate (AOM/DSS), which induces inflammation-driven colon tumors. Tumors were then flow-sorted into fractions of epithelial cells that expressed high or low levels of Lgr5 and were molecularly characterized using gene expression profiling and array comparative genomic hybridization. Silencing of LGR5 in SW480 CRC cells resulted in a depletion of spheres but did not affect adherently growing cells. Spheres expressed higher levels of several stem cell-associated genes than adherent cells, including LGR5. Silencing of LGR5 reduced proliferation, migration and colony formation in vitro and tumorigenicity in vivo. In accordance with these results, NOTCH signaling was downregulated upon LGR5 silencing. In AOM/DSS-induced colon tumors, Lgr5 high cells showed higher levels of several stem cell-associated genes and higher Wnt signaling than Lgr5 low tumor cells and Lgr5 high normal colon cells. Array comparative genomic hybridization revealed no genomic imbalances in either tumor cell fraction. Our data elucidate mechanisms that define the role of LGR5 as a marker for stem-like cells in CRC. JF - Carcinogenesis AU - Hirsch, Daniela AU - Barker, Nick AU - McNeil, Nicole AU - Hu, Yue AU - Camps, Jordi AU - McKinnon, Katherine AU - Clevers, Hans AU - Ried, Thomas AU - Gaiser, Timo AD - Section of Cancer Genomics, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 849 EP - 858 VL - 35 IS - 4 KW - LGR5 protein, human KW - 0 KW - Receptors, G-Protein-Coupled KW - Receptors, Notch KW - Index Medicus KW - Gene Silencing KW - Humans KW - Cell Line, Tumor KW - Receptors, Notch -- metabolism KW - Colorectal Neoplasms -- pathology KW - Neoplastic Stem Cells -- pathology KW - Receptors, G-Protein-Coupled -- metabolism KW - Receptors, G-Protein-Coupled -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514432490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=LGR5+positivity+defines+stem-like+cells+in+colorectal+cancer.&rft.au=Hirsch%2C+Daniela%3BBarker%2C+Nick%3BMcNeil%2C+Nicole%3BHu%2C+Yue%3BCamps%2C+Jordi%3BMcKinnon%2C+Katherine%3BClevers%2C+Hans%3BRied%2C+Thomas%3BGaiser%2C+Timo&rft.aulast=Hirsch&rft.aufirst=Daniela&rft.date=2014-04-01&rft.volume=35&rft.issue=4&rft.spage=849&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt377 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-05-27 N1 - Date created - 2014-04-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2001 Nov 1;414(6859):105-11 [11689955] Oncogene. 2004 May 6;23(21):3813-21 [15021908] Cell. 1990 Jun 1;61(5):759-67 [2188735] Genes Chromosomes Cancer. 1996 Apr;15(4):234-45 [8703849] Cancer Biol Ther. 2006 Apr;5(4):419-26 [16575208] Cancer Res. 2006 Oct 1;66(19):9339-44 [16990346] Cancer Res. 2007 Jan 1;67(1):41-56 [17210682] Nat Protoc. 2007;2(8):1998-2004 [17703211] Nature. 2007 Oct 25;449(7165):1003-7 [17934449] Cancer Res. 2008 Mar 1;68(5):1284-95 [18316590] Am J Pathol. 2008 Sep;173(3):835-43 [18688030] Nat Rev Cancer. 2008 Oct;8(10):755-68 [18784658] Nature. 2009 Jan 29;457(7229):608-11 [19092804] Carcinogenesis. 2009 Feb;30(2):183-96 [19037092] Cancer Res. 2009 Apr 15;69(8):3382-9 [19336570] Dev Biol. 2009 Jul 1;331(1):58-67 [19394326] Cancer Res. 2010 Feb 15;70(4):1469-78 [20145124] Cancer Sci. 2009 Dec;100(12):2275-82 [19737148] Proc Natl Acad Sci U S A. 2010 Feb 23;107(8):3722-7 [20133591] Nat Cell Biol. 2010 May;12(5):468-76 [20418870] Cancer Sci. 2010 Jul;101(7):1731-7 [20384634] World J Gastroenterol. 2010 Aug 21;16(31):3871-7 [20712047] Mol Cancer. 2010;9:212 [20691072] OMICS. 2010 Aug;14(4):369-84 [20726797] J Clin Invest. 2010 Nov;120(11):3969-78 [20978345] Cancer. 2010 Nov 15;116(22):5207-18 [20665495] Nature. 2011 Jan 20;469(7330):314-22 [21248838] EMBO Rep. 2011 Feb;12(2):113-22 [21252944] Am J Pathol. 2011 Apr;178(4):1478-88 [21435437] Cell Stem Cell. 2011 May 6;8(5):511-24 [21419747] Cancer Lett. 2011 Aug 1;307(1):26-36 [21463919] Proc Natl Acad Sci U S A. 2011 Jul 12;108(28):11452-7 [21693646] PLoS One. 2011;6(7):e22733 [21829496] Nature. 2011 Aug 18;476(7360):293-7 [21727895] Carcinogenesis. 2011 Dec;32(12):1824-31 [21983179] Nat Rev Cancer. 2012 Feb;12(2):133-43 [22237392] Cancer Res. 2012 Mar 15;72(6):1547-56 [22318865] Mol Cancer Ther. 2012 Apr;11(4):963-72 [22319203] J Cell Biochem. 2012 May;113(5):1501-13 [22173954] Nat Rev Cancer. 2012 May;12(5):323-34 [22513401] Pathologe. 2012 May;33 Suppl 1:5-175 [22585318] Biochim Biophys Acta. 2012 Jul;1819(7):784-93 [22426433] EMBO J. 2012 Jul 18;31(14):3079-91 [22692129] Science. 2012 Aug 10;337(6095):730-5 [22855427] Stem Cells. 2012 Nov;30(11):2378-86 [22969042] Brain Pathol. 2013 Jan;23(1):60-72 [22805276] Cancer Res. 2013 Mar 15;73(6):2003-13 [23319804] Carcinogenesis. 2013 May;34(5):1150-7 [23349017] Breast Cancer Res. 2012;14(5):R126 [22992387] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgt377 ER - TY - JOUR T1 - The interplay between hypoxia, endothelial and melanoma cells regulates vascularization and cell motility through endothelin-1 and vascular endothelial growth factor. AN - 1514426591; 24473118 AB - Reciprocal growth factor exchanges between endothelial and malignant cells within the hypoxic microenvironment determine tumor progression. However, the nature of these exchanges has not yet been fully explored. We studied the mutual regulation between endothelial cells (EC), melanoma cells and hypoxia that dictate tumor aggressiveness and angiogenic activity. Here, we investigated the presence of bidirectional autocrine/paracrine endothelin (ET)-1/ET receptor (ETBR) signaling in melanoma cells, blood and lymphatic EC. In all these cells, hypoxia enhanced ET-1 expression, which in turn induced vascular endothelial growth factor (VEGF)-A and VEGF-C secretion, through the hypoxia-inducible growth factor (HIF)-1α and HIF-2α. Autocrine/paracrine exchanges of ET-1, VEGF-A and VEGF-C promoted tumor aggressiveness and morphological changes in blood and lymphatic EC. Furthermore, conditioned media from EC enhanced melanoma cell migration and vessel-like channel formation. This regulation was inhibited by ETBR blockade, by using the selective ETBR antagonist, or ETBR small interfering RNA (siRNA), and by VEGFR-2/-3 antibodies, indicating that ET-1, VEGF-A/VEGF-C, produced by melanoma cells or EC mediated inter-regulation between these cells. Interestingly, HIF-1α/HIF-2α siRNA, impaired this reciprocal regulation, demonstrating the key role of these transcriptional factors in signaling exchanges. In melanoma xenografts, the ETBR antagonist reduced tumor growth and the number of blood and lymphatic vessels. These results reveal an interplay between melanoma cells and EC mediated by ET-1 and VEGF-A/-C and coordinated by the hypoxic microenvironment through HIF-1α/2α transcriptional programs. Thus, targeting ETBR may improve melanoma treatment for tumor and EC, by inhibiting autocrine/paracrine signaling that sustains melanoma progression. JF - Carcinogenesis AU - Spinella, Francesca AU - Caprara, Valentina AU - Cianfrocca, Roberta AU - Rosanò, Laura AU - Di Castro, Valeriana AU - Garrafa, Emirena AU - Natali, Pier Giorgio AU - Bagnato, Anna AD - Experimental Oncology Department, Regina Elena National Cancer Institute, 00144 Rome. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 840 EP - 848 VL - 35 IS - 4 KW - Endothelin-1 KW - 0 KW - Vascular Endothelial Growth Factor A KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Animals KW - Humans KW - Enzyme-Linked Immunosorbent Assay KW - Mice, Nude KW - Mice KW - Human Umbilical Vein Endothelial Cells KW - Female KW - Endothelin-1 -- metabolism KW - Cell Movement KW - Melanoma -- pathology KW - Endothelium, Vascular -- pathology KW - Neovascularization, Pathologic KW - Cell Hypoxia KW - Melanoma -- blood supply KW - Vascular Endothelial Growth Factor A -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1514426591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=The+interplay+between+hypoxia%2C+endothelial+and+melanoma+cells+regulates+vascularization+and+cell+motility+through+endothelin-1+and+vascular+endothelial+growth+factor.&rft.au=Spinella%2C+Francesca%3BCaprara%2C+Valentina%3BCianfrocca%2C+Roberta%3BRosan%C3%B2%2C+Laura%3BDi+Castro%2C+Valeriana%3BGarrafa%2C+Emirena%3BNatali%2C+Pier+Giorgio%3BBagnato%2C+Anna&rft.aulast=Spinella&rft.aufirst=Francesca&rft.date=2014-04-01&rft.volume=35&rft.issue=4&rft.spage=840&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgu018 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-05-27 N1 - Date created - 2014-04-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2000 Feb 1;60(3):733-40 [10676661] Nat Rev Clin Oncol. 2010 Aug;7(8):446-54 [20567244] Nature. 2000 Sep 14;407(6801):249-57 [11001068] Am J Pathol. 2000 Nov;157(5):1703-11 [11073829] EMBO J. 2002 Sep 2;21(17):4593-9 [12198161] Trends Endocrinol Metab. 2003 Jan;14(1):44-50 [12475611] Cell Res. 2003 Oct;13(5):309-17 [14672554] Cancer Res. 2004 Feb 15;64(4):1436-43 [14973117] J Pathol. 2004 Sep;204(1):1-10 [15307132] Blood. 2010 Nov 18;116(20):4376-84 [20716773] Cancer Res. 2011 Feb 1;71(3):976-87 [21148069] J Pathol. 2011 Oct;225(2):305-14 [21826669] Proc Natl Acad Sci U S A. 2011 Sep 27;108(39):16369-74 [21911388] Mol Cancer Res. 2011 Dec;9(12):1668-85 [22013079] Cell. 2012 Feb 3;148(3):399-408 [22304911] Am J Pathol. 2012 Oct;181(4):1115-25 [22944600] Cancer Res. 2012 Oct 1;72(19):5111-8 [22865455] Life Sci. 2012 Oct 15;91(13-14):638-43 [22552325] J Clin Invest. 2013 Jan;123(1):189-205 [23318994] J Mol Med (Berl). 2013 Mar;91(3):395-405 [22965194] Cancer Res. 2013 Jul 15;73(14):4212-21 [23695550] Nat Rev Cancer. 2013 Sep;13(9):637-51 [23884378] Oncogene. 2014 Mar 27;33(13):1725-35 [23584483] N Engl J Med. 1971 Nov 18;285(21):1182-6 [4938153] Am J Physiol. 1995 Aug;269(2 Pt 2):H686-95 [7653633] Am J Pathol. 1999 Sep;155(3):739-52 [10487832] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11496-500 [10500205] Cancer Cell. 2005 Jun;7(6):513-20 [15950901] Nat Rev Cancer. 2005 Sep;5(9):735-43 [16079909] Curr Vasc Pharmacol. 2005 Oct;3(4):309-14 [16248773] Breast Cancer Res Treat. 2006 Sep;99(2):135-41 [16555123] Am J Pathol. 2007 Feb;170(2):774-86 [17255343] Cancer Res. 2007 Feb 15;67(4):1725-34 [17308114] Nat Med. 2008 Jan;14(1):28-36 [18157142] Adv Cancer Res. 2008;100:113-31 [18620094] Anticancer Res. 2008 May-Jun;28(3A):1659-66 [18630523] Blood. 2008 Aug 1;112(3):856-65 [18411415] Cancer Res. 2008 Sep 15;68(18):7293-303 [18794116] Cell Tissue Res. 2009 Jan;335(1):223-40 [19015885] Cancer Res. 2009 Mar 15;69(6):2669-76 [19276384] J Neurooncol. 2009 Aug;94(1):1-19 [19468690] Nat Rev Cancer. 2010 Feb;10(2):138-46 [20094048] Biochim Biophys Acta. 2010 Aug;1806(1):18-28 [20079807] PLoS One. 2010;5(6):e11241 [20574527] Cancer Res. 2010 Jul 15;70(14):5649-69 [20610625] Nature. 2000 Aug 3;406(6795):536-40 [10952317] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgu018 ER - TY - JOUR T1 - Cigarette smoking and endometrial carcinoma risk: the role of effect modification and tumor heterogeneity AN - 1512331030; 19380752 AB - Purpose: The inverse relationship between cigarette smoking and endometrial carcinoma risk is well established. We examined effect modification of this relationship and associations with tumor characteristics in the National Institutes of Health-AARP Diet and Health Study. Methods: We examined the association between cigarette smoking and endometrial carcinoma risk among 110,304 women. During 1,029,041 person years of follow-up, we identified 1,476 incident endometrial carcinoma cases. Multivariable Cox proportional hazards regression models were used to estimate relative risks (RRs) and 95 % confidence intervals (CIs) for the association between smoking status, years since smoking cessation, and endometrial carcinoma risk overall and within strata of endometrial carcinoma risk factors. Effect modification was assessed using likelihood ratio test statistics. Smoking associations by histologic subtype/grade and stage at diagnosis were also evaluated. Results: Reduced endometrial carcinoma risk was evident among former (RR 0.89, 95 % CI 0.80, 1.00) and current (RR 0.65, 95 % CI 0.55, 0.78) smokers compared with never smokers. Smoking cessation 1-4 years prior to baseline was significantly associated with endometrial carcinoma risk (RR 0.65, 95 % CI 0.48, 0.89), while cessation greater than or equal to 10 years before baseline was not. The association between smoking and endometrial carcinoma risk was not significantly modified by any endometrial carcinoma risk factor, nor did we observe major differences in risk associations by tumor characteristics. Conclusion: The cigarette smoking-endometrial carcinoma risk relationship was consistent within strata of important endometrial carcinoma risk factors and by clinically relevant tumor characteristics. JF - Cancer Causes & Control AU - Felix, Ashley S AU - Yang, Hannah P AU - Gierach, Gretchen L AU - Park, Yikyung AU - Brinton, Louise A AD - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 9609 Medical Center Drive, Bethesda, MD, 20892-9774, USA, ashley.felix@gmail.com Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 479 EP - 489 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 25 IS - 4 SN - 0957-5243, 0957-5243 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Risk assessment KW - Diets KW - Health risks KW - Cigarettes KW - Risk factors KW - Tumors 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/1512331030?accountid=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+and+endometrial+carcinoma+risk%3A+the+role+of+effect+modification+and+tumor+heterogeneity&rft.au=Felix%2C+Ashley+S%3BYang%2C+Hannah+P%3BGierach%2C+Gretchen+L%3BPark%2C+Yikyung%3BBrinton%2C+Louise+A&rft.aulast=Felix&rft.aufirst=Ashley&rft.date=2014-04-01&rft.volume=25&rft.issue=4&rft.spage=479&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-014-0350-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Number of references - 62 N1 - Last updated - 2014-05-29 N1 - SubjectsTermNotLitGenreText - Diets; Risk assessment; Health risks; Cigarettes; Risk factors; Tumors; Cancer DO - http://dx.doi.org/10.1007/s10552-014-0350-1 ER - TY - JOUR T1 - Enhancers are major targets for murine leukemia virus vector integration. AN - 1511393839; 24501411 AB - Retroviral vectors have been used in successful gene therapies. However, in some patients, insertional mutagenesis led to leukemia or myelodysplasia. Both the strong promoter/enhancer elements in the long terminal repeats (LTRs) of murine leukemia virus (MLV)-based vectors and the vector-specific integration site preferences played an important role in these adverse clinical events. MLV integration is known to prefer regions in or near transcription start sites (TSS). Recently, BET family proteins were shown to be the major cellular proteins responsible for targeting MLV integration. Although MLV integration sites are significantly enriched at TSS, only a small fraction of the MLV integration sites (<15%) occur in this region. To resolve this apparent discrepancy, we created a high-resolution genome-wide integration map of more than one million integration sites from CD34(+) hematopoietic stem cells transduced with a clinically relevant MLV-based vector. The integration sites form ∼60,000 tight clusters. These clusters comprise ∼1.9% of the genome. The vast majority (87%) of the integration sites are located within histone H3K4me1 islands, a hallmark of enhancers. The majority of these clusters also have H3K27ac histone modifications, which mark active enhancers. The enhancers of some oncogenes, including LMO2, are highly preferred targets for integration without in vivo selection. We show that active enhancer regions are the major targets for MLV integration; this means that MLV preferentially integrates in regions that are favorable for viral gene expression in a variety of cell types. The results provide insights for MLV integration target site selection and also explain the high risk of insertional mutagenesis that is associated with gene therapy trials using MLV vectors. JF - Journal of virology AU - De Ravin, Suk See AU - Su, Ling AU - Theobald, Narda AU - Choi, Uimook AU - Macpherson, Janet L AU - Poidinger, Michael AU - Symonds, Geoff AU - Pond, Susan M AU - Ferris, Andrea L AU - Hughes, Stephen H AU - Malech, Harry L AU - Wu, Xiaolin AD - Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 4504 EP - 4513 VL - 88 IS - 8 KW - Histones KW - 0 KW - Index Medicus KW - Animals KW - Genome, Human KW - Cells, Cultured KW - Humans KW - Histones -- metabolism KW - Mice KW - Genetic Therapy KW - Hematopoietic Stem Cells -- virology KW - Mutagenesis, Insertional KW - Histones -- genetics KW - Leukemia Virus, Murine -- physiology KW - Leukemia Virus, Murine -- genetics KW - Genetic Vectors -- physiology KW - Enhancer Elements, Genetic KW - Genetic Vectors -- genetics KW - Virus Integration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1511393839?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Enhancers+are+major+targets+for+murine+leukemia+virus+vector+integration.&rft.au=De+Ravin%2C+Suk+See%3BSu%2C+Ling%3BTheobald%2C+Narda%3BChoi%2C+Uimook%3BMacpherson%2C+Janet+L%3BPoidinger%2C+Michael%3BSymonds%2C+Geoff%3BPond%2C+Susan+M%3BFerris%2C+Andrea+L%3BHughes%2C+Stephen+H%3BMalech%2C+Harry+L%3BWu%2C+Xiaolin&rft.aulast=De+Ravin&rft.aufirst=Suk&rft.date=2014-04-01&rft.volume=88&rft.issue=8&rft.spage=4504&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.00011-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-24 N1 - Date created - 2014-03-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Genome Res. 2007 Aug;17(8):1186-94 [17545577] Annu Rev Biochem. 2007;76:75-100 [17362198] J Clin Invest. 2008 Sep;118(9):3132-42 [18688285] J Clin Invest. 2008 Sep;118(9):3143-50 [18688286] Cell. 2008 Nov 14;135(4):649-61 [18992931] Blood. 2009 May 21;113(21):5104-10 [19286997] Genome Biol. 2008;9(9):R137 [18798982] Hum Mol Genet. 2009 Oct 15;18(R2):R195-201 [19808796] Blood. 2010 Jan 28;115(4):783-91 [19965657] Bioinformatics. 2010 Mar 15;26(6):841-2 [20110278] Blood. 2010 Aug 12;116(6):900-8 [20457870] Nat Biotechnol. 2010 Oct;28(10):1045-8 [20944595] Blood. 2010 Dec 16;116(25):5507-17 [20864581] EMBO Mol Med. 2011 Feb;3(2):89-101 [21243617] Proc Natl Acad Sci U S A. 2010 Dec 14;107(50):21931-6 [21106759] Nature. 2011 May 5;473(7345):43-9 [21441907] J Virol. 2011 Jul;85(14):7393-401 [21561906] J Biol Chem. 2012 Dec 14;287(51):43137-55 [23086925] Nucleic Acids Res. 2013 Apr 1;41(6):3924-36 [23396443] Proc Natl Acad Sci U S A. 2013 Jul 16;110(29):12036-41 [23818621] Science. 2013 Aug 23;341(6148):1233151 [23845947] Science. 2013 Aug 23;341(6148):1233158 [23845948] J Virol. 2013 Dec;87(23):12721-36 [24049186] Mol Biol Cell. 2013 Nov;24(22):3557-68 [24048450] Cell Rep. 2013 Nov 27;5(4):886-94 [24183673] Cell. 2002 Aug 23;110(4):521-9 [12202041] Science. 2003 Jun 13;300(5626):1749-51 [12805549] Mol Cell. 2004 Jan 16;13(1):33-43 [14731392] Proc Natl Acad Sci U S A. 2005 Nov 29;102(48):17308-13 [16260736] Nat Med. 2005 Dec;11(12):1287-9 [16311605] Nat Med. 2006 Apr;12(4):401-9 [16582916] J Biol Chem. 2007 Feb 9;282(6):4193-201 [17148447] Cell. 2007 May 18;129(4):823-37 [17512414] Retrovirology. 2008;5:48 [18554410] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/JVI.00011-14 ER - TY - JOUR T1 - Pentraxins and IgA share a binding hot-spot on FcαRI. AN - 1510111583; 24407959 AB - The pentraxins, C-reactive protein (CRP), and serum amyloid P component (SAP) have previously been shown to function as innate opsonins through interactions with Fcγ receptors. The molecular details of these interactions were elucidated by the crystal structure of SAP in complex with FcγRIIA. More recently, pentraxins were shown to bind and activate FcαRI (CD89), the receptor for IgA. Here, we used mutations of the receptor based on a docking model to further examine pentraxin recognition by FcαRI. The solution binding of pentraxins to six FcαRI alanine cluster mutants revealed that mutations Y35A and R82A, on the C-and F-strands of the D1 domain, respectively, markedly reduced receptor binding to CRP and SAP. These residues are in the IgA-binding site of the receptor, and thus, significantly affected receptor binding to IgA. The shared pentraxin and IgA-binding site on FcαRI is further supported by the results of a solution binding competition assay. In addition to the IgA-binding site, pentraxins appear to interact with a broader region of the receptor as the mutation in the C'-strand (R48A/E49A) enhanced pentraxin binding. Unlike Fcγ receptors, the H129A/I130A and R178A mutations on the BC- and FG-loops of D2 domain, respectively, had little effect on FcαRI binding to the pentraxins. In conclusion, our data suggest that the pentraxins recognize a similar site on FcαRI as IgA. © 2014 The Protein Society. JF - Protein science : a publication of the Protein Society AU - Lu, Jinghua AU - Marjon, Kristopher D AU - Mold, Carolyn AU - Marnell, Lorraine AU - Du Clos, Terry W AU - Sun, Peter AD - Structural Immunology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, 20852. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 378 EP - 386 VL - 23 IS - 4 KW - Antigens, CD KW - 0 KW - Fc(alpha) receptor KW - Immunoglobulin A KW - Receptors, Fc KW - Serum Amyloid P-Component KW - C-Reactive Protein KW - 9007-41-4 KW - Index Medicus KW - surface plasmon resonance KW - site-directed mutagenesis KW - competition KW - Neutrophils -- metabolism KW - Humans KW - Mutation KW - Binding Sites KW - Receptors, Fc -- chemistry KW - Immunoglobulin A -- chemistry KW - Antigens, CD -- chemistry KW - C-Reactive Protein -- chemistry KW - Antigens, CD -- metabolism KW - Antigens, CD -- genetics KW - Receptors, Fc -- metabolism KW - Serum Amyloid P-Component -- chemistry KW - Receptors, Fc -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510111583?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.atitle=Pentraxins+and+IgA+share+a+binding+hot-spot+on+Fc%CE%B1RI.&rft.au=Lu%2C+Jinghua%3BMarjon%2C+Kristopher+D%3BMold%2C+Carolyn%3BMarnell%2C+Lorraine%3BDu+Clos%2C+Terry+W%3BSun%2C+Peter&rft.aulast=Lu&rft.aufirst=Jinghua&rft.date=2014-04-01&rft.volume=23&rft.issue=4&rft.spage=378&rft.isbn=&rft.btitle=&rft.title=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.issn=1469-896X&rft_id=info:doi/10.1002%2Fpro.2419 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-07 N1 - Date created - 2014-03-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Exp Immunol. 2000 Jul;121(1):106-11 [10886246] J Biol Chem. 2011 Nov 25;286(47):40608-13 [21965667] J Biol Chem. 2001 May 11;276(19):16469-77 [11297532] Curr Opin Infect Dis. 2001 Jun;14(3):289-93 [11964845] Annu Rev Immunol. 2003;21:177-204 [12524384] Nature. 2003 Jun 5;423(6940):614-20 [12768205] Acta Crystallogr D Biol Crystallogr. 2003 Dec;59(Pt 12):2251-3 [14646085] Proc Soc Exp Biol Med. 1971 Feb;136(2):612-4 [4395924] J Immunol. 1974 Jun;112(6):2135-47 [4151108] Clin Exp Immunol. 1978 Apr;32(1):119-24 [668189] Nature. 1979 Mar 15;278(5701):259-61 [423976] J Immunol. 1988 Dec 15;141(12):4266-70 [3198919] J Exp Med. 1990 Mar 1;171(3):597-613 [2137852] J Exp Med. 1990 Jul 1;172(1):13-8 [2358775] J Biol Chem. 1991 Feb 5;266(4):2167-71 [1989977] J Immunol. 1991 Feb 15;146(4):1220-5 [1991964] Nature. 1994 Jan 27;367(6461):338-45 [8114934] Immunol Today. 1994 Feb;15(2):81-8 [8155266] J Immunol. 1995 Aug 15;155(4):2185-93 [7636267] Nat Struct Biol. 1996 Apr;3(4):346-54 [8599761] Clin Immunol Immunopathol. 1996 Nov;81(2):153-60 [8906746] Annu Rev Immunol. 1997;15:203-34 [9143687] J Immunol. 1999 Feb 15;162(4):2146-53 [9973489] Structure. 1999 Feb 15;7(2):169-77 [10368284] J Exp Med. 1999 Aug 16;190(4):585-90 [10449529] Clin Immunol. 2005 Nov;117(2):104-11 [16214080] Novartis Found Symp. 2006;279:80-6; discussion 86-91, 216-9 [17278387] Nature. 2008 Dec 18;456(7224):989-92 [19011614] Proc Natl Acad Sci U S A. 2011 Mar 22;108(12):4974-9 [21383176] J Immunol. 2011 Sep 15;187(6):3208-17 [21856937] J Immunol. 2001 Feb 1;166(3):1781-9 [11160224] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/pro.2419 ER - TY - JOUR T1 - Aberrant microRNA expression likely controls RAS oncogene activation during malignant transformation of human prostate epithelial and stem cells by arsenic. AN - 1509415401; 24431212 AB - Inorganic arsenic (iAs), a human carcinogen, potentially targets the prostate. iAs malignantly transforms the RWPE-1 human prostate epithelial line to CAsE-PE cells, and a derivative normal stem cell (SC) line, WPE-stem, to As-Cancer SC (As-CSC) line. MicroRNAs (miRNA) are noncoding but exert negative control on expression by degradation or translational repression of target mRNAs. Aberrant miRNA expression is important in carcinogenesis. A miRNA array of CAsE-PE and As-CSC revealed common altered expression in both for pathways concerning oncogenesis, miRNA biogenesis, cell signaling, proliferation, and tumor metastasis and invasion. The KRAS oncogene is overexpressed in CAsE-PE cells but not by mutation or promoter hypomethylation, and is intensely overexpressed in As-CSC cells. In both transformants, decreased miRNAs targeting KRAS and RAS superfamily members occurred. Reduced miR-134, miR-373, miR-155, miR-138, miR-205, miR-181d, miR-181c, and let-7 in CAsE-PE cells correlated with increased target RAS oncogenes, RAN, RAB27A, RAB22A mRNAs, and KRAS protein. Reduced miR-143, miR-34c-5p, and miR-205 in As-CSC correlated with increased target RAN mRNA, and KRAS, NRAS, and RRAS proteins. The RAS/ERK and PI3K/PTEN/AKT pathways control cell survival, differentiation, and proliferation, and when dysregulated promote a cancer phenotype. iAs transformation increased expression of activated ERK kinase in both transformants and altered components of the PI3K/PTEN/AKT pathway including decreased PTEN and increases in BCL2, BCL-XL, and VEGF in the absence of AKT activation. Thus, dysregulated miRNA expression may be linked to RAS activation in both transformants. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Ngalame, Ntube N O AU - Tokar, Erik J AU - Person, Rachel J AU - Xu, Yuanyuan AU - Waalkes, Michael P AD - Inorganic Toxicology Group, National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 268 EP - 277 VL - 138 IS - 2 KW - Arsenites KW - 0 KW - Carcinogens, Environmental KW - KRAS protein, human KW - MicroRNAs KW - Proto-Oncogene Proteins KW - Sodium Compounds KW - sodium arsenite KW - 48OVY2OC72 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - ras Proteins KW - Index Medicus KW - KRAS KW - prostate cells KW - arsenic KW - microRNA KW - stem/progenitor cells KW - cancer KW - Real-Time Polymerase Chain Reaction KW - Gene Expression -- drug effects KW - ras Proteins -- genetics KW - Blotting, Western KW - Humans KW - Proto-Oncogene Proteins -- genetics KW - Male KW - Cell Line KW - Prostate -- drug effects KW - Genes, ras -- drug effects KW - MicroRNAs -- genetics KW - Neoplastic Stem Cells -- pathology KW - Arsenites -- toxicity KW - Prostate -- metabolism KW - Carcinogens, Environmental -- toxicity KW - Neoplastic Stem Cells -- drug effects KW - Neoplastic Stem Cells -- metabolism KW - Epithelial Cells -- metabolism KW - Epithelial Cells -- drug effects KW - Genes, ras -- genetics KW - Epithelial Cells -- pathology KW - Sodium Compounds -- toxicity KW - Cell Transformation, Neoplastic -- chemically induced KW - Prostate -- pathology KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1509415401?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Aberrant+microRNA+expression+likely+controls+RAS+oncogene+activation+during+malignant+transformation+of+human+prostate+epithelial+and+stem+cells+by+arsenic.&rft.au=Ngalame%2C+Ntube+N+O%3BTokar%2C+Erik+J%3BPerson%2C+Rachel+J%3BXu%2C+Yuanyuan%3BWaalkes%2C+Michael+P&rft.aulast=Ngalame&rft.aufirst=Ntube+N&rft.date=2014-04-01&rft.volume=138&rft.issue=2&rft.spage=268&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%2Fkfu002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-10 N1 - Date created - 2014-03-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460] J Pathol. 2006 Apr;208(5):699-707 [16402365] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945] Environ Health Perspect. 2007 Feb;115(2):243-7 [17384772] Cell Res. 2007 Jun;17(6):531-6 [17404601] Cancer Res. 2007 Jul 1;67(13):6130-5 [17616669] Carcinogenesis. 2007 Jul;28(7):1379-86 [17341655] Stem Cells. 2008 Jan;26(1):17-29 [17916804] Environ Health Perspect. 2008 Feb;116(2):158-64 [18288312] Cancer Res. 2008 Oct 15;68(20):8278-85 [18922899] Nature. 2008 Oct 23;455(7216):1124-8 [18806776] FASEB J. 2009 Mar;23(3):806-12 [18952709] PLoS One. 2009;4(10):e7542 [19855844] J Natl Cancer Inst. 2009 Dec 16;101(24):1670-81 [19933942] Environ Health Perspect. 2010 Jan;118(1):108-15 [20056578] J Natl Cancer Inst. 2010 May 5;102(9):638-49 [20339138] Toxicol Sci. 2011 Jan;119(1):73-83 [20937726] Nat Med. 2011 Feb;17(2):211-5 [21240262] Mol Cell Biochem. 2011 Apr;350(1-2):207-13 [21197560] Cancer Res. 2011 Sep 15;71(18):5950-4 [21917736] J Cell Physiol. 2011 Dec;226(12):3225-32 [21344382] Nature. 2011 Oct 20;478(7369):399-403 [22012397] Toxicol Sci. 2012 Jan;125(1):20-9 [22011395] Mol Biol Rep. 2012 Feb;39(2):1595-9 [21607617] Expert Opin Ther Targets. 2012 Apr;16 Suppl 2:S17-27 [22443084] Cancer Res. 2012 Apr 1;72(7):1878-89 [22350410] Environ Health Perspect. 2012 Jun;120(6):865-71 [22472196] Cancer Res. 2012 Jul 1;72(13):3393-404 [22719071] Mol Oncol. 2013 Jun;7(3):531-42 [23384558] Mol Carcinog. 2001 Feb;30(2):79-87 [11241755] Cancer Res. 2002 Apr 1;62(7):2175-83 [11929841] Carcinogenesis. 2002 May;23(5):777-85 [12016150] J Natl Cancer Inst. 2002 Dec 18;94(24):1888-91 [12488483] J Cell Biochem. 2004 Jan 1;91(1):13-25 [14689577] Cell. 2004 Jan 23;116(2):281-97 [14744438] Cell Commun Adhes. 2004 Jan-Feb;11(1):1-11 [15500293] Carcinogenesis. 1997 Jun;18(6):1215-23 [9214605] Toxicol Appl Pharmacol. 2005 Aug 15;206(3):288-98 [16039940] Differentiation. 2005 Dec;73(9-10):463-73 [16351690] Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1480-5 [16432235] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kfu002 ER - TY - JOUR T1 - A copper chelate selectively triggers apoptosis in myeloid-derived suppressor cells in a drug-resistant tumor model and enhances antitumor immune response. AN - 1509407973; 24611750 AB - Myeloid-derived suppressor cells (MDSCs), one of the major orchestrators of immunosuppressive network are present in the tumor microenvironment suppress antitumor immunity by subverting Th1 response in tumor site and considered as a great obstacle for advancement of different cancer immunotherapeutic protocols. Till date, various pharmacological approaches have been explored to modulate the suppressive functions of MDSCs in vivo. The present study describes our endeavor to explore a possibility of eradicating MDSCs by the application of a copper chelate, namely copper N-(2-hydroxy acetophenone) glycinate (CuNG), previously found to be a potential immunomodulator that can elicit antitumorogenic Th1 response in doxorubicin-resistant EAC (EAC/Dox) bearing mice. Herein, we demonstrated that CuNG treatment could reduce Gr-1+CD11b+ MDSC accumulation in ascitic fluid and spleen of EAC/Dox tumor model. Furthermore, we found that CuNG mediated reduction in MDSCs is associated with induction of Th1 response and reduction in Treg cells. Moreover, we observed that CuNG could deplete MDSCs by inducing Fas-FasL mediated apoptotic cell death where death receptor Fas expression is enhanced in MDSCs and FasL is provided by activated T cells. However, MDSC expansion from bone marrow cells and their differentiation was not affected by CuNG. Altogether, these findings suggest that the immunomodulatory property of CuNG is attributed to, at least in part, by its selective cytotoxic action on MDSCs. So, this preclinical study unveils a new mechanism of regulating MDSC levels in drug-resistant cancer model and holds promise of translating the findings into clinical settings. JF - Immunopharmacology and immunotoxicology AU - Chakraborty, Paramita AU - Das, Satyajit AU - Banerjee, Kaushik AU - Sinha, Abhinaba AU - Roy, Susmita AU - Chatterjee, Mitali AU - Choudhuri, Soumitra Kumar AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute , Kolkata, West Bengal , India and. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 165 EP - 175 VL - 36 IS - 2 KW - Antigens, CD95 KW - 0 KW - Antineoplastic Agents KW - Chelating Agents KW - Copper KW - 789U1901C5 KW - Doxorubicin KW - 80168379AG KW - Index Medicus KW - Bone Marrow Cells -- drug effects KW - Th1 Cells -- immunology KW - Animals KW - T-Lymphocytes, Regulatory -- drug effects KW - CD4-Positive T-Lymphocytes -- immunology KW - Cell Line, Tumor KW - Mice KW - CD4-Positive T-Lymphocytes -- drug effects KW - Antigens, CD95 -- immunology KW - Lymphocyte Activation -- drug effects KW - Bone Marrow Cells -- metabolism KW - Doxorubicin -- pharmacology KW - Lymphocyte Activation -- immunology KW - Th1 Cells -- drug effects KW - T-Lymphocytes, Regulatory -- immunology KW - Chelating Agents -- pharmacology KW - Antineoplastic Agents -- immunology KW - Apoptosis -- drug effects KW - Myeloid Cells -- immunology KW - Apoptosis -- immunology KW - Myeloid Cells -- drug effects KW - Copper -- pharmacology KW - Copper -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1509407973?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunopharmacology+and+immunotoxicology&rft.atitle=A+copper+chelate+selectively+triggers+apoptosis+in+myeloid-derived+suppressor+cells+in+a+drug-resistant+tumor+model+and+enhances+antitumor+immune+response.&rft.au=Chakraborty%2C+Paramita%3BDas%2C+Satyajit%3BBanerjee%2C+Kaushik%3BSinha%2C+Abhinaba%3BRoy%2C+Susmita%3BChatterjee%2C+Mitali%3BChoudhuri%2C+Soumitra+Kumar&rft.aulast=Chakraborty&rft.aufirst=Paramita&rft.date=2014-04-01&rft.volume=36&rft.issue=2&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Immunopharmacology+and+immunotoxicology&rft.issn=1532-2513&rft_id=info:doi/10.3109%2F08923973.2014.897727 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-10 N1 - Date created - 2014-03-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/08923973.2014.897727 ER - TY - JOUR T1 - Safety and efficacy evaluation of albumin-bound paclitaxel. AN - 1508942012; 24559090 AB - Nanoparticle albumin-bound paclitaxel (nab-paclitaxel) is a novel solvent-free formulation of paclitaxel, which was developed to avoid toxicities associated with Cremophor EL® vehicle used in solvent-based paclitaxel. It is approved as monotherapy for treatment of metastatic breast cancer (MBC) in Europe and the US; in combination therapy for non-small-cell lung cancer (NSCLC) and for first-line treatment of advanced pancreatic cancer (PC) only in the US. The European Medicines Agency has recently released only a positive opinion for use of nab-paclitaxel in PC. This review reports the clinical findings and the safety data of nab-paclitaxel for MBC, NSCLC and PC. In MBC, nab-paclitaxel has demonstrated a good safety and an efficacy profile compared with other taxanes, but no strong data on overall survival are available. Considering the role of markers or predictive factors for nab-paclitaxel effectiveness in the metastatic setting would be useful. In PC, nab-paclitaxel and gemcitabine represent a new therapeutic choice with significant improvement in survival. In a Phase III study with NSCLC patients, nab-paclitaxel showed better results in a subgroup of patients with squamous histology, for whom results with conventional therapies are still poor and improved therapeutic options are needed. JF - Expert opinion on drug safety AU - Cecco, Sara AU - Aliberti, Maria AU - Baldo, Paolo AU - Giacomin, Elisa AU - Leone, Roberto AD - CRO Aviano National Cancer Institute, Hospital Pharmacy , Via F. Gallini, 2, 33081, Aviano , Italy. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 511 EP - 520 VL - 13 IS - 4 KW - Albumin-Bound Paclitaxel KW - 0 KW - Albumins KW - Antineoplastic Agents KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Albumins -- adverse effects KW - Clinical Trials, Phase III as Topic KW - Humans KW - Albumins -- therapeutic use KW - Neoplasms -- drug therapy KW - Paclitaxel -- adverse effects KW - Paclitaxel -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1508942012?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+drug+safety&rft.atitle=Safety+and+efficacy+evaluation+of+albumin-bound+paclitaxel.&rft.au=Cecco%2C+Sara%3BAliberti%2C+Maria%3BBaldo%2C+Paolo%3BGiacomin%2C+Elisa%3BLeone%2C+Roberto&rft.aulast=Cecco&rft.aufirst=Sara&rft.date=2014-04-01&rft.volume=13&rft.issue=4&rft.spage=511&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+drug+safety&rft.issn=1744-764X&rft_id=info:doi/10.1517%2F14740338.2014.893293 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-10 N1 - Date created - 2014-03-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1517/14740338.2014.893293 ER - TY - JOUR T1 - Phase I/II study of erlotinib and temsirolimus for patients with recurrent malignant gliomas: North American Brain Tumor Consortium trial 04-02. AN - 1508677717; 24470557 AB - Inhibition of epidermal growth factor receptor (EGFR) and the mechanistic target of rapamycin (mTOR) may have synergistic antitumor effects in high-grade glioma patients. We conducted a phase I/II study of the EGFR inhibitor erlotinib (150 mg/day) and the mTOR inhibitor temsirolimus. Patients initially received temsirolimus 50 mg weekly, and the dose adjusted based on toxicities. In the phase II component, the primary endpoint was 6-month progression-free survival (PFS6) among glioblastoma patients. Twenty-two patients enrolled in phase I, 47 in phase II. Twelve phase I patients treated at the maximum tolerated dosage were included in the phase II cohort for analysis. The maximum tolerated dosage was 15 mg temsirolimus weekly with erlotinib 150 mg daily. Dose-limiting toxicities were rash and mucositis. Among 42 evaluable glioblastoma patients, 12 (29%) achieved stable disease, but there were no responses, and PFS6 was 13%. Among 16 anaplastic glioma patients, 1 (6%) achieved complete response, 1 (6%) partial response, and 2 (12.5%) stable disease, with PFS6 of 8%. Tumor levels of both drugs were low, and posttreatment tissue in 3 patients showed no reduction in the mTOR target phosphorylated (phospho-)S6(S235/236) but possible compensatory increase in phospho-Akt(S473). Presence of EGFR variant III, phospho-EGFR, and EGFR amplification did not correlate with survival, but patients with elevated phospho-extracellular signal-regulated kinase or reduced phosphatase and tensin homolog protein expression had decreased progression-free survival at 4 months. Because of increased toxicity, the maximum tolerated dosage of temsirolimus in combination with erlotinib proved lower than expected. Insufficient tumor drug levels and redundant signaling pathways may partly explain the minimal antitumor activity noted. JF - Neuro-oncology AU - Wen, Patrick Y AU - Chang, Susan M AU - Lamborn, Kathleen R AU - Kuhn, John G AU - Norden, Andrew D AU - Cloughesy, Timothy F AU - Robins, H Ian AU - Lieberman, Frank S AU - Gilbert, Mark R AU - Mehta, Minesh P AU - Drappatz, Jan AU - Groves, Morris D AU - Santagata, Sandro AU - Ligon, Azra H AU - Yung, W K Alfred AU - Wright, John J AU - Dancey, Janet AU - Aldape, Kenneth D AU - Prados, Michael D AU - Ligon, Keith L AD - Center for Neuro-Oncology, Dana Farber/Brigham and Women's Cancer Center, Boston, Massachusetts (P.Y.W., A.D.N., J.D.); Department of Neurosurgery, University of California, San Francisco, San Francisco, California (S.M.C., K.R.L., M.D.P.); University of Texas Health Science Center, San Antonio, Texas (J.G.K.); Division of Neuro-Oncology, Department of Neurology, University of California, Los Angeles, Los Angeles, California (T.F.C.); University of Wisconsin, Madison Wisconsin (H.I.R., M.P.M.); Neurooncology Program, Division of Hematology/Oncology, University of Pittsburgh Medical Center Cancer Pavilion, Pittsburgh, Pennsylvania (F.S.L.); Division of Neuro-Oncology, MD Anderson Cancer Center, Houston, Texas (M.R.G., M.D.G., W.K.A.Y., K.D.A.); Center for Molecular Oncologic Pathology, Dana Farber/Brigham and Women's Cancer Center, Boston, Massachusetts (S.S., A.H.L.); Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts (S.S., A.H.L., K.L.L.); Investigational Drug Branch, Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, Maryland (J.D.*, J.J.W.). Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 567 EP - 578 VL - 16 IS - 4 KW - Quinazolines KW - 0 KW - temsirolimus KW - 624KN6GM2T KW - Erlotinib Hydrochloride KW - DA87705X9K KW - Sirolimus KW - W36ZG6FT64 KW - Index Medicus KW - epidermal growth factor KW - clinical trial KW - anaplastic glioma KW - glioblastoma KW - erlotinib KW - Young Adult KW - Sirolimus -- administration & dosage KW - Neoplasm Staging KW - Humans KW - Prognosis KW - Aged KW - Tissue Distribution KW - Quinazolines -- administration & dosage KW - Survival Rate KW - Adult KW - Follow-Up Studies KW - Middle Aged KW - Female KW - Male KW - Sirolimus -- analogs & derivatives KW - Brain Neoplasms -- pathology KW - Glioma -- pathology KW - Glioma -- drug therapy KW - Brain Neoplasms -- drug therapy KW - Neoplasm Recurrence, Local -- drug therapy KW - Brain Neoplasms -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacokinetics KW - Glioma -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Neoplasm Recurrence, Local -- pathology KW - Neoplasm Recurrence, Local -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1508677717?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+I%2FII+study+of+erlotinib+and+temsirolimus+for+patients+with+recurrent+malignant+gliomas%3A+North+American+Brain+Tumor+Consortium+trial+04-02.&rft.au=Wen%2C+Patrick+Y%3BChang%2C+Susan+M%3BLamborn%2C+Kathleen+R%3BKuhn%2C+John+G%3BNorden%2C+Andrew+D%3BCloughesy%2C+Timothy+F%3BRobins%2C+H+Ian%3BLieberman%2C+Frank+S%3BGilbert%2C+Mark+R%3BMehta%2C+Minesh+P%3BDrappatz%2C+Jan%3BGroves%2C+Morris+D%3BSantagata%2C+Sandro%3BLigon%2C+Azra+H%3BYung%2C+W+K+Alfred%3BWright%2C+John+J%3BDancey%2C+Janet%3BAldape%2C+Kenneth+D%3BPrados%2C+Michael+D%3BLigon%2C+Keith+L&rft.aulast=Wen&rft.aufirst=Patrick&rft.date=2014-04-01&rft.volume=16&rft.issue=4&rft.spage=567&rft.isbn=&rft.btitle=&rft.title=Neuro-oncology&rft.issn=1523-5866&rft_id=info:doi/10.1093%2Fneuonc%2Fnot247 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-06 N1 - Date created - 2014-03-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2009 Mar 24;106(12):4834-9 [19261849] Cancer Res. 1998 Jan 1;58(1):29-33 [9426052] J Neurooncol. 2010 Jan;96(2):219-30 [19562254] Neuro Oncol. 2010 Jan;12(1):95-103 [20150372] Neuro Oncol. 2010 Oct;12(10):1061-70 [20615922] Genes Dev. 2012 Apr 15;26(8):756-84 [22508724] Cancer Discov. 2012 May;2(5):458-71 [22588883] Neuro Oncol. 2012 Jul;14(7):819-29 [22619466] Cancer Res. 2000 Mar 1;60(5):1383-7 [10728703] Cancer Res. 2001 Feb 15;61(4):1527-32 [11245461] J Clin Oncol. 2001 Jul 1;19(13):3267-79 [11432895] J Clin Oncol. 2004 Mar 1;22(5):909-18 [14990647] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840] Science. 1997 Mar 28;275(5308):1943-7 [9072974] Cancer Res. 1997 Oct 1;57(19):4183-6 [9331071] J Clin Oncol. 1999 Aug;17(8):2572-8 [10561324] Science. 2005 Feb 18;307(5712):1098-101 [15718470] J Natl Cancer Inst. 2005 Jun 15;97(12):880-7 [15956649] Invest New Drugs. 2005 Aug;23(4):357-61 [16012795] J Clin Oncol. 2005 Aug 10;23(23):5294-304 [15998902] Cancer Res. 2005 Aug 15;65(16):7052-8 [16103051] Neoplasia. 2005 Oct;7(10):921-9 [16242075] Clin Cancer Res. 2005 Nov 1;11(21):7841-50 [16278407] N Engl J Med. 2005 Nov 10;353(19):2012-24 [16282176] Cancer Res. 2006 Feb 1;66(3):1500-8 [16452206] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):860-8 [16467100] Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2166-71 [16609030] Neurology. 2006 Jul 11;67(1):156-8 [16832099] Cancer Res. 2006 Aug 15;66(16):7864-9 [16912159] Clin Cancer Res. 2006 Oct 1;12(19):5755-63 [17020981] Clin Cancer Res. 2006 Dec 15;12(24):7261-70 [17189397] J Clin Invest. 2007 Mar;117(3):730-8 [17290308] Br J Cancer. 2007 Apr 10;96(7):1047-51 [17353924] Mol Cancer Ther. 2007 Jul;6(7):1909-19 [17620423] Cancer Res. 2007 Sep 1;67(17):7960-5 [17804702] Science. 2007 Oct 12;318(5848):287-90 [17872411] Clin Cancer Res. 2007 Dec 15;13(24):7401-6 [18094423] Clin Cancer Res. 2008 Jan 15;14(2):488-93 [18223223] PLoS Med. 2008 Jan 22;5(1):e8 [18215105] N Engl J Med. 2008 Jul 31;359(5):492-507 [18669428] J Neurooncol. 2008 Oct;90(1):89-97 [18581057] J Clin Invest. 2008 Sep;118(9):3065-74 [18725988] Nature. 2008 Oct 23;455(7216):1061-8 [18772890] Diagn Mol Pathol. 2008 Dec;17(4):227-30 [18382350] Cancer Biol Ther. 2008 Dec;7(12):1952-8 [18981735] J Neurooncol. 2009 Mar;92(1):99-105 [19018475] J Clin Oncol. 2009 Mar 10;27(8):1268-74 [19204207] Clin Cancer Res. 2009 Oct 15;15(20):6430-7 [19808867] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/neuonc/not247 ER - TY - JOUR T1 - Species and gender differences in the carcinogenic activity of trimethylolpropane triacrylate in rats and mice. AN - 1508423030; 24503412 AB - Trimethylolpropane triacrylate (TMPTA) is a multifunctional monomer with industrial applications. To determine the carcinogenic potential, male and female F344/N rats and B6C3F1/N mice were administered TMPTA (0, 0.3, 1.0, or 3.0mg/kg) in acetone dermally for 2 years. There were no differences in the body weights and survival in the treated animals compared to controls. Nonneoplastic skin lesions at the site of application included epidermal hyperplasia and hyperkeratosis in both rats and mice. There were no incidences of tumors at the site of application in rats and mice. Rare malignant liver neoplasms were observed in female mice that included hepatoblastoma in the 0.3 and 3.0mg/kg groups, and hepatocholangiocarcinoma in the 1.0 and 3.0mg/kg groups. The incidences of uterine stromal polyp and stromal polyp or stromal sarcoma (combined) in female mice occurred with positive trends and the incidences were significantly increased in the 3.0mg/kg group. A marginal increase in the incidences of malignant mesothelioma in male rats may have been related to TMPTA treatment. In conclusion, our studies show that TMPTA is a dermal irritant in both rats and mice of either sex. Increased incidences of tumor formation were observed in female mice and male rats. Published by Elsevier Ltd. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Surh, Inok AU - Rao, Deepa B AU - Cesta, Mark F AU - Hébert, Charles D AU - Mann, Jill F AU - Cunny, Helen AU - Kissling, Grace E AU - Malarkey, David AU - Chhabra, Rajendra S AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Electronic address: surhi@niehs.nih.gov. ; National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA; Integrated Laboratory Systems, Inc., Research Triangle Park, NC 27709, USA. ; National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; Southern Research Institute, Birmingham, AL 35255, USA. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 254 EP - 261 VL - 66 KW - Acrylates KW - 0 KW - Carcinogens KW - trimethylolpropane triacrylate KW - 4B67KGL96S KW - Index Medicus KW - Skin KW - Carcinogenicity KW - Uterine KW - Trimethylolpropane triacrylate KW - Liver KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Mice KW - Species Specificity KW - Male KW - Female KW - Sex Factors KW - Carcinogens -- toxicity KW - Acrylates -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1508423030?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.atitle=Species+and+gender+differences+in+the+carcinogenic+activity+of+trimethylolpropane+triacrylate+in+rats+and+mice.&rft.au=Surh%2C+Inok%3BRao%2C+Deepa+B%3BCesta%2C+Mark+F%3BH%C3%A9bert%2C+Charles+D%3BMann%2C+Jill+F%3BCunny%2C+Helen%3BKissling%2C+Grace+E%3BMalarkey%2C+David%3BChhabra%2C+Rajendra+S&rft.aulast=Surh&rft.aufirst=Inok&rft.date=2014-04-01&rft.volume=66&rft.issue=&rft.spage=254&rft.isbn=&rft.btitle=&rft.title=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.issn=1873-6351&rft_id=info:doi/10.1016%2Fj.fct.2014.01.048 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-05 N1 - Date created - 2014-03-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Sci. 2000 Feb;53(2):213-23 [10696769] Obstet Gynecol. 2013 Sep;122(3):676-83 [23921879] Toxicol Pathol. 2002 Sep-Oct;30(5):580-91 [12371667] Br J Dermatol. 1978 May;98(5):541-52 [148898] Contact Dermatitis. 1980 Oct;6(6):405-9 [6449348] Contact Dermatitis. 1983 Jan;9(1):55-60 [6839739] Contact Dermatitis. 1983 Mar;9(2):122-4 [6221863] Br J Ind Med. 1983 Aug;40(3):241-50 [6223656] Contact Dermatitis. 1984 Oct;11(4):236-46 [6499426] Drug Chem Toxicol. 1984;7(6):527-40 [6534730] J Toxicol Environ Health. 1986;19(2):149-64 [3531535] Contact Dermatitis. 1986 Aug;15(2):92-3 [2946530] Biometrics. 1988 Jun;44(2):417-31 [3390507] Toxicol Pathol. 1988;16(3):321-6 [3194653] Fundam Appl Toxicol. 1989 May;12(4):731-7 [2744275] Mutagenesis. 1989 Sep;4(5):381-93 [2687634] Proc Natl Acad Sci U S A. 1990 Dec;87(23):9178-82 [2251261] Environ Mol Mutagen. 1991;17(4):264-71 [2050134] Biometrics. 1993 Sep;49(3):793-801 [8241374] Contact Dermatitis. 1994 Nov;31(5):281-7 [7867323] Ann Bot. 1989;64:271-7 [11537658] Histopathology. 1997 May;30(5):403-18 [9181361] Mol Carcinog. 1997 Sep;20(1):108-14 [9328441] Contact Dermatitis. 1998 May;38(5):292-4 [9667458] Toxicol Lett. 1998 Dec 28;102-103:277-82 [10022266] Toxicol Pathol. 2005;33(6):631-40 [16176922] Mutat Res. 2008 Jul-Aug;659(1-2):15-30 [18485806] Natl Toxicol Program Genet Modif Model Rep. 2005 Oct;(3):1-195 [18784763] Contact Dermatitis. 2008 Dec;59(6):372-3 [19076890] Crit Rev Toxicol. 2009;39(6):512-37 [19545199] Toxicol Pathol. 2010 Jan;38(1):9-36 [20008954] Toxicol Pathol. 2011 Jan;39(1):240-66 [21177527] Eur J Radiol. 2011 Apr;78(1):30-40 [21247711] Toxicol Pathol. 2012 Apr;40(3):419-24 [22215514] Toxicol Pathol. 2001;29 Suppl:51-9 [11695562] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.fct.2014.01.048 ER - TY - JOUR T1 - Adjuvant high-dose chemotherapy with autologous hematopoietic stem cell support for high-risk primary breast cancer: results from the Italian national registry. AN - 1508414648; 24374214 AB - The efficacy of high-dose chemotherapy (HDC) and autologous hemopoietic progenitor cell transplantation (AHPCT) for breast cancer (BC) patients has been an area of intense controversy among the medical oncology community. The aim of this study was to assess toxicity and efficacy of this procedure in a large cohort of high-risk primary BC patients who underwent AHPCT in Italy. A total of 1183 patients receiving HDC for high-risk BC (HRBC) (>3 positive nodes) were identified in the Italian registry. The median age was 46 years, 62% of patients were premenopausal at treatment, 60.1% had endocrine-responsive tumors, and 20.7% had a human epidermal growth factor receptor 2 (HER2)-positive tumor. The median number of positive lymph nodes (LN) at surgery was 15, with 71.5% of patients having ≥ 10 positive nodes. Seventy-three percent received an alkylating agent-based HDC as a single procedure, whereas 27% received epirubicin or mitoxantrone-containing HDC, usually within a multitransplantation program. The source of stem cells was peripheral blood in the vast majority of patients. Transplantation-related mortality was .8%, whereas late cardiac and secondary tumor-related mortality were around 1%, overall. With a median follow-up of 79 months, median disease-free and overall survival (OS) in the entire population were 101 and 134 months, respectively. Subgroup analysis demonstrated that OS was significantly better in patients with endocrine-responsive tumors and in patients receiving multiple transplantation procedures. HER2 status did not affect survival probability. The size of the primary tumor and number of involved LN negatively affected OS. Adjuvant HDC with AHPCT has a low mortality rate and provides impressive long-term survival rates in patients with high-risk primary BC. Our results suggest that this treatment modality should be proposed in selected HRBC patients and further investigated in clinical trials. Copyright © 2014 American Society for Blood and Marrow Transplantation. Published by Elsevier Inc. All rights reserved. JF - Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation AU - Pedrazzoli, Paolo AU - Martinelli, Giovanni AU - Gianni, Alessandro Massimo AU - Da Prada, Gian Antonio AU - Ballestrero, Alberto AU - Rosti, Giovanni AU - Frassineti, Giovanni Luca AU - Aieta, Michele AU - Secondino, Simona AU - Cinieri, Saverio AU - Fedele, Roberta AU - Bengala, Carmelo AU - Bregni, Marco AU - Grasso, Donatella AU - De Giorgi, Ugo AU - Lanza, Francesco AU - Castagna, Luca AU - Bruno, Barbara AU - Martino, Massimo AU - of Gruppo Italiano per il Trapianto di Midollo Osseo, Cellule staminali emopoietiche e terapia cellulare (GITMO) – Sezione Tumori Solidi AD - Medical Oncology, IRCCS Foundation, San Matteo Hospital, Pavia, Italy. ; Medical Oncology, European Institute of Oncology, Milan, Italy. ; Medical Oncology, IRCCS Foundation, National Cancer Institute, Milan, Italy. ; Medical Oncology, IRCCS Maugeri Foundation, Pavia, Italy. ; Department of Internal Medicine, University Hospital, Genova, Italy. ; Medical Oncology, Civil Hospital, Ravenna, Italy. ; Department of Medical Oncology, IRCCS Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori, Meldola, Italy. ; Medical Oncology, IRCCS Casa Sollievo della Sofferenza, San Giovanni Rotondo (FG), Italy. ; Medical Oncology, Niguarda Ca', Granda Hospital, Milan, Italy. ; Hematology and Bone Marrow Transplant Unit, Azienda Ospedaliera "BMM", Reggio Calabria, Italy. ; Medical Oncology, University Hospital, Pisa, Italy. ; Hematology Unit, San Raffaele Scientific Institute, Milan, Italy. ; Section of Hematology and Bone Marrow Transplant Unit, Cremona, Italy. ; Hematology Unit, Humanitas Cancer Center, Rozzano, Milan, Italy. ; National Registry GITMO & Data Managing, Ospedale San Martino, Genova, Italy. ; Hematology and Bone Marrow Transplant Unit, Azienda Ospedaliera "BMM", Reggio Calabria, Italy. Electronic address: dr.massimomartino@gmail.com. ; of Gruppo Italiano per il Trapianto di Midollo Osseo, Cellule staminali emopoietiche e terapia cellulare (GITMO) – Sezione Tumori Solidi Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 501 EP - 506 VL - 20 IS - 4 KW - Antineoplastic Agents, Alkylating KW - 0 KW - Epirubicin KW - 3Z8479ZZ5X KW - Mitoxantrone KW - BZ114NVM5P KW - ERBB2 protein, human KW - EC 2.7.10.1 KW - Receptor, ErbB-2 KW - Index Medicus KW - High-dose chemotherapy KW - Autologous hematopoietic progenitor cell support KW - High-risk breast cancer KW - Receptor, ErbB-2 -- genetics KW - Drug Administration Schedule KW - Lymphatic Metastasis KW - Humans KW - Gene Expression KW - Mitoxantrone -- administration & dosage KW - Aged KW - Antineoplastic Agents, Alkylating -- administration & dosage KW - Transplantation, Autologous KW - Italy KW - Risk KW - Adult KW - Receptor, ErbB-2 -- immunology KW - Middle Aged KW - Epirubicin -- administration & dosage KW - Female KW - Survival Analysis KW - Registries KW - Breast Neoplasms -- immunology KW - Breast Neoplasms -- mortality KW - Peripheral Blood Stem Cell Transplantation KW - Breast Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols KW - Breast Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1508414648?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adjuvant+high-dose+chemotherapy+with+autologous+hematopoietic+stem+cell+support+for+high-risk+primary+breast+cancer%3A+results+from+the+Italian+national+registry.&rft.au=Pedrazzoli%2C+Paolo%3BMartinelli%2C+Giovanni%3BGianni%2C+Alessandro+Massimo%3BDa+Prada%2C+Gian+Antonio%3BBallestrero%2C+Alberto%3BRosti%2C+Giovanni%3BFrassineti%2C+Giovanni+Luca%3BAieta%2C+Michele%3BSecondino%2C+Simona%3BCinieri%2C+Saverio%3BFedele%2C+Roberta%3BBengala%2C+Carmelo%3BBregni%2C+Marco%3BGrasso%2C+Donatella%3BDe+Giorgi%2C+Ugo%3BLanza%2C+Francesco%3BCastagna%2C+Luca%3BBruno%2C+Barbara%3BMartino%2C+Massimo%3Bof+Gruppo+Italiano+per+il+Trapianto+di+Midollo+Osseo%2C+Cellule+staminali+emopoietiche+e+terapia+cellulare+%28GITMO%29+%E2%80%93+Sezione+Tumori+Solidi&rft.aulast=Pedrazzoli&rft.aufirst=Paolo&rft.date=2014-04-01&rft.volume=20&rft.issue=4&rft.spage=501&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.2013.12.569 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-03 N1 - Date created - 2014-03-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbmt.2013.12.569 ER - TY - JOUR T1 - Perilipin 5, a lipid droplet protein adapted to mitochondrial energy utilization. AN - 1507791951; 24535284 AB - We summarize recent mechanistic and physiological studies related to the role of perilipin 5 (Plin5) in regulating lipid droplet accumulation and protection to fatty acids in tissues with high lipid oxidative metabolism. Plin5 is a lipid droplet targeting protein that promotes association of lipid droplets with mitochondria and is most highly expressed in oxidative tissues, including cardiac and skeletal muscle. Recent in-vivo and in-vitro data indicate an important role for Plin5 in the regulation of cardiac lipid storage and function. Targeted overexpression of Plin5 in heart causes steatosis, mild mitochondria dysfunction, and hypertrophy in cardiac tissue, but without affecting cardiac function. In contrast, whole body ablation of Plin5 (Plin5  mice) reduces cardiac lipid droplet formation, increases cardiac fatty acid oxidation, and promotes cardiac dysfunction; cardiac defects can be prevented with antioxidative therapy. These data suggest a cytoprotective role for Plin5 to promote lipid storage but to limit fatty acid toxicity, parameters critical for tissues with high lipid oxidative metabolism. In-vivo and in-vitro data suggest that Plin5 is part of a cell-adaptive response to high lipid oxidative metabolism to protect lipid droplet storage against neutral lipases and, so, limit fatty acid accumulation. Although the specific mechanisms that underlie Plin5 lipid droplet storage protection in oxidative tissues remain to be fully elucidated, Plin5 provides a basis for the novel cytoprotective nature of lipid droplets. JF - Current opinion in lipidology AU - Kimmel, Alan R AU - Sztalryd, Carole AD - aLaboratory of Cellular and Developmental Biology (50/3351), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland bThe Geriatric Research, Education and Clinical Center, Baltimore Veterans Affairs Healthcare Center, Division of Endocrinology, Department of Medicine, School of Medicine, University of Maryland, Baltimore, Maryland, USA. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 110 EP - 117 VL - 25 IS - 2 KW - Intracellular Signaling Peptides and Proteins KW - 0 KW - Muscle Proteins KW - Perilipin-5 KW - Plin5 protein, mouse KW - Proteins KW - lipid storage droplet protein 5, mouse KW - Index Medicus KW - Animals KW - Humans KW - Muscle Proteins -- metabolism KW - Muscle Proteins -- genetics KW - Organelles -- metabolism KW - Intracellular Signaling Peptides and Proteins -- genetics KW - Intracellular Signaling Peptides and Proteins -- metabolism KW - Mitochondria -- metabolism KW - Energy Metabolism KW - Proteins -- metabolism KW - Proteins -- genetics KW - Lipid Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1507791951?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lipidology&rft.atitle=Perilipin+5%2C+a+lipid+droplet+protein+adapted+to+mitochondrial+energy+utilization.&rft.au=Kimmel%2C+Alan+R%3BSztalryd%2C+Carole&rft.aulast=Kimmel&rft.aufirst=Alan&rft.date=2014-04-01&rft.volume=25&rft.issue=2&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+lipidology&rft.issn=1473-6535&rft_id=info:doi/10.1097%2FMOL.0000000000000057 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-05 N1 - Date created - 2014-03-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Annu Rev Biochem. 2012;81:687-714 [22524315] PLoS One. 2012;7(6):e36712 [22675471] J Biol Chem. 2012 Jul 6;287(28):23852-63 [22532565] J Biol Chem. 2012 Jul 20;287(30):25038-48 [22685301] Trends Endocrinol Metab. 2012 Aug;23(8):391-8 [22721584] J Lipid Res. 2012 Sep;53(9):1800-10 [22701043] J Lipid Res. 2013 Feb;54(2):522-34 [23175776] Cell. 1998 Mar 20;92(6):829-39 [9529258] Methods Mol Biol. 1999;109:279-302 [9918030] Biochimie. 2005 Jan;87(1):45-9 [15733736] Methods Mol Biol. 2008;456:299-306 [18516570] J Lipid Res. 2008 Jul;49(7):1395-408 [18387886] Curr Opin Lipidol. 2009 Feb;20(1):50-6 [19133412] J Biol Chem. 2009 Jan 30;284(5):3049-57 [19064991] Biochim Biophys Acta. 2009 Jun;1791(6):419-40 [19375517] J Lipid Res. 2009 Aug;50(8):1621-9 [19304987] J Biol Chem. 2009 Nov 6;284(45):30941-8 [19748893] J Biol Chem. 2009 Nov 13;284(46):32116-25 [19717842] J Biol Chem. 2009 Dec 25;284(52):36312-23 [19778901] Biochim Biophys Acta. 2010 Mar;1801(3):209-14 [19948243] Cell Metab. 2010 Mar 3;11(3):194-205 [20197052] Prog Lipid Res. 2011 Jan;50(1):14-27 [21087632] Hepatology. 2011 Jan;53(1):116-26 [20967758] J Biol Chem. 2011 Feb 18;286(7):5126-35 [21148142] PLoS Genet. 2011 Mar;7(3):e1001324 [21423719] J Biol Chem. 2011 May 6;286(18):15707-15 [21393244] J Clin Invest. 2011 Jun;121(6):2102-10 [21633178] Trends Endocrinol Metab. 2011 Jun;22(6):197-203 [21632259] Nat Med. 2011 Sep;17(9):1076-85 [21857651] Diabetes. 2011 Oct;60(10):2588-97 [21873552] J Lipid Res. 2011 Dec;52(12):2159-68 [21885430] Am J Physiol Regul Integr Comp Physiol. 2012 Jan 1;302(1):R29-36 [22012700] Biochim Biophys Acta. 2012 Feb;1821(2):268-78 [22063271] Prog Lipid Res. 2012 Jan;51(1):36-49 [22120643] Histochem Cell Biol. 2012 Feb;137(2):205-16 [22127648] Cell. 2012 Mar 2;148(5):852-71 [22385956] Cell Metab. 2012 Mar 7;15(3):279-91 [22405066] J Mol Cell Cardiol. 2013 Feb;55:101-10 [22789525] Biochim Biophys Acta. 2013 Apr;1831(4):844-52 [23353597] J Lipid Res. 2013 Apr;54(4):1092-102 [23345410] J Lipid Res. 2013 Apr;54(4):953-65 [23345411] J Lipid Res. 2013 Apr;54(4):876-7 [23417737] J Biol Chem. 2013 Apr 5;288(14):9892-904 [23413028] J Lipid Res. 2013 May;54(5):1346-59 [23402988] Mol Cell Biol. 2006 Feb;26(3):1063-76 [16428458] Science. 2006 May 5;312(5774):734-7 [16675698] J Biol Chem. 2006 May 19;281(20):14232-40 [16571721] Diabetes. 2006 Dec;55(12):3418-28 [17130488] Proc Natl Acad Sci U S A. 2007 Jan 30;104(5):1488-93 [17242355] Biochim Biophys Acta. 2007 Feb;1771(2):210-27 [17234449] Am J Physiol Regul Integr Comp Physiol. 2007 Mar;292(3):R1271-8 [17095651] J Lipid Res. 2007 Dec;48(12):2547-59 [17878492] Nat Genet. 2000 Dec;26(4):474-9 [11101849] Semin Cell Dev Biol. 2012 Aug;23(6):631-9 [22273692] Trends Endocrinol Metab. 2012 Sep;23(9):459-66 [22817841] Mol Cell Endocrinol. 2013 May 22;371(1-2):15-9 [23089211] Am J Physiol Regul Integr Comp Physiol. 2013 Apr 15;304(8):R644-50 [23408028] J Lipid Res. 2013 Jul;54(7):1949-63 [23606724] EMBO Mol Med. 2013 Jul;5(7):905-15 [23740690] Cardiovasc Res. 2013 Aug 1;99(3):442-51 [23708736] Oxid Med Cell Longev. 2013;2013:327167 [24175011] J Clin Endocrinol Metab. 2013 Dec;98(12):4863-71 [24178794] Biochimie. 2014 Jan;96:96-101 [24036367] Biochim Biophys Acta. 2014 Mar;1842(3):393-401 [23688782] Proc Natl Acad Sci U S A. 2001 May 22;98(11):6494-9 [11371650] Mamm Genome. 2001 Sep;12(9):741-9 [11641724] J Clin Endocrinol Metab. 2003 Dec;88(12):6056-62 [14671211] J Biol Chem. 2004 Mar 12;279(11):10070-6 [14704148] Endocrinology. 2004 May;145(5):2346-56 [14726448] Diabetes. 2004 May;53(5):1243-52 [15111493] Diabetes. 2012 Nov;61(11):2679-90 [22807032] J Cell Sci. 2012 Sep 1;125(Pt 17):4067-76 [22685330] Trends Endocrinol Metab. 2013 Jan;24(1):4-12 [23043895] Genetics. 2013 Jan;193(1):1-50 [23275493] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/MOL.0000000000000057 ER - TY - JOUR T1 - Alterations of the lung methylome in allergic airway hyper-responsiveness. AN - 1506407114; 24446183 AB - Asthma is a chronic airway disorder characterized by recurrent attacks of breathlessness and wheezing, affecting 300 million people around the world (available at: www.who.int). To date, genetic factors associated with asthma susceptibility have been unable to explain the full etiology of asthma. Recent studies have demonstrated that the epigenetic disruption of gene expression plays an equally important role in the development of asthma through interaction with our environment. We sensitized 6-week-old C57BL/6J mice with house-dust-mite (HDM) extracts intraperitoneally followed by 5 weeks of exposure to HDM challenges (three times a week) intratracheally. HDM-exposed mice showed an increase in airway hyper-responsiveness (AHR) and inflammation together with structural remodeling of the airways. We applied methylated DNA immunoprecipitation-next generation sequencing (MeDIP-seq) for profiling of DNA methylation changes in the lungs in response to HDM. We observed about 20 million reads by a single-run of massive parallel sequencing. We performed bioinformatics and pathway analysis on the raw sequencing data to identify differentially methylated candidate genes in HDM-exposed mice. Specifically, we have revealed that the transforming growth factor beta signaling pathway is epigenetically modulated by chronic exposure to HDM. Here, we demonstrated that a specific allergen may play a role in AHR through an epigenetic mechanism by disrupting the expression of genes in lungs that might be involved in airway inflammation and remodeling. Our findings provide new insights into the potential mechanisms by which environmental allergens induce allergic asthma and such insights may assist in the development of novel preventive and therapeutic options for this debilitative disease. Copyright © 2014 Wiley Periodicals, Inc. JF - Environmental and molecular mutagenesis AU - Cheng, Robert Ys AU - Shang, Yan AU - Limjunyawong, Nathachit AU - Dao, Tyna AU - Das, Sandhya AU - Rabold, Richard AU - Sham, James Sk AU - Mitzner, Wayne AU - Tang, Wan-Yee AD - Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 244 EP - 255 VL - 55 IS - 3 KW - Transforming Growth Factor beta KW - 0 KW - Index Medicus KW - house dust mite KW - airway hyperresponsiveness KW - asthma KW - DNA methylation KW - next generation sequencing KW - Animals KW - Pyroglyphidae KW - Immunoprecipitation KW - Mice KW - Computational Biology KW - Epigenesis, Genetic KW - Inflammation KW - Gene Expression Profiling KW - Cells, Cultured KW - Bronchoalveolar Lavage Fluid KW - Mice, Inbred C57BL KW - Trachea -- metabolism KW - Transforming Growth Factor beta -- metabolism KW - Signal Transduction KW - Male KW - High-Throughput Nucleotide Sequencing KW - Lung -- immunology KW - Hypersensitivity -- immunology KW - Asthma -- metabolism KW - DNA Methylation KW - Lung -- metabolism KW - Hypersensitivity -- metabolism KW - Asthma -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1506407114?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alterations+of+the+lung+methylome+in+allergic+airway+hyper-responsiveness.&rft.au=Cheng%2C+Robert+Ys%3BShang%2C+Yan%3BLimjunyawong%2C+Nathachit%3BDao%2C+Tyna%3BDas%2C+Sandhya%3BRabold%2C+Richard%3BSham%2C+James+Sk%3BMitzner%2C+Wayne%3BTang%2C+Wan-Yee&rft.aulast=Cheng&rft.aufirst=Robert&rft.date=2014-04-01&rft.volume=55&rft.issue=3&rft.spage=244&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21851 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-05-01 N1 - Date created - 2014-03-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Rev Endocr Metab Disord. 2007 Jun;8(2):173-82 [17638084] Pulm Pharmacol Ther. 2009 Oct;22(5):370-8 [19114115] Proc Am Thorac Soc. 2008 Jan 1;5(1):89-96 [18094090] Toxicol Sci. 2008 Mar;102(1):76-81 [18042818] J Clin Immunol. 2008 Mar;28(2):139-46 [18004650] Nat Med. 2008 May;14(5):565-73 [18454155] Curr Allergy Asthma Rep. 2008 Nov;8(6):540-7 [18940147] PLoS One. 2009;4(2):e4488 [19221603] Environ Health Perspect. 2009 Feb;117(2):217-22 [19270791] Science. 2009 May 15;324(5929):930-5 [19372391] Genome Res. 2009 Jun;19(6):1044-56 [19273619] Respiration. 2012;84(1):4-11 [22759947] Environ Health Perspect. 2012 Aug;120(8):1195-200 [22562770] J Med Genet. 2001 May;38(5):285-303 [11333864] Cell Signal. 2013 Jan;25(1):159-67 [22986000] Pulm Pharmacol Ther. 2013 Feb;26(1):75-85 [22800879] PLoS Genet. 2013;9(2):e1003250 [23408899] BMC Med Genet. 2013;14:39 [23521807] Am J Respir Crit Care Med. 2009 Sep 1;180(5):462-7 [19498054] Neuropharmacology. 2013 Dec;75:233-45 [23958448] Annu Rev Genet. 2009;43:143-66 [19659441] PLoS One. 2010;5(3):e9674 [20300191] Clin Respir J. 2010 May;4 Suppl 1:28-34 [20500607] Lab Invest. 2010 Jul;90(7):997-1003 [20386537] Eur Respir J. 2010 Oct;36(4):950-61 [20889464] Am J Respir Cell Mol Biol. 2011 Feb;44(2):127-33 [20525803] Respirology. 2011 May;16(4):589-97 [21435099] Nature. 2011 May 19;473(7347):389-93 [21451524] Lancet. 2011 Sep 10;378(9795):1006-14 [21907864] Mol Cell Endocrinol. 2012 Apr 4;351(2):167-75 [22266540] J Allergy Clin Immunol. 2012 Apr;129(4):990-7.e6 [22227417] Environ Health Perspect. 2012 May;120(5):733-8 [22256332] J Allergy Clin Immunol. 2012 Jun;129(6):1602-10.e6 [22277202] Allergy. 2012 Jul;67(7):904-10 [22583153] Epigenetics. 2011 Sep 1;6(9):1131-7 [21975512] Carcinogenesis. 2002 Feb;23(2):335-9 [11872642] J Allergy Clin Immunol. 2002 Aug;110(2):249-54 [12170265] Oncogene. 2002 Dec 16;21(58):8935-48 [12483510] Am J Respir Crit Care Med. 2004 Feb 1;169(3):378-85 [14597485] Cancer Res. 2004 Jun 1;64(11):3844-8 [15172992] Exp Lung Res. 2004 Apr-May;30(3):223-50 [15195555] Am J Pathol. 2004 Oct;165(4):1097-106 [15466377] Annu Rev Genomics Hum Genet. 2004;5:479-510 [15485357] J Appl Physiol (1985). 1995 Aug;79(2):560-6 [7592218] J Immunol. 2004 Nov 15;173(10):6384-92 [15528378] J Allergy Clin Immunol. 2005 Jan;115(1):110-7 [15637555] J Allergy Clin Immunol. 2005 Jul;116(1):94-101 [15990780] J Clin Invest. 2006 Mar;116(3):783-96 [16511606] Curr Drug Targets. 2006 May;7(5):547-65 [16719766] Pflugers Arch. 2007 Jan;453(4):531-41 [17093969] Cancer Res. 2007 Feb 1;67(3):876-80 [17283117] Pediatr Res. 2007 May;61(5 Pt 2):5R-10R [17413851] J Immunol. 2007 Jun 1;178(11):7310-6 [17513781] Clin Exp Allergy. 2007 Aug;37(8):1165-74 [17651146] Nat Methods. 2007 Aug;4(8):651-7 [17558387] Curr Top Dev Biol. 2013;104:47-83 [23587238] Am J Respir Cell Mol Biol. 2013 Aug;49(2):279-87 [23526225] Proc Am Thorac Soc. 2008 Jan 1;5(1):15-22 [18094080] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/em.21851 ER - TY - JOUR T1 - High miR-21 expression from FFPE tissues is associated with poor survival and response to adjuvant chemotherapy in colon cancer AN - 1505334743; 19297133 AB - Colon cancer (CC) is a leading cause of cancer mortality. Novel biomarkers are needed to identify CC patients at high risk of recurrence and those who may benefit from therapeutic intervention. The aim of this study is to investigate if miR-21 expression from RNA isolated from formalin-fixed paraffin-embedded (FFPE) tissue sections is associated with prognosis and therapeutic outcome for patients with CC. The expression of miR-21 was measured by quantitative reverse transcriptase-polymerase chain reaction in a Japanese cohort (stage I-IV, n = 156) and a German cohort (stage II, n = 145). High miR-21 expression in tumors was associated with poor survival in both the stage II/III Japanese (p = 0.0008) and stage II German (p = 0.047) cohorts. These associations were independent of other clinical covariates in multivariable models. Receipt of adjuvant chemotherapy was not beneficial in patients with high miR-21 in either cohort. In the Japanese cohort, high miR-21 expression was significantly associated with poor therapeutic outcome (p = 0.0001) and adjuvant therapy was associated with improved survival in patients with low miR-21 (p = 0.001). These results suggest that miR-21 is a promising biomarker to identify patients with poor prognosis and can be accurately measured in FFPE tissues. The expression of miR-21 may also identify patients who will benefit from adjuvant chemotherapy. What's new? While many stage II colorectal cancer patients benefit from adjuvant therapy, others may be harmed, making the decision to use additional chemotherapy in these populations controversial. This study describes a candidate biomarker, miR-21, that could help overcome this problem. High expression of miR-21 in formalin-fixed paraffin-embedded (FFPE) tissues was associated with poor survival in two independent cohorts of colon cancer patients from Japan and Germany. Low miR-21 expression, on the other hand, was associated with improved survival with adjuvant therapy. JF - International Journal of Cancer AU - Oue, Naohide AU - Anami, Katsuhiro AU - Schetter, Aaron J AU - Moehler, Markus AU - Okayama, Hirokazu AU - Khan, Mohammed A AU - Bowman, Elise D AU - Mueller, Annett AU - Schad, Arno AU - Shimomura, Manabu AU - Hinoi, Takao AU - Aoyagi, Kazuhiko AU - Sasaki, Hiroki AU - Okajima, Masazumi AU - Ohdan, Hideki AU - Galle, Peter R AU - Yasui, Wataru AU - Harris, Curtis C AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 2014/04// PY - 2014 DA - Apr 2014 SP - 1926 EP - 1934 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 134 IS - 8 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Bioindicators KW - Tissues KW - Mortality KW - Chemotherapy KW - Survival KW - Intervention KW - Tumors KW - Cancer KW - Health risks KW - Colorectal carcinoma KW - Germany KW - Japan 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/1505334743?accountid=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=High+miR-21+expression+from+FFPE+tissues+is+associated+with+poor+survival+and+response+to+adjuvant+chemotherapy+in+colon+cancer&rft.au=Oue%2C+Naohide%3BAnami%2C+Katsuhiro%3BSchetter%2C+Aaron+J%3BMoehler%2C+Markus%3BOkayama%2C+Hirokazu%3BKhan%2C+Mohammed+A%3BBowman%2C+Elise+D%3BMueller%2C+Annett%3BSchad%2C+Arno%3BShimomura%2C+Manabu%3BHinoi%2C+Takao%3BAoyagi%2C+Kazuhiko%3BSasaki%2C+Hiroki%3BOkajima%2C+Masazumi%3BOhdan%2C+Hideki%3BGalle%2C+Peter+R%3BYasui%2C+Wataru%3BHarris%2C+Curtis+C&rft.aulast=Oue&rft.aufirst=Naohide&rft.date=2014-04-01&rft.volume=134&rft.issue=8&rft.spage=1926&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28522 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Bioindicators; Mortality; Tissues; Health risks; Chemotherapy; Colorectal carcinoma; Intervention; Survival; Tumors; Cancer; Germany; Japan DO - http://dx.doi.org/10.1002/ijc.28522 ER - TY - JOUR T1 - Telmisartan ameliorates glutamate-induced neurotoxicity: roles of AT(1) receptor blockade and PPARγ activation. AN - 1504149624; 24316465 AB - Sartans (Angiotensin II AT(1) Receptor Blockers, ARBs) are powerful neuroprotective agents in vivo and protect against IL-1β neurotoxicity in vitro. The purpose of this research was to determine the extent of sartan neuroprotection against glutamate excitotoxicity, a common cause of neuronal injury and apoptosis. The results show that sartans are neuroprotective, significantly reducing glutamate-induced neuronal injury and apoptosis in cultured rat primary cerebellar granule cells (CGCs). Telmisartan was the most potent sartan studied, with an order of potency telmisartan > candesartan > losartan > valsartan. Mechanisms involved reduction of pro-apoptotic caspase-3 activation, protection of the survival PI3K/Akt/GSK-3β pathway and prevention of glutamate-induced ERK1/2 activation. NMDA receptor stimulation was essential for glutamate-induced cell injury and apoptosis. Participation of AT(1A) receptor was supported by glutamate-induced upregulation of AT(1A) gene expression and AT(1) receptor binding. Conversely, AT(1B) or AT(2) receptors played no role. Glutamate-induced neuronal injury and the neuroprotective effect of telmisartan were decreased, but not abolished, in CGCs obtained from AT(1A) knock-out mice. This indicates that although AT(1) receptors are necessary for glutamate to exert its full neurotoxic potential, part of the neuroprotective effect of telmisartan is independent of AT(1) receptor blockade. PPARγ activation was also involved in the neuroprotective effects of telmisartan, as telmisartan enhanced PPARγ nuclear translocation and the PPARγ antagonist GW9662 partially reversed the neuroprotective effects of telmisartan. The present results substantiate the therapeutic use of sartans, in particular telmisartan, in neurodegenerative diseases and traumatic brain disorders where glutamate neurotoxicity plays a significant role. Published by Elsevier Ltd. JF - Neuropharmacology AU - Wang, Juan AU - Pang, Tao AU - Hafko, Roman AU - Benicky, Julius AU - Sanchez-Lemus, Enrique AU - Saavedra, Juan M AD - Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA. Electronic address: jw543@georgetown.edu. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA; New Drug Screening Center, China Pharmaceutical University, Nanjing 210009, PR China. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA. Electronic address: jb2304@georgetown.edu. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA. Electronic address: scientificsupport@mesoscale.com. ; Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, 20892, USA; Department of Pharmacology and Physiology, Georgetown University Medical Center, Washington, DC 20057, USA. Electronic address: jms522@georgetown.edu. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 249 EP - 261 VL - 79 KW - Agtr1a protein, mouse KW - 0 KW - Angiotensin II Type 1 Receptor Blockers KW - Benzimidazoles KW - Benzoates KW - Neuroprotective Agents KW - PPAR gamma KW - Receptor, Angiotensin, Type 1 KW - Glutamic Acid KW - 3KX376GY7L KW - telmisartan KW - U5SYW473RQ KW - Index Medicus KW - Apoptosis KW - Angiotensin II AT(1) Receptor Blockers KW - Neuroprotection KW - Telmisartan KW - PPARγ KW - Glutamate neurotoxicity KW - Animals KW - Apoptosis -- physiology KW - Mice KW - Mice, Transgenic KW - Angiotensin II Type 1 Receptor Blockers -- pharmacology KW - Cerebellum -- metabolism KW - Mice, Knockout KW - Rats KW - Rats, Sprague-Dawley KW - Cells, Cultured KW - Cerebellum -- drug effects KW - Apoptosis -- drug effects KW - Mice, Inbred C57BL KW - Female KW - Male KW - Glutamic Acid -- toxicity KW - Receptor, Angiotensin, Type 1 -- genetics KW - PPAR gamma -- antagonists & inhibitors KW - Neurons -- drug effects KW - Benzimidazoles -- pharmacology KW - Neurons -- physiology KW - PPAR gamma -- metabolism KW - Receptor, Angiotensin, Type 1 -- metabolism KW - Benzoates -- pharmacology KW - Neuroprotective Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504149624?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropharmacology&rft.atitle=Telmisartan+ameliorates+glutamate-induced+neurotoxicity%3A+roles+of+AT%281%29+receptor+blockade+and+PPAR%CE%B3+activation.&rft.au=Wang%2C+Juan%3BPang%2C+Tao%3BHafko%2C+Roman%3BBenicky%2C+Julius%3BSanchez-Lemus%2C+Enrique%3BSaavedra%2C+Juan+M&rft.aulast=Wang&rft.aufirst=Juan&rft.date=2014-04-01&rft.volume=79&rft.issue=&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=1873-7064&rft_id=info:doi/10.1016%2Fj.neuropharm.2013.11.022 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-03 N1 - Date created - 2014-03-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Front Biosci. 2008;13:1813-26 [17981670] Eur J Neurosci. 2008 Jan;27(2):343-51 [18190523] J Neurosci. 2008 Mar 5;28(10):2576-88 [18322101] J Neurosci Res. 2008 Apr;86(5):1096-105 [18041091] J Neurochem. 2008 May;105(3):994-1005 [18088378] J Mol Med (Berl). 2008 Jun;86(6):715-22 [18385968] Brain Res. 2008 Dec 9;1244:164-72 [18948087] Neurobiol Dis. 2008 Dec;32(3):486-98 [18930139] J Vis Exp. 2009;(23). pii: 990. doi: 10.3791/990 [19229177] J Cereb Blood Flow Metab. 2009 Mar;29(3):640-7 [19127280] Chin J Physiol. 2008 Dec 31;51(6):357-62 [19280879] Curr Opin Nephrol Hypertens. 2009 Mar;18(2):128-33 [19434050] Lab Invest. 2009 Aug;89(8):887-902 [19451898] Hypertension. 2009 Oct;54(4):782-7 [19635982] J Hypertens. 2009 Dec;27(12):2365-76 [19730394] Lancet. 2009 Nov 28;374(9704):1840-8 [19922995] BMJ. 2010;340:b5465 [20068258] Am J Cardiol. 2010 Jan 4;105(1 Suppl):21A-9A [20102970] J Hypertens. 2010 Mar;28(3):429 [20160578] Methods Mol Biol. 2010;633:233-9 [20204632] Curr Clin Pharmacol. 2010 May;5(2):89-95 [20156154] Rejuvenation Res. 2010 Apr-Jun;13(2-3):195-201 [20370487] Pflugers Arch. 2010 Jul;460(2):525-42 [20229265] Physiology (Bethesda). 2010 Jun;25(3):176-85 [20551231] Hypertens Res. 2010 Aug;33(8):831-5 [20505677] J Neurosurg. 2010 Sep;113(3):564-70 [20113156] Hypertens Res. 2010 Oct;33(10):1044-52 [20668453] Psychoneuroendocrinology. 2011 Jan;36(1):1-18 [21035950] Lancet Neurol. 2011 Jan;10(1):43-53 [20980201] Exp Neurol. 2011 Jan;227(1):128-35 [20965168] PLoS One. 2011;6(1):e16037 [21297982] Neuropsychopharmacology. 2011 Mar;36(4):857-70 [21150913] J Renin Angiotensin Aldosterone Syst. 2011 Mar;12(1):1-7 [20603272] J Alzheimers Dis. 2011;26(4):699-708 [21709373] J Hypertens. 2012 Jan;30(1):87-96 [22124178] Crit Care Med. 2012 Mar;40(3):935-44 [21926585] Cell Mol Neurobiol. 2012 Mar;32(2):191-200 [21822733] Hypertension. 2012 May;59(5):1079-88 [22454480] J Clin Pharm Ther. 2012 Jun;37(3):319-27 [21848583] Expert Opin Drug Saf. 2012 Jul;11(4):565-79 [22616948] Clin Sci (Lond). 2012 Nov;123(10):567-90 [22827472] J Neuroinflammation. 2012;9:102 [22642771] Curr HIV Res. 2012 Jul;10(5):392-406 [22591363] Neuropsychopharmacology. 2012 Dec;37(13):2817-29 [22892395] J Neuroinflammation. 2012;9:275 [23259598] Neurochem Int. 2013 Mar;62(4):468-77 [23357479] Br J Pharmacol. 2013 Jul;169(6):1404-16 [23647130] Pharmacol Rev. 2000 Sep;52(3):415-72 [10977869] J Int Med Res. 2000 Jul-Aug;28(4):149-67 [11014323] Stroke. 2000 Oct;31(10):2478-86 [11022082] Endocrinology. 2001 Sep;142(9):3880-9 [11517166] J Pharmacol Exp Ther. 2002 May;301(2):494-500 [11961048] J Neurotrauma. 2002 May;19(5):627-38 [12042097] Stroke. 2002 Sep;33(9):2297-303 [12215602] Physiol Genomics. 2002 Oct 2;11(1):21-30 [12361987] J Cereb Blood Flow Metab. 2003 Mar;23(3):371-80 [12621312] Cerebellum. 2002 Jan-Mar;1(1):41-55 [12879973] Biochem Biophys Res Commun. 2003 Aug 29;308(3):505-10 [12914779] J Clin Endocrinol Metab. 2003 Sep;88(9):4496-501 [12970329] J Neurosci. 2003 Sep 24;23(25):8692-700 [14507968] Eur J Clin Pharmacol. 2004 Feb;59(12):863-8 [14747881] Hypertension. 2004 May;43(5):993-1002 [15007034] Stroke. 2004 Jul;35(7):1726-31 [15143297] Biochem Biophys Res Commun. 1992 May 29;185(1):253-9 [1599461] Neuroreport. 1992 Oct;3(10):922-4 [1358253] Pharmacol Rev. 1993 Jun;45(2):205-51 [8372104] Science. 1993 Oct 29;262(5134):689-95 [7901908] Biochem Biophys Res Commun. 1993 Dec 15;197(2):440-9 [8267579] Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3521-5 [7724593] Brain Res. 1995 Dec 12;703(1-2):63-71 [8719616] Prostaglandins. 1997 Sep;54(3):601-24 [9373877] J Neuroendocrinol. 1998 Jan;10(1):67-72 [9510060] Cell Mol Neurobiol. 1999 Apr;19(2):277-88 [10081610] Crit Rev Neurobiol. 1999;13(1):45-82 [10223523] J Cereb Blood Flow Metab. 2005 Jul;25(7):878-86 [15729290] J Neurochem. 2005 Sep;94(5):1395-401 [15992368] Hypertension. 2006 Jul;48(1):141-8 [16769992] J Neurosci. 2006 Jul 12;26(28):7502-12 [16837598] Eur J Pharmacol. 2006 Dec 15;552(1-3):112-22 [17064684] Vascul Pharmacol. 2006 Sep;45(3):154-62 [16765099] Clin Sci (Lond). 2007 Jun;112(7):375-84 [17324119] J Clin Invest. 2007 Nov;117(11):3393-402 [17965777] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.neuropharm.2013.11.022 ER - TY - JOUR T1 - 9-Cis retinoic acid protects against methamphetamine-induced neurotoxicity in nigrostriatal dopamine neurons. AN - 1503552675; 23884514 AB - Methamphetamine (MA) is a drug of abuse as well as a dopaminergic neurotoxin. 9-Cis retinoic acid (9cRA), a biologically active derivative of vitamin A, has protective effects against damage caused by H(2)O(2) and oxygen-glucose deprivation in vitro as well as infarction and terminal deoxynucleotidyl transferase-mediated dNTP nick-end labeling (TUNEL) labeling in ischemic brain. The purpose of this study was to examine if there was a protective role for 9cRA against MA toxicity in nigrostriatal dopaminergic neurons. Primary dopaminergic neurons, prepared from rat embryonic ventral mesencephalic tissue, were treated with MA. High doses of MA decreased tyrosine hydroxylase (TH) immunoreactivity while increasing TUNEL labeling. These toxicities were significantly reduced by 9cRA. 9cRA also inhibited the export of Nur77 from nucleus to cytosol, a response that activates apoptosis. The interaction of 9cRA and MA in vivo was next examined in adult rats. 9cRA was delivered intracerebroventricularly; MA was given (5 mg/kg, 4×) one day later. Locomotor behavior was measured 2 days after surgery for a period of 48 h. High doses of MA significantly reduced locomotor activity and TH immunoreactivity in striatum. Administration of 9cRA antagonized these changes. Previous studies have shown that 9cRA can induce bone morphogenetic protein-7 (BMP7) expression and that administration of BMP7 attenuates MA toxicity. We demonstrated that MA treatment significantly reduced BMP7 mRNA expression in nigra. Noggin (a BMP antagonist) antagonized 9cRA-induced behavioral recovery and 9cRA-induced normalization of striatal TH levels. Our data suggest that 9cRA has a protective effect against MA-mediated neurodegeneration in dopaminergic neurons via upregulation of BMP. JF - Neurotoxicity research AU - Reiner, David J AU - Yu, Seong-Jin AU - Shen, Hui AU - He, Yi AU - Bae, Eunkyung AU - Wang, Yun AD - Neural Protection and Regeneration Section, Intramural Research Program, National Institute on Drug Abuse, NIH, Baltimore, MD, 21224, USA. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 248 EP - 261 VL - 25 IS - 3 KW - Bmp7 protein, rat KW - 0 KW - Bone Morphogenetic Protein 7 KW - Carrier Proteins KW - Neuroprotective Agents KW - Nr4a1 protein, rat KW - Nuclear Receptor Subfamily 4, Group A, Member 1 KW - RNA, Messenger KW - noggin protein KW - 148294-77-3 KW - alitretinoin KW - 1UA8E65KDZ KW - Methamphetamine KW - 44RAL3456C KW - Tretinoin KW - 5688UTC01R KW - Tyrosine 3-Monooxygenase KW - EC 1.14.16.2 KW - Index Medicus KW - Animals KW - Bone Morphogenetic Protein 7 -- metabolism KW - Tyrosine 3-Monooxygenase -- metabolism KW - Carrier Proteins -- metabolism KW - Nerve Degeneration -- physiopathology KW - Substantia Nigra -- drug effects KW - Nerve Degeneration -- chemically induced KW - Nuclear Receptor Subfamily 4, Group A, Member 1 -- metabolism KW - Motor Activity -- physiology KW - Rats KW - Nerve Degeneration -- drug therapy KW - Substantia Nigra -- physiopathology KW - Rats, Sprague-Dawley KW - Corpus Striatum -- physiopathology KW - RNA, Messenger -- metabolism KW - Cells, Cultured KW - Corpus Striatum -- drug effects KW - Motor Activity -- drug effects KW - Male KW - Tretinoin -- pharmacology KW - Dopaminergic Neurons -- drug effects KW - Neurotoxicity Syndromes -- prevention & control KW - Neurotoxicity Syndromes -- physiopathology KW - Dopaminergic Neurons -- physiology KW - Neuroprotective Agents -- pharmacology KW - Methamphetamine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1503552675?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicity+research&rft.atitle=9-Cis+retinoic+acid+protects+against+methamphetamine-induced+neurotoxicity+in+nigrostriatal+dopamine+neurons.&rft.au=Reiner%2C+David+J%3BYu%2C+Seong-Jin%3BShen%2C+Hui%3BHe%2C+Yi%3BBae%2C+Eunkyung%3BWang%2C+Yun&rft.aulast=Reiner&rft.aufirst=David&rft.date=2014-04-01&rft.volume=25&rft.issue=3&rft.spage=248&rft.isbn=&rft.btitle=&rft.title=Neurotoxicity+research&rft.issn=1476-3524&rft_id=info:doi/10.1007%2Fs12640-013-9413-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-05 N1 - Date created - 2014-02-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Neurosci Lett. 2004 Oct 14;369(2):138-41 [15450683] BMC Neurosci. 2012;13:120 [23040108] Nature. 1992 Jan 23;355(6358):359-61 [1309942] J Neurosci Res. 1995 Jan 1;40(1):1-9 [7714916] Dev Dyn. 1995 Mar;202(3):312-23 [7780180] Mol Cell Biol. 1995 Oct;15(10):5576-85 [7565709] J Neurosci Res. 1999 Nov 1;58(3):426-35 [10518116] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):868-73 [15644446] Neurotoxicology. 2006 Jan;27(1):131-6 [16165214] Neuropsychopharmacology. 2006 Nov;31(11):2359-67 [16855532] Neuroscience. 2008 Jan 2;151(1):92-103 [18082966] Acta Neurochir Suppl. 2008;101:93-8 [18642641] Neurosci Lett. 2008 Sep 5;442(1):15-8 [18598737] Prog Neuropsychopharmacol Biol Psychiatry. 2008 Dec 12;32(8):1957-66 [18930103] J Neurosci Res. 2009 Feb;87(2):545-55 [18803283] Neurotoxicology. 2009 Jan;30(1):127-35 [19056420] Neurotoxicology. 2009 May;30(3):436-44 [19442829] FASEB J. 2009 Jun;23(6):1958-68 [19218497] Neurochem Int. 2010 Mar;56(4):620-6 [20096738] Science. 2000 Aug 18;289(5482):1159-64 [10947977] Brain Res Mol Brain Res. 2000 Nov 10;83(1-2):121-4 [11072101] Science. 2000 Dec 15;290(5499):2140-4 [11118147] Brain Res Mol Brain Res. 2001 Sep 10;93(1):64-9 [11532339] Arch Biochem Biophys. 2001 Sep 15;393(2):262-70 [11556813] Dev Dyn. 2001 Nov;222(3):341-53 [11747070] Synapse. 2002 Jun 1;44(3):158-65 [11954047] Mol Cells. 2002 Apr 30;13(2):221-7 [12018843] Nephrol Dial Transplant. 2002;17 Suppl 9:84-7 [12386300] Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7135-40 [12782789] FASEB J. 2003 Oct;17(13):1775-88 [14519657] Arch Biochem Biophys. 2003 Dec 1;420(1):185-93 [14622989] PLoS One. 2010;5(12):e15193 [21151937] Brain Res Bull. 2011 Jul 15;85(6):380-4 [21600965] Annu Rev Nutr. 2011 Aug 21;31:321-51 [21756134] Neuroscience. 2011 Oct 27;194:170-80 [21867746] Psychopharmacology (Berl). 2012 Jun;221(3):479-92 [22160138] J Biol Chem. 2012 Jul 6;287(28):23726-39 [22511762] Mol Cell Biol. 2004 Nov;24(22):9705-25 [15509776] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s12640-013-9413-4 ER - TY - JOUR T1 - Molecular cloning and knockdown of galactocerebrosidase in zebrafish: new insights into the pathogenesis of Krabbe's disease. AN - 1501834079; 24463171 AB - The lysosomal hydrolase galactocerebrosidase (GALC) catalyzes the removal of galactose from galactosylceramide and from other sphingolipids. GALC deficiency is responsible for globoid cell leukodystrophy (GLD), or Krabbe's disease, an early lethal inherited neurodegenerative disorder characterized by the accumulation of the neurotoxic metabolite psychosine in the central nervous system (CNS). The poor outcome of current clinical treatments calls for novel model systems to investigate the biological impact of GALC down-regulation and for the search of novel therapeutic strategies in GLD. Zebrafish (Danio rerio) represents an attractive vertebrate model for human diseases. Here, lysosomal GALC activity was demonstrated in the brain of zebrafish adults and embryos. Accordingly, we identified two GALC co-orthologs (named galca and galcb) dynamically co-expressed in CNS during zebrafish development. Both genes encode for lysosomal enzymes endowed with GALC activity. Single down-regulation of galca or galcb by specific antisense morpholino oligonucleotides results in a partial decrease of GALC activity in zebrafish embryos that was abrogated in double galca/galcb morphants. However, no psychosine accumulation was observed in galca/galcb double morphants. Nevertheless, double galca/galcb knockdown caused reduction and partial disorganization of the expression of the early neuronal marker neuroD and an increase of apoptotic events during CNS development. These observations provide new insights into the pathogenesis of GLD, indicating that GALC loss-of-function may have pathological consequences in developing CNS independent of psychosine accumulation. Also, they underscore the potentiality of the zebrafish system in studying the pathogenesis of lysosomal neurodegenerative diseases, including GLD. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biochimica et biophysica acta AU - Zizioli, Daniela AU - Guarienti, Michela AU - Tobia, Chiara AU - Gariano, Giuseppina AU - Borsani, Giuseppe AU - Bresciani, Roberto AU - Ronca, Roberto AU - Giacopuzzi, Edoardo AU - Preti, Augusto AU - Gaudenzi, Germano AU - Belleri, Mirella AU - Di Salle, Emanuela AU - Fabrias, Gemma AU - Casas, Josefina AU - Ribatti, Domenico AU - Monti, Eugenio AU - Presta, Marco AD - Unit of Biotechnology, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. ; Unit of Oncology and Experimental Immunology, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. ; Unit of Biology and Genetics, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. ; Department of Biology, University of Milan, Milan, Italy. ; Research Unit on Bioactive Molecules (RUBAM), Department of Biomedicinal Chemistry, Institute for Advanced Chemistry of Catalonia (IQAC), Spanish Council for Scientific Research (CSIC), Barcelona, Spain. ; Department of Basic Biomedical Sciences, Unit of Human Anatomy and Histology, University of Bari, Bari, Italy; National Cancer Institute, Giovanni Paolo II, Bari, Italy. ; Unit of Oncology and Experimental Immunology, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy. Electronic address: presta@med.unibs.it. Y1 - 2014/04// PY - 2014 DA - April 2014 SP - 665 EP - 675 VL - 1842 IS - 4 SN - 0006-3002, 0006-3002 KW - Galactosylceramidase KW - EC 3.2.1.46 KW - Index Medicus KW - Krabbe disease KW - Embryonic development KW - Sphingolipid KW - Zebrafish KW - Brain -- enzymology KW - Animals KW - Humans KW - Brain -- embryology KW - Disease Models, Animal KW - Cloning, Molecular KW - Leukodystrophy, Globoid Cell -- etiology KW - Galactosylceramidase -- genetics KW - Zebrafish -- metabolism KW - Galactosylceramidase -- physiology KW - Zebrafish -- embryology KW - Leukodystrophy, Globoid Cell -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1501834079?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Molecular+cloning+and+knockdown+of+galactocerebrosidase+in+zebrafish%3A+new+insights+into+the+pathogenesis+of+Krabbe%27s+disease.&rft.au=Zizioli%2C+Daniela%3BGuarienti%2C+Michela%3BTobia%2C+Chiara%3BGariano%2C+Giuseppina%3BBorsani%2C+Giuseppe%3BBresciani%2C+Roberto%3BRonca%2C+Roberto%3BGiacopuzzi%2C+Edoardo%3BPreti%2C+Augusto%3BGaudenzi%2C+Germano%3BBelleri%2C+Mirella%3BDi+Salle%2C+Emanuela%3BFabrias%2C+Gemma%3BCasas%2C+Josefina%3BRibatti%2C+Domenico%3BMonti%2C+Eugenio%3BPresta%2C+Marco&rft.aulast=Zizioli&rft.aufirst=Daniela&rft.date=2014-04-01&rft.volume=1842&rft.issue=4&rft.spage=665&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbadis.2014.01.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-23 N1 - Date created - 2014-02-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbadis.2014.01.008 ER - TY - JOUR T1 - Semiparametric Bayesian joint modeling of a binary and continuous outcome with applications in toxicological risk assessment. AN - 1504450317; 24123309 AB - Many dose-response studies collect data on correlated outcomes. For example, in developmental toxicity studies, uterine weight and presence of malformed pups are measured on the same dam. Joint modeling can result in more efficient inferences than independent models for each outcome. Most methods for joint modeling assume standard parametric response distributions. However, in toxicity studies, it is possible that response distributions vary in location and shape with dose, which may not be easily captured by standard models. To address this issue, we propose a semiparametric Bayesian joint model for a binary and continuous response. In our model, a kernel stick-breaking process prior is assigned to the distribution of a random effect shared across outcomes, which allows flexible changes in distribution shape with dose shared across outcomes. The model also includes outcome-specific fixed effects to allow different location effects. In simulation studies, we found that the proposed model provides accurate estimates of toxicological risk when the data do not satisfy assumptions of standard parametric models. We apply our method to data from a developmental toxicity study of ethylene glycol diethyl ether. Copyright © 2013 John Wiley & Sons, Ltd. JF - Statistics in medicine AU - Hwang, Beom Seuk AU - Pennell, Michael L AD - Biostatistics and Bioinformatics Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, U.S.A. Y1 - 2014/03/30/ PY - 2014 DA - 2014 Mar 30 SP - 1162 EP - 1175 VL - 33 IS - 7 KW - Ethyl Ethers KW - 0 KW - Ethylene Glycols KW - ethylene glycol diethyl ether KW - 629-14-1 KW - Index Medicus KW - kernel stick-breaking process KW - nonparametric Bayes KW - benchmark dose KW - developmental toxicology study KW - Animals KW - Ethylene Glycols -- toxicity KW - Computer Simulation KW - Mice KW - Markov Chains KW - Uterus -- pathology KW - Monte Carlo Method KW - Organ Size KW - Female KW - Pregnancy KW - Ethyl Ethers -- toxicity KW - Bayes Theorem KW - Toxicology -- methods KW - Models, Statistical KW - Risk Assessment -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504450317?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Statistics+in+medicine&rft.atitle=Semiparametric+Bayesian+joint+modeling+of+a+binary+and+continuous+outcome+with+applications+in+toxicological+risk+assessment.&rft.au=Hwang%2C+Beom+Seuk%3BPennell%2C+Michael+L&rft.aulast=Hwang&rft.aufirst=Beom&rft.date=2014-03-30&rft.volume=33&rft.issue=7&rft.spage=1162&rft.isbn=&rft.btitle=&rft.title=Statistics+in+medicine&rft.issn=1097-0258&rft_id=info:doi/10.1002%2Fsim.6007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-06 N1 - Date created - 2014-03-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/sim.6007 ER - TY - JOUR T1 - The steric gate of DNA polymerase ι regulates ribonucleotide incorporation and deoxyribonucleotide fidelity. AN - 1511822636; 24532793 AB - Accurate DNA synthesis in vivo depends on the ability of DNA polymerases to select dNTPs from a nucleotide pool dominated by NTPs. High fidelity replicative polymerases have evolved to efficiently exclude NTPs while copying long stretches of undamaged DNA. However, to bypass DNA damage, cells utilize specialized low fidelity polymerases to perform translesion DNA synthesis (TLS). Of interest is human DNA polymerase ι (pol ι), which has been implicated in TLS of oxidative and UV-induced lesions. Here, we evaluate the ability of pol ι to incorporate NTPs during DNA synthesis. pol ι incorporates and extends NTPs opposite damaged and undamaged template bases in a template-specific manner. The Y39A "steric gate" pol ι mutant is considerably more active in the presence of Mn(2+) compared with Mg(2+) and exhibits a marked increase in NTP incorporation and extension, and surprisingly, it also exhibits increased dNTP base selectivity. Our results indicate that a single residue in pol ι is able to discriminate between NTPs and dNTPs during DNA synthesis. Because wild-type pol ι incorporates NTPs in a template-specific manner, certain DNA sequences may be "at risk" for elevated mutagenesis during pol ι-dependent TLS. Molecular modeling indicates that the constricted active site of wild-type pol ι becomes more spacious in the Y39A variant. Therefore, the Y39A substitution not only permits incorporation of ribonucleotides but also causes the enzyme to favor faithful Watson-Crick base pairing over mutagenic configurations. JF - The Journal of biological chemistry AU - Donigan, Katherine A AU - McLenigan, Mary P AU - Yang, Wei AU - Goodman, Myron F AU - Woodgate, Roger AD - From the Laboratory of Genomic Integrity, NICHD and. Y1 - 2014/03/28/ PY - 2014 DA - 2014 Mar 28 SP - 9136 EP - 9145 VL - 289 IS - 13 KW - DNA Primers KW - 0 KW - Deoxyribonucleotides KW - Ribonucleotides KW - Tyrosine KW - 42HK56048U KW - Manganese KW - 42Z2K6ZL8P KW - DNA KW - 9007-49-2 KW - DNA polymerase iota KW - EC 2.7.7.- KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - DNA Synthesis KW - DNA Repair KW - Steric Gate Mutant KW - DNA Polymerase Iota KW - DNA-binding Protein KW - Ribonucleotide Incorporation KW - Y Family DNA Polymerase KW - Mutagenesis KW - Enzyme Kinetics KW - Manganese -- pharmacology KW - Models, Molecular KW - DNA Damage KW - DNA Primers -- genetics KW - DNA -- metabolism KW - Humans KW - Catalytic Domain KW - Amino Acid Sequence KW - DNA -- biosynthesis KW - Base Pairing KW - Conserved Sequence KW - DNA -- genetics KW - Molecular Sequence Data KW - DNA -- chemistry KW - Substrate Specificity KW - Mutation KW - Ribonucleotides -- metabolism KW - Deoxyribonucleotides -- metabolism KW - DNA-Directed DNA Polymerase -- genetics KW - DNA-Directed DNA Polymerase -- metabolism KW - DNA-Directed DNA Polymerase -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1511822636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+steric+gate+of+DNA+polymerase+%CE%B9+regulates+ribonucleotide+incorporation+and+deoxyribonucleotide+fidelity.&rft.au=Donigan%2C+Katherine+A%3BMcLenigan%2C+Mary+P%3BYang%2C+Wei%3BGoodman%2C+Myron+F%3BWoodgate%2C+Roger&rft.aulast=Donigan&rft.aufirst=Katherine&rft.date=2014-03-28&rft.volume=289&rft.issue=13&rft.spage=9136&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M113.545442 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-05-21 N1 - Date created - 2014-03-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Science. 1999 Dec 3;286(5446):1897-905 [10583946] Mol Cell. 2013 May 9;50(3):437-43 [23603118] Nature. 2000 Aug 31;406(6799):1015-9 [10984059] EMBO J. 2000 Oct 2;19(19):5259-66 [11013228] EMBO J. 2002 Nov 15;21(22):6246-56 [12426396] J Biol Chem. 2003 Aug 8;278(32):29649-54 [12777390] Mol Cell Biol. 2004 Jan;24(2):936-43 [14701763] Proc Natl Acad Sci U S A. 1983 Jan;80(2):487-91 [6300848] Proc Natl Acad Sci U S A. 1984 Mar;81(5):1494-8 [6369329] J Biol Chem. 1987 May 15;262(14):6864-70 [3571289] J Biol Chem. 1987 Oct 25;262(30):14689-96 [3667598] J Biol Chem. 1989 Aug 25;264(24):14415-23 [2474545] Bioessays. 1991 Feb;13(2):79-84 [2029269] Mol Cell Biochem. 1994 Nov 9;140(1):1-22 [7877593] Adv Protein Chem. 2004;69:205-28 [15588844] Mol Cell. 2005 May 27;18(5):499-505 [15916957] Structure. 2005 Oct;13(10):1569-77 [16216587] Nat Struct Mol Biol. 2006 Jul;13(7):619-25 [16819516] J Biol Chem. 2006 Sep 15;281(37):27286-91 [16831866] Cancer Res. 2007 Apr 1;67(7):3018-26 [17409408] J Biol Chem. 2007 Aug 24;282(34):24689-96 [17609217] Nucleic Acids Res. 2008 Feb;36(2):411-22 [18039710] Biochemistry. 2008 Aug 5;47(31):8048-57 [18616290] EMBO J. 2008 Nov 5;27(21):2883-95 [18923427] J Biol Chem. 2009 Jan 16;284(3):1732-40 [18984581] Science. 2001 Mar 16;291(5511):2156-9 [11251121] Structure. 2009 Apr 15;17(4):530-7 [19368886] EMBO J. 2009 Jun 3;28(11):1644-54 [19440206] J Bacteriol. 2009 Aug;191(15):4815-23 [19482923] Structure. 2009 Jul 15;17(7):974-80 [19604477] Proc Natl Acad Sci U S A. 2010 Mar 16;107(11):4949-54 [20194773] Nucleic Acids Res. 2010 Apr;38(6):e85 [20008099] J Biol Chem. 2010 Aug 6;285(32):24457-65 [20519499] Nat Chem Biol. 2010 Oct;6(10):774-81 [20729855] Biochemistry. 2011 Feb 22;50(7):1135-42 [21226515] Proc Natl Acad Sci U S A. 2011 Feb 22;108(8):3210-5 [21300901] Nat Rev Mol Cell Biol. 2012 Mar;13(3):141-52 [22358330] Cell. 2012 May 25;149(5):1008-22 [22579044] Nucleic Acids Res. 2012 Jul;40(13):6144-57 [22422840] Anal Biochem. 2012 Oct 15;429(2):132-9 [22828411] Mol Cell. 2012 Sep 28;47(6):980-6 [22864116] Nucleic Acids Res. 2013 Feb 1;41(3):1649-60 [23248005] Mol Cell. 2013 May 9;50(3):323-32 [23603115] Genes Dev. 2000 Jul 1;14(13):1642-50 [10887158] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M113.545442 ER - TY - JOUR T1 - Epidemiologic contributions to recent cancer trends among HIV-infected people in the United States AN - 1765982938; PQ0002610751 AB - Objective: HIV-infected people have elevated risk for some cancers. Changing incidence of these cancers over time may reflect changes in three factors: HIV population demographic structure (e.g. age distribution), general population (background) cancer rates, and HIV-associated relative risks. We assessed the contributions of these factors to time trends for 10 cancers during 1996-2010. Design: Population-based registry linkage study. Methods: We applied Poisson models to data from the U.S. HIV/AIDS Cancer Match Study to estimate annual percentage changes (APCs) in incidence rates of AIDS-defining cancers [ADCs: Kaposi sarcoma, non-Hodgkin lymphoma (NHL), and cervical cancer] and seven non-AIDS-defining cancers (NADCs). We evaluated HIV-infected cancer trends with and without adjustment for demographics, trends in background rates, and trends in standardized incidence ratios (SIRs, to capture relative risk). Results: Cancer rates among HIV-infected people rose over time for anal (APC 3.8%), liver (8.5%), and prostate (9.8%) cancers, but declined for Kaposi sarcoma (1996-2000: -29.3%; 2000-2010: -7.8%), NHL (1996-2003: -15.7%; 2003-2010: -5.5%), cervical cancer (-11.1%), Hodgkin lymphoma (-4.0%), and lung cancer (-2.8%). Breast and colorectal cancer incidence did not change over time. Based on comparison to adjusted models, changing demographics contributed to trends for Kaposi sarcoma and breast, colorectal, liver, lung, and prostate cancers (all P < 0.01). Trends in background rates were notable for liver (APC 5.6%) and lung (-3.2%) cancers. SIRs declined for ADCs, Hodgkin lymphoma (APC -3.2%), and lung cancer (-4.4%). Conclusion: Demographic shifts influenced several cancer trends among HIV-infected individuals. Falling relative risks largely explained ADC declines, while background incidence contributed to some NADC trends. JF - AIDS AU - Robbins, Hilary A AU - Shiels, Meredith S AU - Pfeiffer, Ruth M AU - Engels, Eric A AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland, USA, hilary.robbins@nih.gov Y1 - 2014/03/27/ PY - 2014 DA - 2014 Mar 27 SP - 881 EP - 890 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 IS - 6 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - cancer KW - HIV/AIDS KW - statistical modeling KW - trends KW - United States KW - Risk assessment KW - Acquired immune deficiency syndrome KW - Hodgkin's disease KW - Cervical cancer KW - Colorectal cancer KW - Models KW - Demography KW - Non-Hodgkin's lymphoma KW - adenomatous polyposis coli KW - Risk factors KW - Lymphoma KW - Lung cancer KW - Age composition KW - Data processing KW - Cancer KW - Health risks KW - USA KW - Prostate cancer KW - Human immunodeficiency virus KW - Sarcoma KW - Liver KW - Breast cancer KW - Standards KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765982938?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Epidemiologic+contributions+to+recent+cancer+trends+among+HIV-infected+people+in+the+United+States&rft.au=Robbins%2C+Hilary+A%3BShiels%2C+Meredith+S%3BPfeiffer%2C+Ruth+M%3BEngels%2C+Eric+A&rft.aulast=Robbins&rft.aufirst=Hilary&rft.date=2014-03-27&rft.volume=28&rft.issue=6&rft.spage=881&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000163 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Risk assessment; Age composition; Acquired immune deficiency syndrome; Hodgkin's disease; Data processing; Cervical cancer; Colorectal cancer; Models; Demography; Prostate cancer; adenomatous polyposis coli; Liver; Sarcoma; Breast cancer; Lung cancer; Cancer; Non-Hodgkin's lymphoma; Health risks; Human immunodeficiency virus; Risk factors; Standards; Lymphoma; USA DO - http://dx.doi.org/10.1097/QAD.0000000000000163 ER - TY - CPAPER T1 - Genetic Medicine in Uganda - The Children's National Medical Center and NIH Experience T2 - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014) AN - 1518616882; 6286300 JF - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014) AU - Kruszka, Paul Y1 - 2014/03/25/ PY - 2014 DA - 2014 Mar 25 KW - Uganda KW - Children UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518616882?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.atitle=Genetic+Medicine+in+Uganda+-+The+Children%27s+National+Medical+Center+and+NIH+Experience&rft.au=Kruszka%2C+Paul&rft.aulast=Kruszka&rft.aufirst=Paul&rft.date=2014-03-25&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.acmgmeeting.net/acmg2014/CUSTOM/images/client/2014/2014%20ACMG%20Program%20Guide.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Glut1 Deficiency and other Metabolic Causes of Microcephaly - Recognizing Treatable Conditions T2 - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014) AN - 1518616866; 6286410 JF - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014) AU - Wolfe, Lynne Y1 - 2014/03/25/ PY - 2014 DA - 2014 Mar 25 KW - Microencephaly UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518616866?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.atitle=Glut1+Deficiency+and+other+Metabolic+Causes+of+Microcephaly+-+Recognizing+Treatable+Conditions&rft.au=Wolfe%2C+Lynne&rft.aulast=Wolfe&rft.aufirst=Lynne&rft.date=2014-03-25&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.acmgmeeting.net/acmg2014/CUSTOM/images/client/2014/2014%20ACMG%20Program%20Guide.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - The Spectrum of Vascular Anomalies in Disorders of the P13K-AKT Pathway T2 - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014) AN - 1518615274; 6286361 JF - 2014 Annual Clinical Genetics Meeting of the American College of Medical Genetics (ACMG 2014) AU - Biesecker, Leslie Y1 - 2014/03/25/ PY - 2014 DA - 2014 Mar 25 KW - Genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518615274?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.atitle=The+Spectrum+of+Vascular+Anomalies+in+Disorders+of+the+P13K-AKT+Pathway&rft.au=Biesecker%2C+Leslie&rft.aulast=Biesecker&rft.aufirst=Leslie&rft.date=2014-03-25&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Clinical+Genetics+Meeting+of+the+American+College+of+Medical+Genetics+%28ACMG+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.acmgmeeting.net/acmg2014/CUSTOM/images/client/2014/2014%20ACMG%20Program%20Guide.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - JOUR T1 - A new approach to radial basis function approximation and its application to QSAR. AN - 1510105943; 24451033 AB - We describe a novel approach to RBF approximation, which combines two new elements: (1) linear radial basis functions and (2) weighting the model by each descriptor's contribution. Linear radial basis functions allow one to achieve more accurate predictions for diverse data sets. Taking into account the contribution of each descriptor produces more accurate similarity values used for model development. The method was validated on 14 public data sets comprising nine physicochemical properties and five toxicity endpoints. We also compared the new method with five different QSAR methods implemented in the EPA T.E.S.T. program. Our approach, implemented in the program GUSAR, showed a reasonable accuracy of prediction and high coverage for all external test sets, providing more accurate prediction results than the comparison methods and even the consensus of these methods. Using our new method, we have created models for physicochemical and toxicity endpoints, which we have made freely available in the form of an online service at http://cactus.nci.nih.gov/chemical/apps/cap. JF - Journal of chemical information and modeling AU - Zakharov, Alexey V AU - Peach, Megan L AU - Sitzmann, Markus AU - Nicklaus, Marc C AD - CADD Group, Chemical Biology Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health , DHHS, NCI-Frederick, , 376 Boyles St., Frederick, Maryland 21702, United States. Y1 - 2014/03/24/ PY - 2014 DA - 2014 Mar 24 SP - 713 EP - 719 VL - 54 IS - 3 KW - Index Medicus KW - Rats KW - Daphnia -- physiology KW - Animals KW - Daphnia -- drug effects KW - Computer Simulation KW - Neural Networks (Computer) KW - Toxicity Tests KW - Databases, Factual KW - Cyprinidae -- physiology KW - Tetrahymena -- drug effects KW - Tetrahymena -- physiology KW - Internet KW - Software KW - Quantitative Structure-Activity Relationship KW - Algorithms KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510105943?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chemical+information+and+modeling&rft.atitle=A+new+approach+to+radial+basis+function+approximation+and+its+application+to+QSAR.&rft.au=Zakharov%2C+Alexey+V%3BPeach%2C+Megan+L%3BSitzmann%2C+Markus%3BNicklaus%2C+Marc+C&rft.aulast=Zakharov&rft.aufirst=Alexey&rft.date=2014-03-24&rft.volume=54&rft.issue=3&rft.spage=713&rft.isbn=&rft.btitle=&rft.title=Journal+of+chemical+information+and+modeling&rft.issn=1549-960X&rft_id=info:doi/10.1021%2Fci400704f LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-24 N1 - Date created - 2014-03-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Chem Inf Comput Sci. 2004 Sep-Oct;44(5):1763-73 [15446835] J Comput Aided Mol Des. 1997 Mar;11(2):135-42 [9089431] SAR QSAR Environ Res. 2007 May-Jun;18(3-4):285-98 [17514571] Methods Mol Biol. 2008;458:137-58 [19065809] Chem Res Toxicol. 2009 Dec;22(12):1913-21 [19845371] Mol Pharm. 2013 Apr 1;10(4):1224-35 [23305561] J Agric Food Chem. 2011 Apr 13;59(7):2909-17 [20879794] Eur J Med Chem. 2011 Sep;46(9):4374-82 [21802177] Future Med Chem. 2012 Oct;4(15):1933-44 [23088274] Chem Res Toxicol. 2012 Nov 19;25(11):2378-85 [23078046] SAR QSAR Environ Res. 2009 Oct;20(7-8):679-709 [20024804] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/ci400704f ER - TY - CPAPER T1 - Fetal Consequences of In Utero Antiretroviral (ARV) Nucleoside Reverse Transcriptase Inhibitor (NRTI) Exposures in Primates T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AN - 1518614783; 6281379 JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AU - Poirier, M AU - Olivero, O AU - Liu, Y AU - Divi, R AU - Woodward, R Y1 - 2014/03/23/ PY - 2014 DA - 2014 Mar 23 KW - Antiviral agents KW - Inhibitors KW - Primates KW - Antiretroviral agents KW - Fetuses KW - nucleoside reverse transcriptase inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518614783?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Fetal+Consequences+of+In+Utero+Antiretroviral+%28ARV%29+Nucleoside+Reverse+Transcriptase+Inhibitor+%28NRTI%29+Exposures+in+Primates&rft.au=Poirier%2C+M%3BOlivero%2C+O%3BLiu%2C+Y%3BDivi%2C+R%3BWoodward%2C+R&rft.aulast=Poirier&rft.aufirst=M&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - From Research to Regulatory Science: Toxicology Careers in Government T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AN - 1518613249; 6281539 JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AU - Germolec, D Y1 - 2014/03/23/ PY - 2014 DA - 2014 Mar 23 KW - Careers KW - Toxicology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518613249?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=From+Research+to+Regulatory+Science%3A+Toxicology+Careers+in+Government&rft.au=Germolec%2C+D&rft.aulast=Germolec&rft.aufirst=D&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Leadership--Doing the Right Things T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AN - 1518613130; 6281582 JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AU - Birnbaum, L Y1 - 2014/03/23/ PY - 2014 DA - 2014 Mar 23 KW - Rights KW - Lead UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518613130?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Leadership--Doing+the+Right+Things&rft.au=Birnbaum%2C+L&rft.aulast=Birnbaum&rft.aufirst=L&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - The Office of Health Assessment and Translation Approach to Evidence Integration for Assessment of Noncancer Health Effects T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AN - 1518611784; 6281524 JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AU - Rooney, A AU - Boyles, A AU - Wolfe, M AU - Thayer, K Y1 - 2014/03/23/ PY - 2014 DA - 2014 Mar 23 KW - Integration KW - Translation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611784?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=The+Office+of+Health+Assessment+and+Translation+Approach+to+Evidence+Integration+for+Assessment+of+Noncancer+Health+Effects&rft.au=Rooney%2C+A%3BBoyles%2C+A%3BWolfe%2C+M%3BThayer%2C+K&rft.aulast=Rooney&rft.aufirst=A&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - The Concepts and Methods for Stem Cells T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AN - 1518609471; 6281297 JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AU - Tokar, E Y1 - 2014/03/23/ PY - 2014 DA - 2014 Mar 23 KW - Stem cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609471?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=The+Concepts+and+Methods+for+Stem+Cells&rft.au=Tokar%2C+E&rft.aulast=Tokar&rft.aufirst=E&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Stem Cells in Carcinogenesis T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AN - 1518609431; 6281298 JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AU - Waalkes, M Y1 - 2014/03/23/ PY - 2014 DA - 2014 Mar 23 KW - Stem cells KW - Carcinogenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609431?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Stem+Cells+in+Carcinogenesis&rft.au=Waalkes%2C+M&rft.aulast=Waalkes&rft.aufirst=M&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Constructing AOPs for Developmental Toxicities T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AN - 1518609386; 6281260 JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AU - Kleinstreuer, N Y1 - 2014/03/23/ PY - 2014 DA - 2014 Mar 23 KW - Toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609386?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Constructing+AOPs+for+Developmental+Toxicities&rft.au=Kleinstreuer%2C+N&rft.aulast=Kleinstreuer&rft.aufirst=N&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Challenges and Recommendations for Future Asbestos Research T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AN - 1518609358; 6281346 JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AU - Miller, A Y1 - 2014/03/23/ PY - 2014 DA - 2014 Mar 23 KW - Asbestos UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609358?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Challenges+and+Recommendations+for+Future+Asbestos+Research&rft.au=Miller%2C+A&rft.aulast=Miller&rft.aufirst=A&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Perinatal Exposures to Environmental Pollutants and Children's Health T2 - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AN - 1518609338; 6281377 JF - 53rd Annual Meeting of the Society of Toxicology (SOT 2014) AU - Heindel, J AU - Schug, T AU - Gray, K Y1 - 2014/03/23/ PY - 2014 DA - 2014 Mar 23 KW - Pollutants KW - Perinatal exposure KW - Children UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609338?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.atitle=Perinatal+Exposures+to+Environmental+Pollutants+and+Children%27s+Health&rft.au=Heindel%2C+J%3BSchug%2C+T%3BGray%2C+K&rft.aulast=Heindel&rft.aufirst=J&rft.date=2014-03-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=53rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2014Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - JOUR T1 - Transgenic mice expressing S129 phosphorylation mutations in α-synuclein. AN - 1506398416; 24486885 AB - Aggregated α-synuclein is a predominant constituent of Lewy bodies, the intracellular protein aggregates seen in Parkinson's disease. While most α-synuclein in the nervous system is unphosphorylated, the majority of α-synuclein in Lewy bodies is phosphorylated at serine 129 (S129). We developed transgenic mice expressing human SNCA with either a phosphomimic (S129D) or a non-phosphorylatable (S129A) mutation, on a mouse Snca knockout background. Transgenic lines with each mutation expressing the human α-synuclein protein at levels ranging from 0.3 to 1.9 fold of endogenous mouse protein were chosen to avoid toxic overexpression effects. We previously demonstrated an altered distribution of presynaptic vesicles in Snca knockout mice, as well as enhanced interaction between presynaptic cytoskeletal proteins and α-synuclein when phosphorylated at S129 or carrying an S129D mutation. We therefore examined α-synuclein's synaptic localization and the distribution of presynaptic vesicles in these mutants. In addition, we evaluated the transgenic lines for reduced colonic motility, an early marker of α-synuclein pathology, and α-synuclein aggregates. No abnormalities were detected in mice expressing either phosphorylation mutant protein as their only α-synuclein protein. These results suggest the S129A and S129D mutations have no obvious effect on α-synuclein function. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Neuroscience letters AU - Escobar, Valerie Drews AU - Kuo, Yien-Ming AU - Orrison, Bonnie M AU - Giasson, Benoit I AU - Nussbaum, Robert L AD - Department of Medicine, University of California San Francisco, San Francisco, CA 94143, USA; Institute for Human Genetics, University of California San Francisco, San Francisco, CA 94143, USA. ; Genetic Disease Research Branch, NHGRI, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. ; Department of Medicine, University of California San Francisco, San Francisco, CA 94143, USA; Institute for Human Genetics, University of California San Francisco, San Francisco, CA 94143, USA. Electronic address: nussbaumr@humgen.ucsf.edu. Y1 - 2014/03/20/ PY - 2014 DA - 2014 Mar 20 SP - 96 EP - 100 VL - 563 KW - alpha-Synuclein KW - 0 KW - Index Medicus KW - Phosphorylation KW - Parkinson's disease KW - Transgenic KW - α-synuclein KW - Lewy bodies KW - Animals KW - Gastrointestinal Motility KW - Humans KW - Brain -- metabolism KW - Mice, Transgenic KW - Lewy Bodies -- pathology KW - Cells, Cultured KW - Brain -- pathology KW - Enteric Nervous System -- physiopathology KW - Colon -- innervation KW - Lewy Bodies -- metabolism KW - Synapses -- metabolism KW - Mutation KW - Colon -- physiopathology KW - Male KW - Female KW - Neurons -- metabolism KW - alpha-Synuclein -- metabolism KW - alpha-Synuclein -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1506398416?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+letters&rft.atitle=Transgenic+mice+expressing+S129+phosphorylation+mutations+in+%CE%B1-synuclein.&rft.au=Escobar%2C+Valerie+Drews%3BKuo%2C+Yien-Ming%3BOrrison%2C+Bonnie+M%3BGiasson%2C+Benoit+I%3BNussbaum%2C+Robert+L&rft.aulast=Escobar&rft.aufirst=Valerie&rft.date=2014-03-20&rft.volume=563&rft.issue=&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=1872-7972&rft_id=info:doi/10.1016%2Fj.neulet.2014.01.033 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-24 N1 - Date created - 2014-03-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Neuron. 2000 Jan;25(1):239-52 [10707987] Neurobiol Dis. 2013 Aug;56:47-58 [23567651] J Neurosci. 2000 May 1;20(9):3214-20 [10777786] J Biol Chem. 2000 Aug 25;275(34):26515-22 [10852916] Genome Res. 2001 Jan;11(1):78-86 [11156617] Nat Cell Biol. 2002 Feb;4(2):160-4 [11813001] Neuron. 2002 May 16;34(4):521-33 [12062037] J Neurosci. 2002 Oct 15;22(20):8797-807 [12388586] Genome Res. 2003 Mar;13(3):476-84 [12618378] Mol Cell Neurosci. 2003 Oct;24(2):419-29 [14572463] J Mol Biol. 2004 Apr 2;337(4):1001-9 [15033366] Nature. 1997 Aug 28;388(6645):839-40 [9278044] Nat Neurosci. 2005 May;8(5):657-63 [15834418] J Biol Chem. 2006 Oct 6;281(40):29739-52 [16847063] Proc Natl Acad Sci U S A. 2008 Jan 15;105(2):763-8 [18178617] J Biol Chem. 2008 Jun 13;283(24):16895-905 [18343814] Mol Cell Proteomics. 2008 Nov;7(11):2123-37 [18614564] Hum Mol Genet. 2009 Mar 1;18(5):872-87 [19074459] Adv Anat Embryol Cell Biol. 2009;201:1-119 [19230552] J Neuropathol Exp Neurol. 2009 May;68(5):515-24 [19525899] J Neurosci. 2010 Mar 3;30(9):3184-98 [20203178] Hum Mol Genet. 2010 May 1;19(9):1633-50 [20106867] Annu Rev Genomics Hum Genet. 2011;12:301-25 [21639795] Nature. 2000 Mar 23;404(6776):394-8 [10746727] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.neulet.2014.01.033 ER - TY - CPAPER T1 - The Evolution of Cancer and Challenges in Drug Development in AIDS Patients T2 - 115th American Society for Clinical Pharmacology and Therapeutics (ASCPT 2014) AN - 1518612912; 6284190 JF - 115th American Society for Clinical Pharmacology and Therapeutics (ASCPT 2014) AU - Little, Richard Y1 - 2014/03/18/ PY - 2014 DA - 2014 Mar 18 KW - Acquired immune deficiency syndrome KW - Drug development KW - Evolution KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518612912?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=115th+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2014%29&rft.atitle=The+Evolution+of+Cancer+and+Challenges+in+Drug+Development+in+AIDS+Patients&rft.au=Little%2C+Richard&rft.aulast=Little&rft.aufirst=Richard&rft.date=2014-03-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=115th+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascpt.org/Portals/8/docs/Meetings/2014%20Annual%20Meeting/Final%20Program%20Proof%204.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - JOUR T1 - Direction pathway analysis of large-scale proteomics data reveals novel features of the insulin action pathway AN - 1516739523; 19505087 AB - Motivation:With the advancement of high-throughput techniques, large-scale profiling of biological systems with multiple experimental perturbations is becoming more prevalent. Pathway analysis incorporates prior biological knowledge to analyze genes/proteins in groups in a biological context. However, the hypotheses under investigation are often confined to a 1D space (i.e. up, down, either or mixed regulation). Here, we develop direction pathway analysis (DPA), which can be applied to test hypothesis in a high-dimensional space for identifying pathways that display distinct responses across multiple perturbations.Results:Our DPA approach allows for the identification of pathways that display distinct responses across multiple perturbations. To demonstrate the utility and effectiveness, we evaluated DPA under various simulated scenarios and applied it to study insulin action in adipocytes. A major action of insulin in adipocytes is to regulate the movement of proteins from the interior to the cell surface membrane. Quantitative mass spectrometry-based proteomics was used to study this process on a large-scale. The combined dataset comprises four separate treatments. By applying DPA, we identified that several insulin responsive pathways in the plasma membrane trafficking are only partially dependent on the insulin-regulated kinase Akt. We subsequently validated our findings through targeted analysis of key proteins from these pathways using immunoblotting and live cell microscopy. Our results demonstrate that DPA can be applied to dissect pathway networks testing diverse hypotheses and integrating multiple experimental perturbations. JF - Bioinformatics AU - Yang, Pengyi AU - Patrick, Ellis AU - Tan, Shi-Xiong AU - Fazakerley, Daniel J AU - Burchfield, James AU - Gribben, Christopher AU - Prior, Matthew J AU - James, David E AU - Hwa Yang, Yee AD - super(1)Systems Biology Group, Biostatistics Branch, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709, USA, super(2)School of Mathematics and Statistics, University of Sydney, super(3)Diabetes and Obesity Program, Garvan Institute of Medical Research, NSW 2006, Australia and super(4)Metabolism in Human Disease Unit, Institute of Molecular and Cellular Biology, A*Star, 61 Biopolis Drive, Proteos 138673, Singapore Y1 - 2014/03/15/ PY - 2014 DA - 2014 Mar 15 SP - 808 EP - 814 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 30 IS - 6 SN - 1367-4803, 1367-4803 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Immunoblotting KW - Cell surface KW - Data processing KW - Insulin KW - Computer programs KW - Plasma membranes KW - Adipocytes KW - Microscopy KW - AKT protein KW - membrane trafficking KW - proteomics KW - Bioinformatics KW - Internet KW - N 14810:Methods KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516739523?accountid=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=Direction+pathway+analysis+of+large-scale+proteomics+data+reveals+novel+features+of+the+insulin+action+pathway&rft.au=Yang%2C+Pengyi%3BPatrick%2C+Ellis%3BTan%2C+Shi-Xiong%3BFazakerley%2C+Daniel+J%3BBurchfield%2C+James%3BGribben%2C+Christopher%3BPrior%2C+Matthew+J%3BJames%2C+David+E%3BHwa+Yang%2C+Yee&rft.aulast=Yang&rft.aufirst=Pengyi&rft.date=2014-03-15&rft.volume=30&rft.issue=6&rft.spage=808&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt616 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Cell surface; Immunoblotting; Data processing; Insulin; Computer programs; Plasma membranes; Adipocytes; Microscopy; membrane trafficking; AKT protein; Bioinformatics; proteomics; Internet DO - http://dx.doi.org/10.1093/bioinformatics/btt616 ER - TY - JOUR T1 - Targeting hydrogen sulfide as a promising therapeutic strategy for atherosclerosis. AN - 1516723998; 24491853 AB - Physiological concentrations of nitric oxide (NO) and carbon monoxide (CO) have multiple protective effects in the cardiovascular system. Recent studies have implicated hydrogen sulfide (H2S) as a new member of vasculoprotective gasotransmitter family, behaving similarly to NO and CO. H2S has been demonstrated to inhibit multiple key aspects of atherosclerosis, including atherogenic modification of LDL, monocytes adhesion to the endothelial cells, macrophage-derived foam cell formation and inflammation, smooth muscle cell proliferation, neointimal hyperplasia, vascular calcification, and thrombogenesis. H2S also decreases plasma homocysteine levels in experimental animal models. In the human body, H2S production is predominantly catalyzed by cystathionine-β-synthase (CBS) and cystathionine γ-lyase (CSE). CSE is the primary H2S-producing enzyme in the vasculature. Growing evidence suggests that atherosclerosis is associated with vascular CSE/H2S deficiency and that H2S supplementation by exogenous H2S donors (such as NaHS and GYY4137) attenuates, and H2S synthesis suppression by inhibitors (such as D, L-propargylglycine) aggravates the development of atherosclerotic plaques. However, it remains elusive whether CSE deficiency plays a causative role in atherosclerosis. A recent study (Circulation. 2013; 127: 2523-2534) demonstrates that decreased endogenous H2S production by CSE genetic deletion accelerates atherosclerosis in athero-prone ApoE-/- mice, pinpointing that endogenously produced H2S by CSE activation may be of benefit in the prevention and treatment of atherosclerosis. This study will facilitate the development of H2S-based pharmaceuticals with therapeutic applications in atherosclerosis-related cardiovascular diseases. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - International journal of cardiology AU - Xu, Suowen AU - Liu, Zhiping AU - Liu, Peiqing AD - Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China; Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1590, USA. Electronic address: suowen.xu@gmail.com. ; Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. ; Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. Electronic address: liupq@mail.sysu.edu.cn. Y1 - 2014/03/15/ PY - 2014 DA - 2014 Mar 15 SP - 313 EP - 317 VL - 172 IS - 2 KW - GYY 4137 KW - 0 KW - Morpholines KW - Organothiophosphorus Compounds KW - Carbon Dioxide KW - 142M471B3J KW - Nitric Oxide KW - 31C4KY9ESH KW - Cystathionine gamma-Lyase KW - EC 4.4.1.1 KW - Hydrogen Sulfide KW - YY9FVM7NSN KW - Index Medicus KW - Atherosclerosis KW - Hydrogen sulfide KW - Gasotransmitter KW - Cystathionine γ-lyase KW - Signal Transduction -- physiology KW - Animals KW - Oxidative Stress -- physiology KW - Humans KW - Morpholines -- pharmacology KW - Nitric Oxide -- metabolism KW - Mice KW - Organothiophosphorus Compounds -- pharmacology KW - Carbon Dioxide -- metabolism KW - Atherosclerosis -- drug therapy KW - Hydrogen Sulfide -- metabolism KW - Atherosclerosis -- etiology KW - Hydrogen Sulfide -- pharmacology KW - Cystathionine gamma-Lyase -- deficiency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516723998?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cardiology&rft.atitle=Targeting+hydrogen+sulfide+as+a+promising+therapeutic+strategy+for+atherosclerosis.&rft.au=Xu%2C+Suowen%3BLiu%2C+Zhiping%3BLiu%2C+Peiqing&rft.aulast=Xu&rft.aufirst=Suowen&rft.date=2014-03-15&rft.volume=172&rft.issue=2&rft.spage=313&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cardiology&rft.issn=1874-1754&rft_id=info:doi/10.1016%2Fj.ijcard.2014.01.068 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-12 N1 - Date created - 2014-03-05 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ijcard.2014.01.068 ER - TY - JOUR T1 - Gallstones, Cholecystectomy, and Risk of Digestive System Cancers AN - 1512331318; 19377170 AB - Gallstones and cholecystectomy may be related to digestive system cancer through inflammation, altered bile flux, and changes in metabolic hormone levels. Although gallstones are recognized causes of gallbladder cancer, associations with other cancers of the digestive system are poorly established. We used the Surveillance, Epidemiology, and End Results (SEER)-Medicare linked database (1992-2005), which includes 17 cancer registries that cover approximately 26% of the US population, to identify first primary cancers (n = 236,850) occurring in persons aged greater than or equal to 66 years and 100,000 cancer-free population-based controls frequency-matched by calendar year, age, and gender. Odds ratios and 95% confidence intervals were calculated using logistic regression analysis, adjusting for the matching factors. Gallstones and cholecystectomy were associated with increased risk of noncardia gastric cancer (odds ratio (OR) = 1.21 (95% confidence interval (CI): 1.11, 1.32) and OR = 1.26 (95% CI: 1.13, 1.40), respectively), small-intestine carcinoid (OR = 1.27 (95% CI: 1.01, 1.60) and OR = 1.78 (95% CI: 1.41, 2.25)), liver cancer (OR = 2.35 (95% CI: 2.18, 2.54) and OR = 1.26 (95% CI: 1.12, 1.41)), and pancreatic cancer (OR = 1.24 (95% CI: 1.16, 1.31) and OR = 1.23 (95% CI: 1.15, 1.33)). Colorectal cancer risk associated with gallstones and cholecystectomy decreased with increasing distance from the common bile duct (P-trend < 0.001). Hence, gallstones and cholecystectomy are associated with the risk of cancers occurring throughout the digestive tract. JF - American Journal of Epidemiology AU - Nogueira, Leticia AU - Freedman, Neal D AU - Engels, Eric A AU - Warren, Joan L AU - Castro, Felipe AU - Koshiol, Jill AD - Correspondence to Dr. Leticia Nogueira, National Cancer Institute, 9609 Medical Center Drive, MSC 7248, Bethesda, MD 20892., leticia.nogueira@nih.gov Y1 - 2014/03/15/ PY - 2014 DA - 2014 Mar 15 SP - 731 EP - 739 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 179 IS - 6 SN - 0002-9262, 0002-9262 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Health risks KW - Age KW - Risk factors KW - Gender KW - Liver KW - Pancreatic cancer KW - Colorectal carcinoma KW - Digestive system KW - Hormones KW - Cancer KW - H 11000:Diseases/Injuries/Trauma KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512331318?accountid=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=Gallstones%2C+Cholecystectomy%2C+and+Risk+of+Digestive+System+Cancers&rft.au=Nogueira%2C+Leticia%3BFreedman%2C+Neal+D%3BEngels%2C+Eric+A%3BWarren%2C+Joan+L%3BCastro%2C+Felipe%3BKoshiol%2C+Jill&rft.aulast=Nogueira&rft.aufirst=Leticia&rft.date=2014-03-15&rft.volume=179&rft.issue=6&rft.spage=731&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwt322 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Health risks; Age; Risk factors; Gender; Pancreatic cancer; Liver; Colorectal carcinoma; Hormones; Digestive system; Cancer DO - http://dx.doi.org/10.1093/aje/kwt322 ER - TY - JOUR T1 - Germline variation in NCF4, an innate immunity gene, is associated with an increased risk of colorectal cancer. AN - 1490742265; 23982929 AB - Chronic inflammation has been implicated in the etiology of colorectal adenoma and cancer; however, few key inflammatory genes mediating this relationship have been identified. In this study, we investigated the association of germline variation in innate immunity genes in relation to the risk of colorectal neoplasia. Our study was based on the analysis of samples collected from the prostate, lung, colorectal and ovarian (PLCO) Cancer Screening Trial. We investigated the association between 196 tag single nucleotide polymorphisms (SNPs) in 20 key innate immunity genes with risk of advanced colorectal adenoma and cancer in 719 adenoma cases, 481 cancer cases and 719 controls. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CIs). After Bonferroni correction, the AG/GG genotype of rs5995355, which is upstream of NCF4, was associated with an increased risk of colorectal cancer (OR = 2.43, 95% CI = 1.73-3.39; p < 0.0001). NCF4 is part of the NAPDH complex, a key factor in biochemical pathways and the innate immune response. While not definitive, our analyses suggest that the variant allele does not affect expression of NCF4, but rather modulates activity of the NADPH complex. Additional studies on the functional consequences of rs5995355 in NCF4 may help to clarify the mechanistic link between inflammation and colorectal cancer. © 2013 UICC. JF - International journal of cancer AU - Ryan, Bríd M AU - Zanetti, Krista A AU - Robles, Ana I AU - Schetter, Aaron J AU - Goodman, Julie AU - Hayes, Richard B AU - Huang, Wen-Yi AU - Gunter, Mark J AU - Yeager, Meredith AU - Burdette, Laurie AU - Berndt, Sonja I AU - Harris, Curtis C AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892. Y1 - 2014/03/15/ PY - 2014 DA - 2014 Mar 15 SP - 1399 EP - 1407 VL - 134 IS - 6 KW - Biomarkers, Tumor KW - 0 KW - RNA, Messenger KW - NADP KW - 53-59-8 KW - NADPH Oxidase KW - EC 1.6.3.1 KW - NCF4 protein, human KW - Index Medicus KW - single nucleotide polymorphism KW - NCF4 KW - innate immunity KW - colorectal cancer KW - Real-Time Polymerase Chain Reaction KW - Cell Movement KW - Apoptosis KW - Neoplasm Staging KW - Humans KW - Prognosis KW - NADP -- metabolism KW - Aged KW - Cell Differentiation KW - Reverse Transcriptase Polymerase Chain Reaction KW - RNA, Messenger -- genetics KW - Cell Proliferation KW - Genotype KW - Blotting, Western KW - Risk Factors KW - Case-Control Studies KW - Early Detection of Cancer KW - Middle Aged KW - Follow-Up Studies KW - Cell Cycle KW - Male KW - Female KW - Cell Adhesion KW - Biomarkers, Tumor -- genetics KW - Colorectal Neoplasms -- pathology KW - Colorectal Neoplasms -- etiology KW - Adenoma -- etiology KW - Immunity, Innate -- genetics KW - Adenoma -- pathology KW - Polymorphism, Single Nucleotide -- genetics KW - NADPH Oxidase -- genetics KW - Germ-Line Mutation -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490742265?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Germline+variation+in+NCF4%2C+an+innate+immunity+gene%2C+is+associated+with+an+increased+risk+of+colorectal+cancer.&rft.au=Ryan%2C+Br%C3%ADd+M%3BZanetti%2C+Krista+A%3BRobles%2C+Ana+I%3BSchetter%2C+Aaron+J%3BGoodman%2C+Julie%3BHayes%2C+Richard+B%3BHuang%2C+Wen-Yi%3BGunter%2C+Mark+J%3BYeager%2C+Meredith%3BBurdette%2C+Laurie%3BBerndt%2C+Sonja+I%3BHarris%2C+Curtis+C&rft.aulast=Ryan&rft.aufirst=Br%C3%ADd&rft.date=2014-03-15&rft.volume=134&rft.issue=6&rft.spage=1399&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.28457 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-02-25 N1 - Date created - 2014-01-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 2003 Sep 15;171(6):3010-8 [12960326] N Engl J Med. 2002 Aug 8;347(6):417-29 [12167685] J Biol Chem. 1969 Jul 25;244(14):3855-63 [4308738] Science. 1988 Dec 2;242(4883):1295-7 [2848318] Life Sci. 1992;50(26):2045-52 [1608288] Arch Biochem Biophys. 1995 Apr 1;318(1):53-8 [7726572] Blood. 1996 Oct 1;88(7):2714-21 [8839867] J Gastroenterol Hepatol. 1999 Jul;14(7):709-14 [10440217] Carcinogenesis. 2004 Dec;25(12):2467-72 [15308583] Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300] J Natl Cancer Inst. 2005 Jul 6;97(13):989-97 [15998952] Gut. 2007 Nov;56(11):1585-9 [17591622] Genes Immun. 2008 Sep;9(6):561-5 [18580884] Clin Cancer Res. 2009 Jan 15;15(2):425-30 [19147746] J Natl Cancer Inst. 2009 Feb 18;101(4):256-66 [19211452] Int J Cancer. 2009 Jul 1;125(1):171-80 [19350627] Crit Rev Oncol Hematol. 2009 Jun;70(3):183-94 [18805702] Clin Cancer Res. 2009 Sep 15;15(18):5878-87 [19737943] Gastroenterology. 2010 Mar;138(3):958-68 [19914252] Nat Genet. 2010 Apr;42(4):332-7 [20228799] Infect Dis Clin North Am. 2010 Dec;24(4):1019-39, x [20937463] Scand J Immunol. 2011 May;73(5):420-7 [21204900] Genome Res. 2005 Nov;15(11):1592-3 [16251469] J Exp Med. 2006 Aug 7;203(8):1927-37 [16880254] J Exp Med. 2006 Aug 7;203(8):1915-25 [16880255] J Exp Med. 2006 Oct 2;203(10):2377-89 [17000866] Nat Genet. 2007 May;39(5):596-604 [17435756] Lancet. 2007 May 12;369(9573):1603-13 [17499602] Lancet. 2007 May 12;369(9573):1627-40 [17499605] Dis Colon Rectum. 2007 Jun;50(6):839-55 [17308939] Cancer Causes Control. 2007 Dec;18(10):1095-105 [17694420] Int J Cancer. 2010 Dec 15;127(12):2822-30 [21351261] Nat Genet. 2010 Dec;42(12):1118-25 [21102463] JAMA. 2011 Sep 28;306(12):1352-8 [21954479] Nat Genet. 2011 Nov;43(11):1066-73 [21983784] Cancer Res. 2012 Mar 15;72(6):1467-77 [22282660] Am J Gastroenterol. 2012 Apr;107(4):589-96 [22158027] Gut. 2012 Jul;61(7):1028-35 [21900546] Gut. 2012 Jul;61(7):1097; author reply 1097-8 [22027479] Dis Colon Rectum. 2012 Jul;55(7):773-7 [22706129] CA Cancer J Clin. 2013 Jan;63(1):11-30 [23335087] Control Clin Trials. 2000 Dec;21(6 Suppl):273S-309S [11189684] Toxicology. 2001 Mar 7;160(1-3):11-8 [11246119] Gut. 2001 Apr;48(4):526-35 [11247898] Nature. 2001 May 31;411(6837):599-603 [11385576] Cancer Epidemiol Biomarkers Prev. 2002 Jul;11(7):622-9 [12101109] Am J Hum Genet. 2004 Jan;74(1):106-20 [14681826] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.28457 ER - TY - JOUR T1 - Anal microbiota profiles in HIV-positive and HIV-negative MSM AN - 1765970151; PQ0002559421 AB - Objective: Because differences in anal microbial populations (microbiota) could affect acquisition of HIV or other conditions, especially among MSM, we profiled the microbiota of the anal canal, assessed its stability, and investigated associations with diversity and composition. Design: Microbiota profiles in anal swabs collected from 76 MSM (52 in 1989, swab-1; 66 1-5 years later, swab-2) were compared by HIV status (25 HIV-positive), T-cell subsets, and questionnaire data. Methods: Bacterial 16S rRNA genes were amplified, sequenced (Illumina MiSeq), and clustered into species-level operational taxonomic units (QIIME and Greengenes). Regression models and Wilcoxon tests were used for associations with alpha diversity (unique operational taxonomic units, Shannon's index). Composition was compared by Adonis (QIIME). Results: Most anal bacteria were Firmicutes (mean 60.6%, range 21.1-91.1%) or Bacteroidetes (29.4%, 4.1-70.8%). Alpha diversity did not change between the two swabs (N = 42 pairs). In swab-2, HIV-positives had lower alpha diversity (P [< or =] 0.04) and altered composition, with fewer Firmicutes and more Fusobacteria taxa (P [< or =] 0.03), not completely attributable to very low CD4 super(+) cell count (median 232 cells/ mu ), prior AIDS clinical diagnosis (N = 17), or trimethoprim-sulfamethoxazole use (N = 6). Similar but weaker differences were observed in swab-1 (HIV-positive median 580 CD4 super(+) cells/( mu l; no trimethoprim-sulfamethoxazole). Associations with T-cell subsets, smoking, and sexual practices were null or inconsistent. Conclusions: The anal microbiota of MSM was relatively stable over 1-5 years. However, with uncontrolled, advanced HIV infection, the microbiota had altered composition and reduced diversity partially attributable to antibiotics. Investigations of microbial community associations with other immune perturbations and clinical abnormalities are needed. JF - AIDS AU - Yu, Guoqin AU - Fadrosh, Doug AU - Ma, Bing AU - Ravel, Jacques AU - Goedert, James J AD - Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, goedertj@mail.nih.gov Y1 - 2014/03/13/ PY - 2014 DA - 2014 Mar 13 SP - 753 EP - 760 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 IS - 5 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - anal KW - HIV KW - human microbiome KW - MSM KW - risk factors KW - sexual activities KW - Inventories KW - Acquired immune deficiency syndrome KW - Data processing KW - Microbial activity KW - trimethoprim-sulfamethoxazole KW - Antibiotics KW - Firmicutes KW - Infection KW - Canals KW - Smoking KW - CD4 antigen KW - Human immunodeficiency virus KW - Lymphocytes T KW - Regression analysis KW - Taxonomy KW - Taxa KW - rRNA 16S KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765970151?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Anal+microbiota+profiles+in+HIV-positive+and+HIV-negative+MSM&rft.au=Yu%2C+Guoqin%3BFadrosh%2C+Doug%3BMa%2C+Bing%3BRavel%2C+Jacques%3BGoedert%2C+James+J&rft.aulast=Yu&rft.aufirst=Guoqin&rft.date=2014-03-13&rft.volume=28&rft.issue=5&rft.spage=753&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000154 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Smoking; Canals; Inventories; Acquired immune deficiency syndrome; CD4 antigen; Data processing; Regression analysis; Lymphocytes T; Antibiotics; trimethoprim-sulfamethoxazole; Infection; rRNA 16S; Human immunodeficiency virus; Taxa; Microbial activity; Taxonomy; Firmicutes DO - http://dx.doi.org/10.1097/QAD.0000000000000154 ER - TY - JOUR T1 - The role of Nrf1 and Nrf2 in the regulation of copper-responsive transcription. AN - 1499153131; 24462598 AB - Recent evidences indicated Nrf2 is more potent than Nrf1 in the activation of antioxidant genes. However, the roles of Nrf proteins in the regulation of copper-responsive transcription have not been well addressed. We took the toxicogenomic approach and the present network and Gene Ontology analyses results showed that Nrf1 and Nrf2 are distinctively involved in copper-responsive transcriptional regulation in HepG2 transcriptome. Cells deficient in either Nrf1 or Nrf2 were more susceptible to copper exposure than wild type cells. Nrf1 and Nrf2 null cells were transfected with the luciferase reporters containing either ARE(s) or a combination of ARE(s) and MREs, and then treated with copper. In Nrf2-null (Nrf2(-/-)) cells, copper did not activate transcription of reporter genes, whereas Nrf1 deficiency did not affect copper-inducible activation. Ectopic expression of Nrf2 restored copper-inducible transcription in Nrf2(-/-) cells. However, the changes in the intrinsic mRNA levels of MT-1 in Nrf null cells following copper treatment showed that Nrf1 and Nrf2 equally contributed to MT-1 activation after 4h, while Nrf1involved more than Nrf2 following 24h exposure. These results suggest that while Nrf2 is crucial for MRE/ARE-mediated transcription in response to copper, Nrf1 may activate MT-1 expression by a mechanism different from that Nrf2 employs. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Experimental cell research AU - Song, Min Ok AU - Mattie, Michael D AU - Lee, Chang-Ho AU - Freedman, Jonathan H AD - Department of Biology, College of Natural Sciences, Gangneung-Wonju National University, Gangwon-do 210-702, Republic of Korea. Electronic address: rotisong@gmail.com. ; Nicholas School of the Environment, Box 90328, Duke University, Durham, NC 27708, USA. Electronic address: mmattie@agensys.com. ; Department of Biology, College of Natural Sciences, Gangneung-Wonju National University, Gangwon-do 210-702, Republic of Korea. ; Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Y1 - 2014/03/10/ PY - 2014 DA - 2014 Mar 10 SP - 39 EP - 50 VL - 322 IS - 1 KW - NF-E2-Related Factor 2 KW - 0 KW - Nfe2l2 protein, mouse KW - Nrf1 protein, mouse KW - Nuclear Respiratory Factor 1 KW - metallothionein-1, mouse KW - Copper KW - 789U1901C5 KW - Metallothionein KW - 9038-94-2 KW - Index Medicus KW - Nrf1 KW - ARE KW - Metallothionein-1 KW - Transcription KW - Nrf2 KW - Gene Expression Profiling KW - Animals KW - Transcription, Genetic -- drug effects KW - Hep G2 Cells KW - Cells, Cultured KW - Humans KW - Gene Regulatory Networks KW - Metallothionein -- genetics KW - Mice KW - Metallothionein -- metabolism KW - Mice, Knockout KW - NF-E2-Related Factor 2 -- physiology KW - NF-E2-Related Factor 2 -- genetics KW - Nuclear Respiratory Factor 1 -- genetics KW - Gene Expression Regulation -- drug effects KW - Nuclear Respiratory Factor 1 -- physiology KW - Copper -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499153131?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+cell+research&rft.atitle=The+role+of+Nrf1+and+Nrf2+in+the+regulation+of+copper-responsive+transcription.&rft.au=Song%2C+Min+Ok%3BMattie%2C+Michael+D%3BLee%2C+Chang-Ho%3BFreedman%2C+Jonathan+H&rft.aulast=Song&rft.aufirst=Min&rft.date=2014-03-10&rft.volume=322&rft.issue=1&rft.spage=39&rft.isbn=&rft.btitle=&rft.title=Experimental+cell+research&rft.issn=1090-2422&rft_id=info:doi/10.1016%2Fj.yexcr.2014.01.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-22 N1 - Date created - 2014-02-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Appl Pharmacol. 2010 Apr 1;244(1):4-15 [20122947] Toxicol Appl Pharmacol. 2010 Apr 1;244(1):37-42 [19538984] Genes Cells. 2011 Jun;16(6):692-703 [21554501] Nucleic Acids Res. 2012 Aug;40(15):7416-29 [22581777] Arch Toxicol. 2013 Jan;87(1):49-72 [22926699] Annu Rev Pharmacol Toxicol. 2013;53:401-26 [23294312] Proc Natl Acad Sci U S A. 1999 Oct 26;96(22):12731-6 [10535991] J Biol Chem. 1999 Dec 24;274(52):37491-8 [10601325] J Biol Chem. 2000 May 19;275(20):15466-73 [10747902] Toxicology. 2000 May 5;146(2-3):171-6 [10814849] Biochim Biophys Acta. 2000 Dec 15;1517(1):19-26 [11118612] Cancer Res. 2001 Apr 15;61(8):3299-307 [11309284] Biochem J. 2002 Jul 15;365(Pt 2):405-16 [11991805] Cancer Res. 2002 Sep 15;62(18):5196-203 [12234984] OMICS. 2003 Fall;7(3):235-52 [14583114] Am J Physiol Cell Physiol. 2004 Feb;286(2):C293-301 [14576086] Free Radic Biol Med. 2004 May 15;36(10):1199-207 [15110384] EMBO J. 1993 Apr;12(4):1355-62 [8467794] Nucleic Acids Res. 1994 Nov 25;22(23):5016-23 [7800494] J Biol Chem. 1995 Mar 24;270(12):6894-900 [7896838] J Biol Chem. 1995 Oct 13;270(41):24468-74 [7592662] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14960-5 [8962164] EMBO J. 1998 Mar 16;17(6):1779-87 [9501099] Chem Biol Interact. 2005 Jan 15;151(2):71-82 [15698579] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4120-5 [15738389] Curr Med Chem. 2005;12(10):1161-208 [15892631] Hepatology. 2006 Jan;43(1):144-53 [16374848] Annu Rev Pharmacol Toxicol. 2007;47:89-116 [16968214] Toxicology. 2008 Apr 3;246(1):24-33 [18083283] Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W358-63 [18487275] Mutat Res. 2008 Jul-Aug;659(1-2):31-9 [18164232] J Biol Chem. 2008 Nov 28;283(48):33554-62 [18826952] J Biol Chem. 2009 May 15;284(20):13291-5 [19182219] Physiol Genomics. 2009 Aug 7;38(3):386-401 [19549813] Toxicol In Vitro. 2010 Sep;24(6):1554-61 [20599494] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.yexcr.2014.01.013 ER - TY - JOUR T1 - Intakes of folate, methionine, vitamin B6, and vitamin B12 with risk of esophageal and gastric cancer in a large cohort study. AN - 1504732509; 24481406 AB - Nutrients in the one-carbon metabolism pathway may be involved in carcinogenesis. Few cohort studies have investigated the intakes of folate and related nutrients in relation to gastric and esophageal cancer. We prospectively examined the association between self-reported intakes of folate, methionine, vitamin B6, and vitamin B12 and gastric and esophageal cancer in 492,293 men and women. We observed an elevated risk of esophageal squamous cell carcinoma with low intake of folate (relative risk (95% confidence interval): Q1 vs Q3, 1.91 (1.17, 3.10)), but no association with high intake. Folate intake was not associated with esophageal adenocarcinoma, gastric cardia adenocarcinoma, or non-cardia gastric adenocarcinoma. The intakes of methionine, vitamin B6, and vitamin B12 were not associated with esophageal and gastric cancer. Low intake of folate was associated with increased risk of esophageal squamous cell carcinoma. JF - British journal of cancer AU - Xiao, Q AU - Freedman, N D AU - Ren, J AU - Hollenbeck, A R AU - Abnet, C C AU - Park, Y AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA. ; National Office for Cancer Prevention and Control, National Cancer Center, Beijing, China. ; AARP, Washington, District of Columbia, USA. Y1 - 2014/03/04/ PY - 2014 DA - 2014 Mar 04 SP - 1328 EP - 1333 VL - 110 IS - 5 KW - Vitamin B 6 KW - 8059-24-3 KW - Folic Acid KW - 935E97BOY8 KW - Methionine KW - AE28F7PNPL KW - Vitamin B 12 KW - P6YC3EG204 KW - Index Medicus KW - Risk KW - Carcinoma, Squamous Cell -- epidemiology KW - Humans KW - Cohort Studies KW - Middle Aged KW - United States -- epidemiology KW - Male KW - Female KW - Vitamin B 6 -- administration & dosage KW - Methionine -- administration & dosage KW - Diet -- statistics & numerical data KW - Vitamin B 12 -- administration & dosage KW - Stomach Neoplasms -- epidemiology KW - Folic Acid -- administration & dosage KW - Esophageal Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504732509?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intakes+of+folate%2C+methionine%2C+vitamin+B6%2C+and+vitamin+B12+with+risk+of+esophageal+and+gastric+cancer+in+a+large+cohort+study.&rft.au=Xiao%2C+Q%3BFreedman%2C+N+D%3BRen%2C+J%3BHollenbeck%2C+A+R%3BAbnet%2C+C+C%3BPark%2C+Y&rft.aulast=Xiao&rft.aufirst=Q&rft.date=2014-03-04&rft.volume=110&rft.issue=5&rft.spage=1328&rft.isbn=&rft.btitle=&rft.title=British+journal+of+cancer&rft.issn=1532-1827&rft_id=info:doi/10.1038%2Fbjc.2014.17 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-23 N1 - Date created - 2014-03-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Nutr. 2003 Nov;133(11 Suppl 1):3748S-3753S [14608109] Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517] J Natl Cancer Inst. 1988 Dec 21;80(20):1620-5 [3193480] J Nutr. 1990 Nov;120 Suppl 11:1508-11 [2243297] Cancer Epidemiol Biomarkers Prev. 1994 Jul-Aug;3(5):393-8 [7920206] J Natl Cancer Inst. 1995 Jan 18;87(2):104-9 [7707381] Nutr Cancer. 1997;27(3):298-309 [9101561] Int J Cancer. 1999 Nov 26;83(5):601-5 [10521793] Nutr Cancer. 2005;52(2):138-46 [16201845] Gastroenterology. 2006 Oct;131(4):1271-83 [17030196] Am J Clin Nutr. 2007 Aug;86(2):271-3 [17684194] Public Health Nutr. 2008 Feb;11(2):183-95 [17610761] Gastroenterol Clin North Am. 2009 Mar;38(1):27-57, vii [19327566] Am J Clin Nutr. 2010 Jun;91(6):1708-15 [20410093] J Natl Cancer Inst. 2010 Sep 8;102(17):1344-53 [20716718] J Nutr. 2011 Feb;141(2):274-83 [21178085] Am J Epidemiol. 2011 May 15;173(10):1171-82 [21447479] Nutr J. 2011;10:137 [22185224] Asian Pac J Cancer Prev. 2011;12(8):2019-23 [22292644] Int J Obes (Lond). 2013 Mar;37(3):448-54 [22546778] Clin Gastroenterol Hepatol. 2013 Sep;11(9):1130-1136.e2 [23591281] Cancer. 2000 Feb 15;88(4):737-48 [10679641] Am J Epidemiol. 2000 Aug 1;152(3):279-86 [10933275] Int J Cancer. 2001 Aug 1;93(3):417-23 [11433408] Am J Epidemiol. 1986 Jul;124(1):17-27 [3521261] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/bjc.2014.17 ER - TY - JOUR T1 - Commentary: When to start and what to use in children - recommendations and rationale AN - 1768567825; PQ0002676694 AB - The 2013 WHO consolidated guidelines recommend treating all HIV-infected children under the age of 5 years regardless of CD4 super(+) T-cell count or WHO clinical stage, and treating children aged 5 years and older according to the same criteria as for adults: WHO clinical stage 3 or 4 or CD4 super(+) T-cell count of 500cells/ mu l or less [1]. Guideline recommendations for what drugs to use for initial antiretroviral therapy (ART) vary by age group: less than 3 years, 3-10 years and above 10 years. JF - AIDS AU - Siberry, George AU - Tindyebwa, Denis AD - Maternal and Pediatric Infectious Disease (MPID) Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA, siberryg@mail.nih.gov Y1 - 2014/03// PY - 2014 DA - March 2014 SP - S133 EP - S135 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - Acquired immune deficiency syndrome KW - Age KW - Human immunodeficiency virus KW - Guidelines KW - Age groups KW - Children KW - Antiretroviral agents KW - Drugs KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768567825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Commentary%3A+When+to+start+and+what+to+use+in+children+-+recommendations+and+rationale&rft.au=Siberry%2C+George%3BTindyebwa%2C+Denis&rft.aulast=Siberry&rft.aufirst=George&rft.date=2014-03-01&rft.volume=28&rft.issue=&rft.spage=S133&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000241 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Age; Acquired immune deficiency syndrome; Guidelines; Age groups; Children; Drugs; Antiretroviral agents; Human immunodeficiency virus DO - http://dx.doi.org/10.1097/QAD.0000000000000241 ER - TY - JOUR T1 - Parenting with bipolar disorder: Coping with risk of mood disorders to children AN - 1692286372; 201504953 AB - Children of individuals with bipolar disorder (BPD) have increased risk for mood disorders and other adverse psychosocial outcomes due to genetic and environmental risk. Though parents with BPD are aware of increased risk to children, little is known about efforts undertaken in response or their perceived utility. Among parents who self-report with BPD, this study identifies key variables associated with parental coping with children's risk of mood disorders; and explores the relationship between monitoring children's moods and perceived coping efficacy. In this U.S. study, active parental coping with, and cognitive distancing from, child's risk were measured using novel scales. Parents (n = 266) who self-identified as having BPD completed a web-based survey. They had at least one unaffected child. Most participants endorsed monitoring their children's moods. Monitoring was associated with increased perceived control over the child's well-being (p < 0.005), but not feeling less worried. Active parental coping with risk to children was positively associated with active coping with own illness (Beta = 0.25, p = 0.001), family history (Beta = 0.24, p = 0.001), and self-report of current depression (Beta = 0.16, p = 0.037), explaining 13.8% of the variance (F = 8.81, p < 0.001). Cognitive distancing from the child's risk was positively associated with confidence in diagnosis (Beta = 0.25, p = 0.001), and negatively associated with self-report of current mania (Beta = -0.19, p = 0.007), perceiving BPD as genetic (Beta = -0.26, p < 0.001) and having more children (Beta = -0.20, p = 0.004); explaining 16.2% of the variance (F = 8.63, p < 0.001). Parents' adaptation to their own BPD was modestly correlated with active coping with child's risk (r = 0.15, p < 0.05) but not with cognitive distancing. The findings support the importance of understanding causal attributions and the value of genetic education and counseling for parents with BPD. Further research is necessary to elucidate the psychological benefits of active coping versus cognitive distancing from child's risk, and explore additional variables that predict parental coping with children's risk of mood disorders. [Copyright Elsevier Ltd.] JF - Social Science & Medicine AU - Peay, Holly Landrum AU - Rosenstein, Donald L AU - Biesecker, Barbara Bowles AD - Social and Behavioral Research Branch, National Human Genome Research Institute, NHGRI Building 31, Room B1B36 31 Center Drive, MSC 2073, Bethesda, MD 20892, USA Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 194 EP - 200 PB - Elsevier Science, Amsterdam The Netherlands VL - 104 SN - 0277-9536, 0277-9536 KW - Bipolar disorder Coping Parent Risk Genetic Children Mood disorder United States KW - Values KW - Genetics KW - Emotions KW - Risk KW - Affective Illness KW - Coping KW - Parents KW - Children KW - Cognition KW - article KW - 6140: illness & health care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1692286372?accountid=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+Science+%26+Medicine&rft.atitle=Parenting+with+bipolar+disorder%3A+Coping+with+risk+of+mood+disorders+to+children&rft.au=Peay%2C+Holly+Landrum%3BRosenstein%2C+Donald+L%3BBiesecker%2C+Barbara+Bowles&rft.aulast=Peay&rft.aufirst=Holly&rft.date=2014-03-01&rft.volume=104&rft.issue=&rft.spage=194&rft.isbn=&rft.btitle=&rft.title=Social+Science+%26+Medicine&rft.issn=02779536&rft_id=info:doi/10.1016%2Fj.socscimed.2013.10.022 LA - English DB - Social Services Abstracts N1 - Date revised - 2015-07-01 N1 - Last updated - 2016-09-28 N1 - CODEN - SSCMAW N1 - SubjectsTermNotLitGenreText - Children; Risk; Parents; Coping; Emotions; Cognition; Genetics; Affective Illness; Values DO - http://dx.doi.org/10.1016/j.socscimed.2013.10.022 ER - TY - JOUR T1 - Influencing the World Versus Adjusting to Constraints AN - 1673613031 AB - Although higher social class carries mental and physical health benefits, these advantages are less robust among members of racial and ethnic minority groups than among European Americans. We explore whether differential reactions to discrimination may be a factor in explaining why. Working-class and middle-class Latino American women engaged in an evaluative interaction with a European American woman who rejected them and held either prejudiced or unprejudiced attitudes. We examined how participants responded to this rejection by measuring neuroendocrine reactivity, executive functioning, and the affective content of their verbal responses during the interaction. Among middle­class Latinas, rejection from a prejudiced, compared to unprejudiced, out-group member was associated with less adaptive stress responses, greater cognitive depletion, and more feelings of uncertainty. In contrast, among working­-class Latinas, neuroendocrine, cognitive, and affective responses were similar across the two sources of rejection. Results suggest that social class is an important moderator of responses to discrimination. JF - Social Psychological & Personality Science AU - Townsend, Sarah S M AU - Eliezer, Dina AU - Major, Brenda AU - Mendes, Wendy Berry AD - Department of Management and Organizations, Kellogg School of Management, Northwestern University, Evanston, IL 60208, USA ; National Institutes of Health, Bethesda, MD, USA ; University of California, Santa Barbara, CA, USA ; University of California, San Francisco, CA, USA ; Department of Management and Organizations, Kellogg School of Management, Northwestern University, Evanston, IL 60208, USA Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 226 EP - 234 CY - Thousand Oaks PB - SAGE PUBLICATIONS, INC. VL - 5 IS - 2 SN - 1948-5506 KW - Psychology KW - socioeconomic status KW - prejudice KW - stress reactions KW - neuroendocrinology KW - Affective responses KW - Women KW - American people KW - Attitudes KW - Depletion KW - Discrimination KW - Executive function KW - Health status KW - Mental health KW - Middle class people KW - Minority groups KW - Reactivity KW - Rejection KW - Social class KW - Social rejection KW - Uncertainty UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673613031?accountid=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+%26+Personality+Science&rft.atitle=Influencing+the+World+Versus+Adjusting+to+Constraints%3A+Social+Class+Moderates+Responses+to+Discrimination&rft.au=Townsend%2C+Sarah+S+M%3BEliezer%2C+Dina%3BMajor%2C+Brenda%3BMendes%2C+Wendy+Berry&rft.aulast=Townsend&rft.aufirst=Sarah+S&rft.date=2014-03-01&rft.volume=5&rft.issue=2&rft.spage=226&rft.isbn=&rft.btitle=&rft.title=Social+Psychological+%26+Personality+Science&rft.issn=19485506&rft_id=info:doi/10.1177%2F1948550613490968 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-03-31 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1177/1948550613490968 ER - TY - JOUR T1 - Investigating the mechanisms of ribonucleotide excision repair in Escherichia coli AN - 1668262104; PQ0001243194 AB - Low fidelity Escherichia coli DNA polymerase V (pol V/UmuD'2C) is best characterized for its ability to perform translesion synthesis (TLS). However, in recA730 lexA(Def) strains, the enzyme is expressed under optimal conditions allowing it to compete with the cell's replicase for access to undamaged chromosomal DNA and leads to a substantial increase in spontaneous mutagenesis. We have recently shown that a Y11A substitution in the "steric gate" residue of UmuC reduces both base and sugar selectivity of pol V, but instead of generating an increased number of spontaneous mutations, strains expressing umuC_Y11A are poorly mutable in vivo. This phenotype is attributed to efficient RNase HII-initiated repair of the misincorporated ribonucleotides that concomitantly removes adjacent misincorporated deoxyribonucleotides. We have utilized the ability of the pol V steric gate mutant to promote incorporation of large numbers of errant ribonucleotides into the E. coli genome to investigate the fundamental mechanisms underlying ribonucleotide excision repair (RER). Here, we demonstrate that RER is normally facilitated by DNA polymerase I (pol I) via classical "nick translation". In vitro, pol I displaces 1-3 nucleotides of the RNA/DNA hybrid and through its 5' arrow right 3' (exo/endo) nuclease activity releases ribo- and deoxyribonucleotides from DNA. In vivo, umuC_Y11A-dependent mutagenesis changes significantly in polymerase-deficient, or proofreading-deficient polA strains, indicating a pivotal role for pol I in ribonucleotide excision repair (RER). However, there is also considerable redundancy in the RER pathway in E. coli. Pol I's strand displacement and FLAP-exo/endonuclease activities can be facilitated by alternate enzymes, while the DNA polymerization step can be assumed by high-fidelity pol III. We conclude that RNase HII and pol I normally act to minimize the genomic instability that is generated through errant ribonucleotide incorporation, but that the "nick-translation" activities encoded by the single pol I polypeptide can be undertaken by a variety of back-up enzymes. JF - Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis AU - Vaisman, Alexandra AU - McDonald, John P AU - Noll, Stephan AU - Huston, Donald AU - Loeb, Gregory 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 - 2014/03// PY - 2014 DA - March 2014 SP - 21 EP - 33 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 761 SN - 0027-5107, 0027-5107 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - pol DNA polymerase KW - nt nucleotide KW - RER ribonucleotide excision repair KW - Top1 topoisomerase 1 KW - Y-family DNA polymerase KW - Steric gate mutant KW - Ribonucleotide excision repair KW - UmuC: spontaneous mutagenesis KW - RNase H KW - Genomes KW - Translation KW - Sugar KW - Polymerization KW - Enzymes KW - Nuclease KW - deoxyribonucleotides KW - Nucleotides KW - replicase KW - Mutagenesis KW - ribonuclease H2 KW - Fidelity KW - Genomic instability KW - RNA KW - Hybrids KW - DNA-directed DNA polymerase KW - ribonucleotides KW - Escherichia coli KW - Ribonuclease KW - Endonuclease KW - Mutation KW - J 02410:Animal Diseases KW - N 14830:RNA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668262104?accountid=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=Mutation+Research%2FFundamental+and+Molecular+Mechanisms+of+Mutagenesis&rft.atitle=Investigating+the+mechanisms+of+ribonucleotide+excision+repair+in+Escherichia+coli&rft.au=Vaisman%2C+Alexandra%3BMcDonald%2C+John+P%3BNoll%2C+Stephan%3BHuston%2C+Donald%3BLoeb%2C+Gregory%3BGoodman%2C+Myron+F%3BWoodgate%2C+Roger&rft.aulast=Vaisman&rft.aufirst=Alexandra&rft.date=2014-03-01&rft.volume=761&rft.issue=&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Mutation+Research%2FFundamental+and+Molecular+Mechanisms+of+Mutagenesis&rft.issn=00275107&rft_id=info:doi/10.1016%2Fj.mrfmmm.2014.01.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Genomes; Sugar; Translation; Polymerization; Nuclease; Enzymes; replicase; Nucleotides; deoxyribonucleotides; Mutagenesis; ribonuclease H2; Fidelity; Genomic instability; RNA; DNA-directed DNA polymerase; Hybrids; ribonucleotides; Ribonuclease; Endonuclease; Mutation; Escherichia coli DO - http://dx.doi.org/10.1016/j.mrfmmm.2014.01.005 ER - TY - JOUR T1 - Cerebral tubercular thrombophlebitis presenting as venous infarct: Magnetic resonance imaging and pathologic correlation AN - 1668257725; PQ0001246003 AB - Central nervous system involvement by tuberculosis to produce basal meningitis, hydrocephalus, arteritis and infarcts is well-known, the brunt of the pathology being borne by the arterial vasculature to produce neurological sequelae. However, tuberculous thrombophlebitis causing venous infarction is exceedingly rare. We present imaging and pathological features of two autopsy proven cases of tuberculous thrombophlebitis with venous infarcts involving superficial venous system in one and deep venous system in the other. This is the first study presenting radiopathologic correlation of this rare complication. Tuberculous thrombophlebitis should be suspected if basal exudates and multiple white matter T2 hyperintensities are seen on neuroimaging and the imaging protocol should include both magnetic resonance arteriogram and venogram. JF - Annals of Indian Academy of Neurology AU - Mangalore, Sandhya AU - Desai, Sunali AU - Mahadevan, Anita AU - Kovoor, Jerry M E AU - Vasudev, M K AU - Tally, Arun Bhagwandas AU - Shankar, Susarla Krishna AD - Department of Neuroimaging and Interventional Radiology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 130 EP - 134 PB - Medknow Publications Pvt. Ltd., A-108/109 Kanara Business Center Mumbai 400075 India VL - 17 IS - 1 SN - 0972-2327, 0972-2327 KW - Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts KW - Central nervous system tuberculosis KW - Magnetic resonance imaging KW - thrombophlebitis KW - venous infarct KW - Autopsy KW - Central nervous system KW - Neuroimaging KW - Mycobacterium KW - Neurological complications KW - Substantia alba KW - Meningitis KW - Exudates KW - N.M.R. KW - Tuberculosis KW - Hydrocephalus KW - Arteritis KW - Infarction KW - Thrombophlebitis KW - J 02490:Miscellaneous KW - N3 11027:Neurology & neuropathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668257725?accountid=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=Annals+of+Indian+Academy+of+Neurology&rft.atitle=Cerebral+tubercular+thrombophlebitis+presenting+as+venous+infarct%3A+Magnetic+resonance+imaging+and+pathologic+correlation&rft.au=Mangalore%2C+Sandhya%3BDesai%2C+Sunali%3BMahadevan%2C+Anita%3BKovoor%2C+Jerry+M+E%3BVasudev%2C+M+K%3BTally%2C+Arun+Bhagwandas%3BShankar%2C+Susarla+Krishna&rft.aulast=Mangalore&rft.aufirst=Sandhya&rft.date=2014-03-01&rft.volume=17&rft.issue=1&rft.spage=130&rft.isbn=&rft.btitle=&rft.title=Annals+of+Indian+Academy+of+Neurology&rft.issn=09722327&rft_id=info:doi/10.4103%2F09722327.128587 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Central nervous system; Autopsy; Neuroimaging; Magnetic resonance imaging; Substantia alba; Neurological complications; Meningitis; Exudates; Tuberculosis; N.M.R.; Arteritis; Hydrocephalus; Infarction; Thrombophlebitis; Mycobacterium DO - http://dx.doi.org/10.4103/09722327.128587 ER - TY - JOUR T1 - Plasmid-mediated transformation tropism of chlamydial biovars AN - 1654678503; 21296957 AB - Chlamydia trachomatis and C. muridarum are human and mouse pathogens, respectively, which show high conservation of gene order and content. Both species contain a common 7.5-kb plasmid that is an important virulence factor. Recently described transformation systems have been used to characterize C. trachomatis L2 plasmid gene functions; however, similar studies have not been reported for C. trachomatis ocular tropic serovar A or the mouse strain, C. muridarum. Here, we have conducted genetic experiments with C. trachomatis serovar A and C. muridarum and report the following: (1) successful transformation of C. muridarum and C. trachomatis serovar A is restricted to a shuttle vector with a C. muridarum or C. trachomatis serovar A plasmid backbone, respectively; (2) transformation of plasmid-deficient C. muridarum with the C. muridarum-based shuttle vector complement glycogen accumulation and inclusion morphology; and (3) C. muridarum plasmid-encoded Pgp4 is a regulator of chromosomal ( glgA ) and plasmid ( pgp3 ) virulence genes. In summary, our findings show a previously unrecognized and unexpected role for the chlamydial plasmid in its transformation tropism and confirm the plasmids regulatory role of virulence genes in C. muridarum. This study is the first to show that plasmid mediated transformation of chlamydiae is biovar-specific; a tropism that provides experimental evidence for a co-evolutionary relationship between plasmid and chromosomal genes. JF - Pathogens and Disease AU - Song, Lihua AU - Carlson, John H AU - Zhou, Bing AU - Virtaneva, Kimmo AU - Whitmire, William M AU - Sturdevant, Gail L AU - Porcella, Stephen F AU - McClarty, Grant AU - Caldwell, Harlan D AD - Laboratory of Intracellular Parasites, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA. Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 189 EP - 193 PB - Wiley Subscription Services, Inc., 1105 N Market St Wilmington DE 19801 England VL - 70 IS - 2 SN - 2049-632X, 2049-632X KW - Microbiology Abstracts B: Bacteriology KW - Transformation KW - Gene order KW - virulence factors KW - Tropism KW - Chlamydia trachomatis KW - shuttle vectors KW - Pathogens KW - Plasmids KW - Glycogen KW - J 02320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654678503?accountid=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=Pathogens+and+Disease&rft.atitle=Plasmid-mediated+transformation+tropism+of+chlamydial+biovars&rft.au=Song%2C+Lihua%3BCarlson%2C+John+H%3BZhou%2C+Bing%3BVirtaneva%2C+Kimmo%3BWhitmire%2C+William+M%3BSturdevant%2C+Gail+L%3BPorcella%2C+Stephen+F%3BMcClarty%2C+Grant%3BCaldwell%2C+Harlan+D&rft.aulast=Song&rft.aufirst=Lihua&rft.date=2014-03-01&rft.volume=70&rft.issue=2&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Pathogens+and+Disease&rft.issn=2049632X&rft_id=info:doi/10.1111%2F2049-632X.12104 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Transformation; Gene order; virulence factors; Tropism; Pathogens; shuttle vectors; Plasmids; Glycogen; Chlamydia trachomatis DO - http://dx.doi.org/10.1111/2049-632X.12104 ER - TY - JOUR T1 - Dendrimers as high relaxivity MR contrast agents AN - 1635018981; 21008404 AB - Dendrimers are versatile macromolecules with tremendous potential as magnetic resonance imaging (MRI) contrast agents. Dendrimer-based agents provide distinct advantages over low-molecular-weight gadolinium chelates, including enhanced r 1 relaxivity due to slow rotational dynamics, tunable pharmacokinetics that can be adapted for blood pool, liver, kidney, and lymphatic imaging, the ability to be a drug carrier, and flexibility for labeling due to their inherent multivalency. Clinical applications are increasingly being developed, particularly in lymphatic imaging. Herein we present a broad overview of dendrimer-based MRI contrast agents with attention to the unique chemistry and physical properties as well as emerging clinical applications. For further resources related to this article, please visit the WIREs website . Conflict of interest: The authors have declared no conflicts of interest for this article. JF - Wiley Interdisciplinary Reviews: Nanomedicine and Nanobiotechnology AU - Longmire, Michelle R AU - Ogawa, Mikako AU - Choyke, Peter L AU - Kobayashi, Hisataka AD - Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 155 EP - 162 PB - Wiley-Blackwell, Baffins Lane Chichester W. Sussex PO19 1UD United Kingdom VL - 6 IS - 2 SN - 1939-5116, 1939-5116 KW - Biotechnology and Bioengineering Abstracts KW - Drug delivery KW - Macromolecules KW - Gadolinium KW - Magnetic resonance imaging KW - Therapeutic applications KW - Pharmacokinetics KW - Blood KW - Reviews KW - Computed tomography KW - Liver KW - Kidney KW - Contrast media KW - Chelates KW - nanotechnology KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635018981?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Wiley+Interdisciplinary+Reviews%3A+Nanomedicine+and+Nanobiotechnology&rft.atitle=Dendrimers+as+high+relaxivity+MR+contrast+agents&rft.au=Longmire%2C+Michelle+R%3BOgawa%2C+Mikako%3BChoyke%2C+Peter+L%3BKobayashi%2C+Hisataka&rft.aulast=Longmire&rft.aufirst=Michelle&rft.date=2014-03-01&rft.volume=6&rft.issue=2&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=Wiley+Interdisciplinary+Reviews%3A+Nanomedicine+and+Nanobiotechnology&rft.issn=19395116&rft_id=info:doi/10.1002%2Fwnan.1250 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Drug delivery; Macromolecules; Magnetic resonance imaging; Gadolinium; Therapeutic applications; Pharmacokinetics; Blood; Reviews; Computed tomography; Contrast media; Kidney; Liver; Chelates; nanotechnology DO - http://dx.doi.org/10.1002/wnan.1250 ER - TY - JOUR T1 - Cumulative Proportion of Responders Analysis (CPRA) as a Tool to Assess Treatment Outcome in Alcohol Clinical Trials AN - 1550984222; 201425362 AB - Objective: Several definitions of treatment response have been proposed for alcohol clinical trials (e.g., abstinence and no heavy drinking). However, each of these outcomes allows only one definition of successful response. In contrast, the cumulative proportion of responders analysis (CPRA) includes all of the possible drinking response cutoff points, providing a more complete picture of the therapeutic effects of a treatment. CPRA has been used to examine the efficacy of analgesics but not alcohol pharmacotherapy. To demonstrate its potential utility, we conducted CPRA in two large alcohol treatment trials: the COMBINE (Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence) trial (naltrexone) and a multisite topiramate trial. CPRA was used to demonstrate the efficacy of naltrexone and topiramate on continuous measures of in-treatment drinkingheavy drinking days and drinks per dayand their reductions from pretreatment. Method: All possible cutoff points were portrayed for each measure. We provide graphs to illustrate the effects of the active medications compared with placebo and examined them statistically over a number of salient drinking outcomes to evaluate their efficacy. Results: Treatment group responder curves were not parallel across the entire range of cutoff points; rather, they separated only at lower levels of drinking. In general, effect sizes increased by 0.10-0.15 when going from the lowest drinking level cutoff (i.e., abstinence and no heavy drinking) to the cutoff associated with the maximal treatment effect. Conclusions: CPRA may be useful in designing subsequent trials and helping to illustrate for treatment providers the likelihood of treatment success given various definitions of a positive response. Adapted from the source document. JF - Journal of Studies on Alcohol and Drugs AU - Falk, Daniel E AU - Litten, Raye Z AU - Anton, Raymond F AU - Kranzler, Henry R AU - Johnson, Bankole A AD - Division of Treatment and Recovery Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland; National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, 5635 Fishers Lane, Room 2040, Rockville, MD 20852 falkde@mail.nih.gov Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 335 EP - 346 PB - Center of Alcohol Studies, Rutgers, The State University of New Jersey, Piscataway VL - 75 IS - 2 SN - 1937-1888, 1937-1888 KW - Clinical outcomes KW - Alcohol consumption KW - Pharmacology KW - Efficacy KW - Naltrexone KW - Clinical trials KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1550984222?accountid=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=Cumulative+Proportion+of+Responders+Analysis+%28CPRA%29+as+a+Tool+to+Assess+Treatment+Outcome+in+Alcohol+Clinical+Trials&rft.au=Falk%2C+Daniel+E%3BLitten%2C+Raye+Z%3BAnton%2C+Raymond+F%3BKranzler%2C+Henry+R%3BJohnson%2C+Bankole+A&rft.aulast=Falk&rft.aufirst=Daniel&rft.date=2014-03-01&rft.volume=75&rft.issue=2&rft.spage=335&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 - 2014-08-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Alcohol consumption; Efficacy; Naltrexone; Pharmacology; Clinical outcomes; Clinical trials ER - TY - JOUR T1 - Accuracy and efficacy of percutaneous biopsy and ablation using robotic assistance under computed tomography guidance: a phantom study AN - 1544002737; 19326088 AB - Objective: To compare the accuracy of a robotic interventional radiologist (IR) assistance platform with a standard freehand technique for computed-tomography (CT)-guided biopsy and simulated radiofrequency ablation (RFA). Methods: The accuracy of freehand single-pass needle insertions into abdominal phantoms was compared with insertions facilitated with the use of a robotic assistance platform (n=20 each). Post-procedural CTs were analysed for needle placement error. Percutaneous RFA was simulated by sequentially placing five 17-gauge needle introducers into 5-cm diameter masses (n=5) embedded within an abdominal phantom. Simulated ablations were planned based on pre-procedural CT, before multi-probe placement was executed freehand. Multi-probe placement was then performed on the same 5-cm mass using the ablation planning software and robotic assistance. Post-procedural CTs were analysed to determine the percentage of untreated residual target. Results: Mean needle tip-to-target errors were reduced with use of the IR assistance platform (both P<0.0001). Reduced percentage residual tumour was observed with treatment planning (P=0.02). Conclusion: Improved needle accuracy and optimised probe geometry are observed during simulated CT-guided biopsy and percutaneous ablation with use of a robotic IR assistance platform. This technology may be useful for clinical CT-guided biopsy and RFA, when accuracy may have an impact on outcome. Key points: : times A recently developed robotic intervention radiology assistance platform facilitates CT-guided interventions. times Improved accuracy of complex needle insertions is achievable. times IR assistance platform use can improve target ablation coverage. JF - European Radiology AU - Koethe, Yilun AU - Xu, Sheng AU - Velusamy, Gnanasekar AU - Wood, Bradford J AU - Venkatesan, Aradhana M AD - Center for Interventional Oncology, NIH Clinical Center, National Institutes of Health, Bethesda, MD, USA, venkatesana@cc.nih.gov Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 723 EP - 730 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 24 IS - 3 SN - 0938-7994, 0938-7994 KW - Biotechnology and Bioengineering Abstracts KW - Computer programs KW - software KW - Computed tomography KW - Probes KW - robotics KW - Biopsy KW - Radiology KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1544002737?accountid=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+Radiology&rft.atitle=Accuracy+and+efficacy+of+percutaneous+biopsy+and+ablation+using+robotic+assistance+under+computed+tomography+guidance%3A+a+phantom+study&rft.au=Koethe%2C+Yilun%3BXu%2C+Sheng%3BVelusamy%2C+Gnanasekar%3BWood%2C+Bradford+J%3BVenkatesan%2C+Aradhana+M&rft.aulast=Koethe&rft.aufirst=Yilun&rft.date=2014-03-01&rft.volume=24&rft.issue=3&rft.spage=723&rft.isbn=&rft.btitle=&rft.title=European+Radiology&rft.issn=09387994&rft_id=info:doi/10.1007%2Fs00330-013-3056-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-07-01 N1 - Number of references - 30 N1 - Last updated - 2014-07-10 N1 - SubjectsTermNotLitGenreText - Computer programs; software; Computed tomography; Probes; Biopsy; robotics; Radiology DO - http://dx.doi.org/10.1007/s00330-013-3056-y ER - TY - JOUR T1 - Alcohol abuse in developed and developing countries in the World Mental Health Surveys: Socially defined consequences or psychiatric disorder? AN - 1541981377; 201417586 AB - Background Previous single country research has raised concerns that: (1) the DSM-IV diagnosis of alcohol abuse (AA) is met primarily through the hazardous use criterion related to drinking and driving and (2) that the hazardous use and social consequences AA criteria primarily reflect varying socioeconomic and cultural factors rather than psychiatric disorder. Methods Using representative cross-national data from the 21 countries in the World Mental Health surveys, adults meeting DSM-IV lifetime criteria for AA but not dependence from 10 developed (n=46,071) and 11 developing (n=49,761) countries were assessed as meeting AA with the hazardous use or the social consequences criteria. Results Between 29.3% (developed) and 16.2% (developing) of respondents with AA met only the hazardous use criterion. AA cases with and without hazardous use were similar in age-of-onset, course, predictors, and psychopathological consequences in both developed and developing countries. Discussion and Conclusions Despite some associations of the AA criteria with socioeconomic factors, the hazardous use and social consequences criteria were significantly associated with psychiatric predictors and sequelae. The findings indicate that these criteria reflect psychiatric disorder and are appropriate for inclusion as DSM-5 Alcohol Use Disorder criteria. Scientific Significance These findings support a psychiatric rather than a sociocultural view of the hazardous use and social consequences symptoms and provide evidence that they are appropriate diagnostic criteria cross-nationally with utility in a wide range of socioeconomic environments. This suggests consideration for their adoption by ICD-11. Further research is needed on the implications of these results for prevention and treatment. Adapted from the source document. JF - The American Journal on Addictions AU - Glantz, Meyer D AU - Medina-Mora, Maria Elena AU - Petukhova, Maria AU - Andrade, Laura Helena AU - Anthony, James C AU - de Girolamo, Giovanni AU - de Graaf, Ron AU - Degenhardt, Louisa AU - Demyttenaere, Koen AU - Florescu, Silvia AU - Gureje, Oye AU - Haro, Josep Maria AU - Horiguchi, Itsuko AU - Karam, Elie G AU - Kostyuchenko, Stanislav AU - Lee, Sing AU - Lepine, Jean-Pierre AU - Matschinger, Herbert AU - Neumark, Yehuda AU - Posada-Villa, Jose AU - Sagar, Rajesh AU - Stein, Dan J AU - Tomov, Toma AU - Wells, J Elisabeth AU - Chatterji, Somnath AU - Kessler, Ronald C AD - Division of Epidemiology, Services, and Prevention Research, National Institute on Drug Abuse, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 145 EP - 155 PB - Wiley Subscription Services, Inc. VL - 23 IS - 2 SN - 1055-0496, 1055-0496 KW - Socioeconomic factors KW - Alcohol abuse KW - Psychiatric disorders KW - Mental health KW - Cultural aspects KW - Developing countries KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541981377?accountid=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=Alcohol+abuse+in+developed+and+developing+countries+in+the+World+Mental+Health+Surveys%3A+Socially+defined+consequences+or+psychiatric+disorder%3F&rft.au=Glantz%2C+Meyer+D%3BMedina-Mora%2C+Maria+Elena%3BPetukhova%2C+Maria%3BAndrade%2C+Laura+Helena%3BAnthony%2C+James+C%3Bde+Girolamo%2C+Giovanni%3Bde+Graaf%2C+Ron%3BDegenhardt%2C+Louisa%3BDemyttenaere%2C+Koen%3BFlorescu%2C+Silvia%3BGureje%2C+Oye%3BHaro%2C+Josep+Maria%3BHoriguchi%2C+Itsuko%3BKaram%2C+Elie+G%3BKostyuchenko%2C+Stanislav%3BLee%2C+Sing%3BLepine%2C+Jean-Pierre%3BMatschinger%2C+Herbert%3BNeumark%2C+Yehuda%3BPosada-Villa%2C+Jose%3BSagar%2C+Rajesh%3BStein%2C+Dan+J%3BTomov%2C+Toma%3BWells%2C+J+Elisabeth%3BChatterji%2C+Somnath%3BKessler%2C+Ronald+C&rft.aulast=Glantz&rft.aufirst=Meyer&rft.date=2014-03-01&rft.volume=23&rft.issue=2&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+on+Addictions&rft.issn=10550496&rft_id=info:doi/10.1111%2Fj.1521-0391.2013.12082.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-07-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Psychiatric disorders; Alcohol abuse; Mental health; Developing countries; Socioeconomic factors; Cultural aspects DO - http://dx.doi.org/10.1111/j.1521-0391.2013.12082.x ER - TY - JOUR T1 - Implementation of a Tailored Kiosk-Based Injury Prevention Program in Pediatric Primary Care AN - 1541979627; 201423512 AB - This study identified behavioral and organizational barriers and facilitators related to the implementation of a clinic-based pediatric injury prevention program. Safe N' Sound (SNS), an evidence-based tailored injury prevention program designed for pediatric primary care, was implemented in five pediatric clinics in North Carolina. Office managers participated in structured interviews; health care providers participated in focus groups. Waiting room observations were conducted in participating clinics. Qualitative data captured perceptions of program implementation, including experience in integrating the program into clinical practice, usage by parents and providers, and recommendations for improving implementation. Reported facilitators of program use included usefulness and likeability of customized materials by parents and physicians and alignment with clinic priorities for injury prevention. Barriers included perceived staff burden despite the program's low staff requirements. Consequently, practices experienced difficulty integrating the program into the waiting room environment and within existing staff roles. Recommendations included formalizing staff roles in implementation. Waiting room observations supported greater technology maintenance and staff involvement. Findings suggest a dynamic relationship between program implementation and the adopting organization. In addition to considering characteristics of the intervention, environment, and personnel in intervention development, implementation may require customization to the organization's capacity. [Reprinted by permission of Sage Publications Inc., copyright holder.] JF - Health Promotion Practice AU - Tse, Julia AU - Nansel, Tonja R AU - Weaver, Nancy L AU - Williams, Janice AU - Botello-Harbaum, Maria AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 243 EP - 251 PB - Sage Publications, Thousand Oaks CA VL - 15 IS - 2 SN - 1524-8399, 1524-8399 KW - injury prevention anticipatory guidance pediatric counseling implementation dissemination evidence-based barriers facilitators KW - Paediatrics KW - Injuries KW - Clinics KW - Facilitators KW - Waiting rooms KW - Preventive programmes KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541979627?accountid=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+Promotion+Practice&rft.atitle=Implementation+of+a+Tailored+Kiosk-Based+Injury+Prevention+Program+in+Pediatric+Primary+Care&rft.au=Tse%2C+Julia%3BNansel%2C+Tonja+R%3BWeaver%2C+Nancy+L%3BWilliams%2C+Janice%3BBotello-Harbaum%2C+Maria&rft.aulast=Tse&rft.aufirst=Julia&rft.date=2014-03-01&rft.volume=15&rft.issue=2&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Health+Promotion+Practice&rft.issn=15248399&rft_id=info:doi/10.1177%2F1524839913504586 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-07-01 N1 - Number of references - 22 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Paediatrics; Injuries; Clinics; Preventive programmes; Waiting rooms; Facilitators DO - http://dx.doi.org/10.1177/1524839913504586 ER - TY - JOUR T1 - Acetaldehyde and the genome: Beyond nuclear DNA adducts and carcinogenesis AN - 1534857380; 19846875 AB - The designation of acetaldehyde associated with the consumption of alcoholic beverages as "carcinogenic to humans" (Group 1) by the International Agency for Research on Cancer (IARC) has brought renewed attention to the biological effects of acetaldehyde, as the primary oxidative metabolite of alcohol. Therefore, the overall focus of this review is on acetaldehyde and its direct and indirect effects on the nuclear and mitochondrial genome. We first consider different acetaldehyde-DNA adducts, including a critical assessment of the evidence supporting a role for acetaldehyde-DNA adducts in alcohol related carcinogenesis, and consideration of additional data needed to make a conclusion. We also review recent data on the role of the Fanconi anemia DNA repair pathway in protecting against acetaldehyde genotoxicity and carcinogenicity, as well as teratogenicity. We also review evidence from the older literature that acetaldehyde may impact the genome indirectly, via the formation of adducts with proteins that are themselves critically involved in the maintenance of genetic and epigenetic stability. Finally, we note the lack of information regarding acetaldehyde effects on the mitochondrial genome, which is notable since aldehyde dehydrogenase 2 (ALDH2), the primary acetaldehyde metabolic enzyme, is located in the mitochondrion, and roughly 30% of East Asian individuals are deficient in ALDH2 activity due to a genetic variant in the ALDH2 gene. In summary, a comprehensive understanding of all of the mechanisms by which acetaldehyde impacts the function of the genome has implications not only for alcohol and cancer, but types of alcohol related pathologies as well. Environ. Mol. Mutagen. 55:77-91, 2014. copyright 2013 Wiley Periodicals, Inc. JF - Environmental and Molecular Mutagenesis AU - Brooks, Philip J AU - Zakhari, Samir AD - Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland. Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 77 EP - 91 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 55 IS - 2 SN - 0893-6692, 0893-6692 KW - Toxicology Abstracts; Health & Safety Science Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts KW - Genomes KW - Mutagens KW - Pathology KW - Acetaldehyde KW - Mitochondria KW - Metabolites KW - Mutagenesis KW - Aldehyde dehydrogenase (NAD) KW - Carcinogenicity KW - epigenetics KW - alcohols KW - Alcohol KW - DNA adducts KW - Alcoholic beverages KW - Data processing KW - Genotoxicity KW - Anemia KW - Enzymes KW - DNA repair KW - Maintenance KW - Cancer KW - Biological effects KW - Reviews KW - Fanconi syndrome KW - Carcinogenesis KW - DNA KW - Proteins KW - Teratogenicity KW - Aldehyde dehydrogenase KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - X 24380:Social Poisons & Drug Abuse KW - N 14820:DNA Metabolism & Structure KW - G 07710:Chemical Mutagenesis & Radiation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534857380?accountid=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+and+Molecular+Mutagenesis&rft.atitle=Acetaldehyde+and+the+genome%3A+Beyond+nuclear+DNA+adducts+and+carcinogenesis&rft.au=Brooks%2C+Philip+J%3BZakhari%2C+Samir&rft.aulast=Brooks&rft.aufirst=Philip&rft.date=2014-03-01&rft.volume=55&rft.issue=2&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/10.1002%2Fem.21824 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Genomes; DNA adducts; Mutagens; Data processing; Alcoholic beverages; Acetaldehyde; Genotoxicity; Mitochondria; Enzymes; Metabolites; DNA repair; Cancer; Mutagenesis; Aldehyde dehydrogenase (NAD); epigenetics; Fanconi syndrome; Reviews; Carcinogenesis; alcohols; Teratogenicity; Aldehyde dehydrogenase; Alcohol; Pathology; Anemia; Maintenance; Biological effects; Carcinogenicity; DNA; Proteins DO - http://dx.doi.org/10.1002/em.21824 ER - TY - JOUR T1 - Effect of acid activated clay minerals on biodegradation of crude oil hydrocarbons AN - 1534850670; 20038826 AB - The role of acid activated clays and unmodified clays in hydrocarbon removal during biodegradation was investigated in aqueous clay/oil microcosm experiments with a hydrocarbon degrading microorganism community. The clay minerals used for this study were Na-montmorillonite, palygorskite, saponite and kaolinite. The clay mineral samples were treated with hydrochloric acid to produce acid activated clays which were used in this study. The study indicated that acid activated clays and untreated kaolinite were inhibitory to biodegradation of the hydrocarbons via different mechanisms whereas the untreated saponite was neutral to biodegradation of the hydrocarbons. However, untreated palygorskite and Namontmorillonite were stimulatory to biodegradation and appears to do so as a result of the clays' ability to provide high surface area for the accumulation of microbes and nutrients such that the nutrients are within the 'vicinity' of the microbes. Adsorption of hydrocarbons was significant during biodegradation especially with unmodified palygorskite, where there was more than 40% removal of total petroleum hydrocarbons (TPH) by adsorption in the experimental microcosm containing 5:1 ratio (w/w) of clay to oil. JF - International Biodeterioration & Biodegradation AU - Ugochukwu, Uzochukwu C AU - Jones, Martin D AU - Head, Ian M AU - Manning, David AC AU - Fialips, Claire I AD - School of Civil Engineering and Geosciences, University of Newcastle Upon Tyne, Drummond Building, NEI 7RU, United Kingdom, ugouzochukwu@yahoo.com Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 185 EP - 191 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 88 SN - 0964-8305, 0964-8305 KW - Environment Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Biotechnology and Bioengineering Abstracts KW - Acid activated clay KW - Unmodified clay KW - Biodegradation KW - Adsorption KW - Total petroleum hydrocarbon KW - Microbial cells KW - Biodeterioration KW - Clay KW - Hydrocarbons KW - Surface area KW - Nutrients KW - kaolinite KW - Clays KW - Oil KW - Crude oil KW - Petroleum KW - Microorganisms KW - Microcosms KW - Minerals KW - Hydrochloric acid KW - Petroleum hydrocarbons KW - ENA 11:Non-Renewable Resources KW - W 30950:Waste Treatment & Pollution Clean-up KW - A 01320:Microbial Degradation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534850670?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Biodeterioration+%26+Biodegradation&rft.atitle=Effect+of+acid+activated+clay+minerals+on+biodegradation+of+crude+oil+hydrocarbons&rft.au=Ugochukwu%2C+Uzochukwu+C%3BJones%2C+Martin+D%3BHead%2C+Ian+M%3BManning%2C+David+AC%3BFialips%2C+Claire+I&rft.aulast=Ugochukwu&rft.aufirst=Uzochukwu&rft.date=2014-03-01&rft.volume=88&rft.issue=&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=International+Biodeterioration+%26+Biodegradation&rft.issn=09648305&rft_id=info:doi/10.1016%2Fj.ibiod.2013.10.018 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2016-07-20 N1 - SubjectsTermNotLitGenreText - Biodeterioration; Biodegradation; Hydrocarbons; Surface area; Nutrients; kaolinite; Clays; Oil; Petroleum; Microorganisms; Adsorption; Microcosms; Minerals; Hydrochloric acid; Crude oil; Clay; Petroleum hydrocarbons DO - http://dx.doi.org/10.1016/j.ibiod.2013.10.018 ER - TY - JOUR T1 - THYROID CANCER STUDY AMONG UKRAINIAN CHILDREN EXPOSED TO RADIATION AFTER THE CHORNOBYL ACCIDENT: IMPROVED ESTIMATES OF THE THYROID DOSES TO THE COHORT MEMBERS AN - 1534846327; 19900498 AB - In collaboration with the Ukrainian Research Center for Radiation Medicine, the U.S. National Cancer Institute initiated a cohort study of children and adolescents exposed to Chornobyl fallout in Ukraine to better understand the long-term health effects of exposure to radioactive iodines. All 13,204 cohort members were subjected to at least one direct thyroid measurement between 30 April and 30 June 1986 and resided at the time of the accident in the northern parts of Kyiv, Zhytomyr, or Chernihiv Oblasts, which were the most contaminated territories of Ukraine as a result of radioactive fallout from the Chornobyl accident. Thyroid doses for the cohort members, which had been estimated following the first round of interviews, were re-evaluated following the second round of interviews. The revised thyroid doses range from 0.35 mGy to 42 Gy, with 95% of the doses between 1 mGy and 4.2 Gy, an arithmetic mean of 0.65 Gy, and a geometric mean of 0.19 Gy. These means are 70% of the previous estimates, mainly because of the use of country-specific thyroid masses. Many of the individual thyroid dose estimates show substantial differences because of the use of an improved questionnaire for the second round of interviews. Limitations of the current set of thyroid dose estimates are discussed. For the epidemiologic study, the most notable improvement is a revised assessment of the uncertainties, as shared and unshared uncertainties in the parameter values were considered in the calculation of the 1,000 stochastic estimates of thyroid dose for each cohort member. This procedure makes it possible to perform a more realistic risk analysis. JF - Health Physics AU - Likhtarov, Ilya AU - Kovgan, Lina AU - Masiuk, Sergii AU - Talerko, Mykola AU - Chepurny, Mykola AU - Ivanova, Olga AU - Gerasymenko, Valentina AU - Boyko, Zulfira AU - Voilleque, Paul AU - Drozdovitch, Vladimir AU - Bouville, Andre AD - State Institution "National Research Centre for Radiation Medicine," National Academy of Medical Sciences of Ukraine, 53 Melnikova Street, 04050 Kyiv, Ukraine, drozdovv@mail.nih.gov. Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 370 EP - 396 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 106 IS - 3 SN - 0017-9078, 0017-9078 KW - Risk Abstracts; Health & Safety Science Abstracts KW - 131I KW - Chernobyl KW - dose assessment KW - thyroid KW - Risk analysis KW - Ukraine KW - Thyroid KW - Territory KW - Children KW - Cancer KW - Health risks KW - USA KW - Accidents KW - Radiation KW - Radioactive fallout KW - Iodine KW - Adolescents 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/1534846327?accountid=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=THYROID+CANCER+STUDY+AMONG+UKRAINIAN+CHILDREN+EXPOSED+TO+RADIATION+AFTER+THE+CHORNOBYL+ACCIDENT%3A+IMPROVED+ESTIMATES+OF+THE+THYROID+DOSES+TO+THE+COHORT+MEMBERS&rft.au=Likhtarov%2C+Ilya%3BKovgan%2C+Lina%3BMasiuk%2C+Sergii%3BTalerko%2C+Mykola%3BChepurny%2C+Mykola%3BIvanova%2C+Olga%3BGerasymenko%2C+Valentina%3BBoyko%2C+Zulfira%3BVoilleque%2C+Paul%3BDrozdovitch%2C+Vladimir%3BBouville%2C+Andre&rft.aulast=Likhtarov&rft.aufirst=Ilya&rft.date=2014-03-01&rft.volume=106&rft.issue=3&rft.spage=370&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0b013e31829f3096 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2015-05-27 N1 - SubjectsTermNotLitGenreText - Health risks; Risk analysis; Accidents; Radiation; Radioactive fallout; Thyroid; Iodine; Territory; Children; Cancer; Adolescents; USA; Ukraine DO - http://dx.doi.org/10.1097/HP.0b013e31829f3096 ER - TY - JOUR T1 - Overfitting, generalization, and MSE in class probability estimation with high-dimensional data AN - 1534827288; 20037663 AB - Accurate class probability estimation is important for medical decision making but is challenging, particularly when the number of candidate features exceeds the number of cases. Special methods have been developed for nonprobabilistic classification, but relatively little attention has been given to class probability estimation with numerous candidate variables. In this paper, we investigate overfitting in the development of regularized class probability estimators. We investigate the relation between overfitting and accurate class probability estimation in terms of mean square error. Using simulation studies based on real datasets, we found that some degree of overfitting can be desirable for reducing mean square error. We also introduce a mean square error decomposition for class probability estimation that helps clarify the relationship between overfitting and prediction accuracy. JF - Biometrical Journal AU - Kim, Kyung In AU - Simon, Richard AD - Biometric Research Branch, National Cancer Institute, 9609 Medical Center Dr, MSC 9735 Bethesda, MD 20892-9735, USA. Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 256 EP - 269 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 56 IS - 2 SN - 0323-3847, 0323-3847 KW - Biotechnology and Bioengineering Abstracts KW - Decision making KW - Data processing KW - Statistics KW - Classification KW - Biometrics KW - Decomposition KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534827288?accountid=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=Overfitting%2C+generalization%2C+and+MSE+in+class+probability+estimation+with+high-dimensional+data&rft.au=Kim%2C+Kyung+In%3BSimon%2C+Richard&rft.aulast=Kim&rft.aufirst=Kyung&rft.date=2014-03-01&rft.volume=56&rft.issue=2&rft.spage=256&rft.isbn=&rft.btitle=&rft.title=Biometrical+Journal&rft.issn=03233847&rft_id=info:doi/10.1002%2Fbimj.201300083 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Decision making; Statistics; Data processing; Classification; Biometrics; Decomposition DO - http://dx.doi.org/10.1002/bimj.201300083 ER - TY - JOUR T1 - ATHENA: the analysis tool for heritable and environmental network associations AN - 1534822276; 19360573 AB - Motivation: Advancements in high-throughput technology have allowed researchers to examine the genetic etiology of complex human traits in a robust fashion. Although genome-wide association studies have identified many novel variants associated with hundreds of traits, a large proportion of the estimated trait heritability remains unexplained. One hypothesis is that the commonly used statistical techniques and study designs are not robust to the complex etiology that may underlie these human traits. This etiology could include non-linear gene gene or gene environment interactions. Additionally, other levels of biological regulation may play a large role in trait variability.Results: To address the need for computational tools that can explore enormous datasets to detect complex susceptibility models, we have developed a software package called the Analysis Tool for Heritable and Environmental Network Associations (ATHENA). ATHENA combines various variable filtering methods with machine learning techniques to analyze high-throughput categorical (i.e. single nucleotide polymorphisms) and quantitative (i.e. gene expression levels) predictor variables to generate multivariable models that predict either a categorical (i.e. disease status) or quantitative (i.e. cholesterol levels) outcomes. The goal of this article is to demonstrate the utility of ATHENA using simulated and biological datasets that consist of both single nucleotide polymorphisms and gene expression variables to identify complex prediction models. Importantly, this method is flexible and can be expanded to include other types of high-throughput data (i.e. RNA-seq data and biomarker measurements). JF - Bioinformatics AU - Holzinger, Emily R AU - Dudek, Scott M AU - Frase, Alex T AU - Pendergrass, Sarah A AU - Ritchie, Marylyn D AD - super(1)Inherited Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Baltimore, MD, USA and super(2)Department of Biochemistry and Molecular Biology, Center for Systems Genomics, Pennsylvania State University, University Park, PA, USA Y1 - 2014/03/01/ PY - 2014 DA - 2014 Mar 01 SP - 698 EP - 705 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 30 IS - 5 SN - 1367-4803, 1367-4803 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Etiology KW - Data processing KW - Statistical analysis KW - Cholesterol KW - Computer applications KW - biomarkers KW - Models KW - Gene expression KW - Computer programs KW - software KW - Single-nucleotide polymorphism KW - Learning algorithms KW - Bioinformatics KW - Internet KW - Heritability KW - N 14810:Methods KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534822276?accountid=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=ATHENA%3A+the+analysis+tool+for+heritable+and+environmental+network+associations&rft.au=Holzinger%2C+Emily+R%3BDudek%2C+Scott+M%3BFrase%2C+Alex+T%3BPendergrass%2C+Sarah+A%3BRitchie%2C+Marylyn+D&rft.aulast=Holzinger&rft.aufirst=Emily&rft.date=2014-03-01&rft.volume=30&rft.issue=5&rft.spage=698&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt572 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Etiology; Data processing; Statistical analysis; Cholesterol; Computer applications; biomarkers; Models; Gene expression; Computer programs; software; Single-nucleotide polymorphism; Bioinformatics; Learning algorithms; Heritability; Internet DO - http://dx.doi.org/10.1093/bioinformatics/btt572 ER - TY - JOUR T1 - Discretized Gaussian mixture for genotyping of microsatellite loci containing homopolymer runs AN - 1534820830; 19360591 AB - Motivation: Inferring lengths of inherited microsatellite alleles with single base pair resolution from short sequence reads is challenging due to several sources of noise caused by the repetitive nature of microsatellites and the technologies used to generate raw sequence data.Results: We have developed a program, GenoTan, using a discretized Gaussian mixture model combined with a rules-based approach to identify inherited variation of microsatellite loci from short sequence reads without paired-end information. It effectively distinguishes length variants from noise including insertion/deletion errors in homopolymer runs by addressing the bidirectional aspect of insertion and deletion errors in sequence reads. Here we first introduce a homopolymer decomposition method which estimates error bias toward insertion or deletion in homopolymer sequence runs. Combining these approaches, GenoTan was able to genotype 94.9% of microsatellite loci accurately from simulated data with 40x sequence coverage quickly while the other programs showed <90% correct calls for the same data and required 5 similar to 30 more computational time than GenoTan. It also showed the highest true-positive rate for real data using mixed sequence data of two Drosophila inbred lines, which was a novel validation approach for genotyping. JF - Bioinformatics AU - Tae, Hongseok AU - Kim, Dong-Yun AU - McCormick, John AU - Settlage, Robert E AU - Garner, Harold R AD - super(1)Virginia Bioinformatics Institute, Virginia Tech, Blacksburg, VA 24061 and super(2)Office of Biostatistics Research, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2014/03/01/ PY - 2014 DA - 2014 Mar 01 SP - 652 EP - 659 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 30 IS - 5 SN - 1367-4803, 1367-4803 KW - Biotechnology and Bioengineering Abstracts KW - Genotyping KW - Microsatellites KW - Genotypes KW - Computer applications KW - Decomposition KW - Models KW - Computer programs KW - software KW - Insertion KW - Inbreeding KW - Bioinformatics KW - Drosophila KW - Internet KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534820830?accountid=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=Discretized+Gaussian+mixture+for+genotyping+of+microsatellite+loci+containing+homopolymer+runs&rft.au=Tae%2C+Hongseok%3BKim%2C+Dong-Yun%3BMcCormick%2C+John%3BSettlage%2C+Robert+E%3BGarner%2C+Harold+R&rft.aulast=Tae&rft.aufirst=Hongseok&rft.date=2014-03-01&rft.volume=30&rft.issue=5&rft.spage=652&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt595 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2014-08-07 N1 - SubjectsTermNotLitGenreText - Computer programs; software; Insertion; Genotyping; Microsatellites; Inbreeding; Genotypes; Bioinformatics; Computer applications; Decomposition; Internet; Models; Drosophila DO - http://dx.doi.org/10.1093/bioinformatics/btt595 ER - TY - JOUR T1 - Serum leptin and loss of control eating in children and adolescents AN - 1524394920; 19750242 AB - Background: Both insufficiency and resistance to the actions of the adipocyte-derived hormone leptin promote hunger, increased food intake and greater body weight. Some studies suggest that adults reporting binge eating have increased serum leptin compared with those without binge eating, even after adjusting for the greater adiposity that characterizes binge eaters. Pediatric binge or loss of control (LOC) eating are prospective risk factors for excessive weight gain and may predict development of metabolic abnormalities, but whether LOC eating is associated with higher leptin among children is unknown. We therefore examined leptin and LOC eating in a pediatric cohort. Methods: A convenience sample of 506 lean and obese youth (7-18 years) was recruited from Washington, DC and its suburbs. Serum leptin was collected after an overnight fast. Adiposity was measured by dual-energy X-ray absorptiometry or air displacement plethysmography. LOC eating was assessed by interview methodology. Results: Leptin was strongly associated with fat mass (r=0.79, P0.05). The relationship between LOC eating and leptin appeared to be significant for females only (P=0.002). Conclusions: Reports of LOC eating were associated with higher fasting leptin in youth, beyond the contributions of body weight. Prospective studies are required to elucidate whether LOC eating promotes greater leptin or whether greater leptin resistance may promote LOC eating. JF - International Journal of Obesity AU - Miller, R AU - Tanofsky-Kraff, M AU - Shomaker, L B AU - Field, S E AU - Hannallah, L AU - Reina, S A AU - Mooreville, M AU - Sedaka, N AU - Brady, S M AU - Condarco, T AU - Reynolds, J C AU - Yanovski, S Z AU - Yanovski, J A AD - 1] Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Hatfield Clinical Research Center, Bethesda, MD, USA [2] Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, Bethesda, MD, USA Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 397 EP - 403 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 38 IS - 3 SN - 0307-0565, 0307-0565 KW - Risk Abstracts KW - Hunger KW - Obesity KW - Body weight KW - Risk factors KW - Children KW - Hormones KW - USA, Washington, D.C. KW - Suburbs KW - Adolescents KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524394920?accountid=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+Obesity&rft.atitle=Serum+leptin+and+loss+of+control+eating+in+children+and+adolescents&rft.au=Miller%2C+R%3BTanofsky-Kraff%2C+M%3BShomaker%2C+L+B%3BField%2C+S+E%3BHannallah%2C+L%3BReina%2C+S+A%3BMooreville%2C+M%3BSedaka%2C+N%3BBrady%2C+S+M%3BCondarco%2C+T%3BReynolds%2C+J+C%3BYanovski%2C+S+Z%3BYanovski%2C+J+A&rft.aulast=Miller&rft.aufirst=R&rft.date=2014-03-01&rft.volume=38&rft.issue=3&rft.spage=397&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2013.126 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-05-29 N1 - SubjectsTermNotLitGenreText - Hunger; Obesity; Body weight; Risk factors; Children; Hormones; Adolescents; Suburbs; USA, Washington, D.C. DO - http://dx.doi.org/10.1038/ijo.2013.126 ER - TY - JOUR T1 - Associations between child disabilities and caregiver discipline and violence in low- and middle-income countries AN - 1521335782; 4555744 AB - Using nationally representative samples of 45,964 two- to nine-year-old children and their primary caregivers in 17 developing countries, this study examined the relations between children's cognitive, language, sensory, and motor disabilities and caregivers' use of discipline and violence. Primary caregivers reported on their child's disabilities and whether they or anyone in their household had used nonviolent discipline, psychological aggression, and physical violence toward the target child and believed that using corporal punishment is necessary. Logistic regression analyses supported the hypothesis that children with disabilities are treated more harshly than children without disabilities. The findings suggest that policies and interventions are needed to work toward the United Nations' goals of ensuring that children with disabilities are protected from abuse and violence. Reprinted by permission of the University of Chicago Press. © All rights reserved JF - Child development AU - Bornstein, Marc H AU - Hendricks, Charlene AU - Lansford, Jennifer E AU - Deater-Deckard, Kirby AD - National Institutes of Health ; Duke University ; Virginia Polytechnic Institute and State University Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 513 EP - 531 VL - 85 IS - 2 SN - 0009-3920, 0009-3920 KW - Sociology KW - Caring KW - Disability KW - Aggression KW - Children KW - Developing countries KW - Violence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521335782?accountid=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=Associations+between+child+disabilities+and+caregiver+discipline+and+violence+in+low-+and+middle-income+countries&rft.au=Bornstein%2C+Marc+H%3BHendricks%2C+Charlene%3BLansford%2C+Jennifer+E%3BDeater-Deckard%2C+Kirby&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2014-03-01&rft.volume=85&rft.issue=2&rft.spage=513&rft.isbn=&rft.btitle=&rft.title=Child+development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fcdev.12132 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-05-06 N1 - Last updated - 2014-05-07 N1 - SubjectsTermNotLitGenreText - 2212; 3584 1678; 2039 13521; 13325; 662; 3480 2958 12092 DO - http://dx.doi.org/10.1111/cdev.12132 ER - TY - JOUR T1 - Limited HIV-1 Superinfection in Seroconverters from the CAPRISA 004 Microbicide Trial AN - 1520373038; 19446612 AB - HIV-1 superinfection (SI) occurs when an infected individual acquires a distinct new viral strain. The rate of superinfection may be reflective of the underlying HIV risk in a population. The Centre for the AIDS Programme of Research in South Africa (CAPRISA) 004 clinical trial demonstrated that women who used a tenofovir-containing microbicide gel had lower rates of HIV infection than women using a placebo gel. Women who contracted HIV-1 during the trial were screened for the occurrence of superinfection by next-generation sequencing of the viral gag and env genes. There were two cases (one in each trial arm) of subtype C superinfection identified from the 76 women with primary infection screened at two time points (rate of superinfection, 1.5/100 person-years). Both women experienced a >0.5-log increase in viral load during the window when superinfection occurred. The rate of superinfection was significantly lower than the overall primary HIV incidence in the microbicide trial (incidence rate ratio [IRR], 0.20; P = 0.003). The women who seroconverted during the trial reported a significant increase in sexual contact with their stable partner 4 months after seroconversion (P < 0.001), which may have lowered the risk of superinfection in this population. The lower frequency of SI compared to the primary incidence is in contrast to a report from a general heterosexual African population but agrees with a study of high-risk women in Kenya. A better understanding of the rate of HIV superinfection could have important implications for ongoing HIV vaccine research. JF - Journal of Clinical Microbiology AU - Redd, Andrew D AU - Mullis, Caroline E AU - Wendel, Sarah K AU - Sheward, Daniel AU - Martens, Craig AU - Bruno, Daniel AU - Werner, Lise AU - Garrett, Nigel J AU - Karim, Quarraisha Abdool AU - Williamson, Carolyn AD - Laboratory of Immunoregulation, Division of Intramural Research, NIAID, NIH, Bethesda, Maryland, USA, aredd2@jhmi.edu. Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 844 EP - 848 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 52 IS - 3 SN - 0095-1137, 0095-1137 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - Acquired immune deficiency syndrome KW - Human immunodeficiency virus KW - Risk factors KW - Human immunodeficiency virus 1 KW - Risk groups KW - Seroconversion KW - Vaccines KW - Superinfection KW - Clinical trials KW - Gag protein KW - microbicides KW - A 01340:Antibiotics & Antimicrobials KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520373038?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Limited+HIV-1+Superinfection+in+Seroconverters+from+the+CAPRISA+004+Microbicide+Trial&rft.au=Redd%2C+Andrew+D%3BMullis%2C+Caroline+E%3BWendel%2C+Sarah+K%3BSheward%2C+Daniel%3BMartens%2C+Craig%3BBruno%2C+Daniel%3BWerner%2C+Lise%3BGarrett%2C+Nigel+J%3BKarim%2C+Quarraisha+Abdool%3BWilliamson%2C+Carolyn&rft.aulast=Redd&rft.aufirst=Andrew&rft.date=2014-03-01&rft.volume=52&rft.issue=3&rft.spage=844&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/10.1128%2FJCM.03143-13 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Number of references - 16 N1 - Last updated - 2015-11-25 N1 - SubjectsTermNotLitGenreText - Acquired immune deficiency syndrome; Risk factors; Seroconversion; Risk groups; Vaccines; Clinical trials; Superinfection; Gag protein; microbicides; Human immunodeficiency virus; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1128/JCM.03143-13 ER - TY - JOUR T1 - Mutagenesis and phenotyping resources in zebrafish for studying development and human disease AN - 1516739585; 19505047 AB - The zebrafish (Danio rerio) is an important model organism for studying development and human disease. The zebrafish has an excellent reference genome and the functions of hundreds of genes have been tested using both forward and reverse genetic approaches. Recent years have seen an increasing number of large-scale mutagenesis projects and the number of mutants or gene knockouts in zebrafish has increased rapidly, including for the first time conditional knockout technologies. In addition, targeted mutagenesis techniques such as zinc finger nucleases, transcription activator-like effector nucleases and clustered regularly interspaced short sequences (CRISPR) or CRISPR-associated (Cas), have all been shown to effectively target zebrafish genes as well as the first reported germline homologous recombination, further expanding the utility and power of zebrafish genetics. Given this explosion of mutagenesis resources, it is now possible to perform systematic, high-throughput phenotype analysis of all zebrafish gene knockouts. JF - Briefings in Functional Genomics AU - Varshney, Gaurav Kumar AU - Burgess, Shawn Michael AD - Corresponding author. Shawn Michael Burgess, Developmental Genomics Section, Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA., burgess@mail.nih.gov Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 82 EP - 94 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 13 IS - 2 SN - 2041-2649, 2041-2649 KW - Genetics Abstracts; ASFA 1: Biological Sciences & Living Resources; Biotechnology and Bioengineering Abstracts KW - zebrafish KW - mutagenesis KW - phenotyping KW - resources KW - knockouts KW - Genomes KW - Human diseases KW - Nuclease KW - Zinc finger proteins KW - Transcription KW - Freshwater KW - Freshwater fish KW - Phenotypes KW - Explosions KW - Models KW - Mutagenesis KW - Danio rerio KW - Phenotyping KW - Recombination KW - targeted mutagenesis KW - homologous recombination KW - Resource development KW - Q1 08604:Stock assessment and management KW - G 07730:Development & Cell Cycle KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516739585?accountid=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=Briefings+in+Functional+Genomics&rft.atitle=Mutagenesis+and+phenotyping+resources+in+zebrafish+for+studying+development+and+human+disease&rft.au=Varshney%2C+Gaurav+Kumar%3BBurgess%2C+Shawn+Michael&rft.aulast=Varshney&rft.aufirst=Gaurav&rft.date=2014-03-01&rft.volume=13&rft.issue=2&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=Briefings+in+Functional+Genomics&rft.issn=20412649&rft_id=info:doi/10.1093%2Fbfgp%2Felt042 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Genomes; Recombination; Human diseases; Transcription; Resource development; Freshwater fish; Phenotypes; Explosions; Mutagenesis; Phenotyping; targeted mutagenesis; Zinc finger proteins; Nuclease; homologous recombination; Models; Danio rerio; Freshwater DO - http://dx.doi.org/10.1093/bfgp/elt042 ER - TY - JOUR T1 - Experience of an information aid for newly diagnosed multiple sclerosis patients: a qualitative study on the SIMS-Trial AN - 1512193795; 201404444 AB - Background The SIMS-Trial (ISRCTN81072971) proved the effectiveness, in terms of patient's knowledge and care satisfaction, of an add-on information aid (personal interview with a physician using a navigable CD and take-home booklet) in 120 newly diagnosed patients with multiple sclerosis (MS) from five Italian centres. Objective To scrutinize the experience of SIMS-Trial participants in order to gain better understanding of the effectiveness of the information aid and its components. Design We performed (i) nine individual semi-structured interviews with a purposeful sample of SIMS-Trial patients who received the information aid, (ii) focus group meeting (FGM) with the physicians who conducted the personal interview, and (iii) FGM with patients' caring neurologists. Results Patients' experience with the information aid was positive as it enhanced their understanding of their disease, being viewed as a guided tour of their medical condition. The physicians who conducted the personal interviews were also positive in their overall evaluation but noted an initial difficulty in using the CD. The caring neurologists had limited direct experience of the aid, and their views were confined to utility of the information aid in general. All participants considered the combination of personal interview, CD navigation and take-home booklet essential, but urged a more flexible scheduling of the personal interview. It also emerged that some content required revision and that the aid was unsuitable for patients with primary progressive MS. Conclusions The results of the study further support the value of the aid and also provide important indications for improving it and refining indications for use. Adapted from the source document. JF - Health Expectations AU - Borreani, Claudia AU - Giordano, Andrea AU - Falautano, Monica AU - Lugaresi, Alessandra AU - Martinelli, Vittorio AU - Granella, Franco AU - Tortorella, Carla AU - Plasmati, Imma AU - Radaelli, Marta AU - Farina, Deborah AU - Dalla Bella, Eleonora AU - Bianchi, Elisabetta AU - Acquarone, Nicola AU - Miccinesi, Guido AU - Solari, Alessandra AD - Psychology Unit, National Cancer Institute Foundation, Milan Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 36 EP - 48 PB - Blackwell Publishing, Oxford UK VL - 17 IS - 1 SN - 1369-6513, 1369-6513 KW - Neurologists KW - Newly diagnosed KW - Doctors KW - Multiple sclerosis KW - Caring KW - Navigation KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512193795?accountid=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+Expectations&rft.atitle=Experience+of+an+information+aid+for+newly+diagnosed+multiple+sclerosis+patients%3A+a+qualitative+study+on+the+SIMS-Trial&rft.au=Borreani%2C+Claudia%3BGiordano%2C+Andrea%3BFalautano%2C+Monica%3BLugaresi%2C+Alessandra%3BMartinelli%2C+Vittorio%3BGranella%2C+Franco%3BTortorella%2C+Carla%3BPlasmati%2C+Imma%3BRadaelli%2C+Marta%3BFarina%2C+Deborah%3BDalla+Bella%2C+Eleonora%3BBianchi%2C+Elisabetta%3BAcquarone%2C+Nicola%3BMiccinesi%2C+Guido%3BSolari%2C+Alessandra&rft.aulast=Borreani&rft.aufirst=Claudia&rft.date=2014-03-01&rft.volume=17&rft.issue=1&rft.spage=36&rft.isbn=&rft.btitle=&rft.title=Health+Expectations&rft.issn=13696513&rft_id=info:doi/10.1111%2Fj.1369-7625.2011.00736.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-04-01 N1 - Last updated - 2016-09-27 N1 - CODEN - HEHPFM N1 - SubjectsTermNotLitGenreText - Multiple sclerosis; Doctors; Newly diagnosed; Caring; Neurologists; Navigation DO - http://dx.doi.org/10.1111/j.1369-7625.2011.00736.x ER - TY - JOUR T1 - Subchronic oral toxicity study of decitabine in combination with tetrahydrouridine in CD-1 mice. AN - 1511820354; 24639139 AB - Decitabine (5-aza-2'-deoxycytidine; DAC) in combination with tetrahydrouridine (THU) is a potential oral therapy for sickle cell disease and β-thalassemia. A study was conducted in mice to assess safety of this combination therapy using oral gavage of DAC and THU administered 1 hour prior to DAC on 2 consecutive days/week for up to 9 weeks followed by a 28-day recovery to support its clinical trials up to 9-week duration. Tetrahydrouridine, a competitive inhibitor of cytidine deaminase, was used in the combination to improve oral bioavailability of DAC. Doses were 167 mg/kg THU followed by 0, 0.2, 0.4, or 1.0 mg/kg DAC; THU vehicle followed by 1.0 mg/kg DAC; or vehicle alone. End points evaluated were clinical observations, body weights, food consumption, clinical pathology, gross/histopathology, bone marrow micronuclei, and toxicokinetics. There were no treatment-related effects noticed on body weight, food consumption, serum chemistry, or urinalysis parameters. Dose- and gender-dependent changes in plasma DAC levels were observed with a Cmax within 1 hour. At the 1 mg/kg dose tested, THU increased DAC plasma concentration (∼ 10-fold) as compared to DAC alone. Severe toxicity occurred in females receiving high-dose 1 mg/kg DAC + THU, requiring treatment discontinuation at week 5. Severity and incidence of microscopic findings increased in a dose-dependent fashion; findings included bone marrow hypocellularity (with corresponding hematologic changes and decreases in white blood cells, red blood cells, hemoglobin, hematocrit, reticulocytes, neutrophils, and lymphocytes), thymic/lymphoid depletion, intestinal epithelial apoptosis, and testicular degeneration. Bone marrow micronucleus analysis confirmed bone marrow cytotoxicity, suppression of erythropoiesis, and genotoxicity. Following the recovery period, a complete or trend toward resolution of these effects was observed. In conclusion, the combination therapy resulted in an increased sensitivity to DAC toxicity correlating with DAC plasma levels, and females are more sensitive compared to their male counterparts. JF - International journal of toxicology AU - Terse, Pramod AU - Engelke, Kory AU - Chan, Kenneth AU - Ling, Yonghua AU - Sharpnack, Douglas AU - Saunthararajah, Yogen AU - Covey, Joseph M AD - Division of Pre-Clinical Innovations, National Center for Advancing Translational Sciences, Bethesda, MD, USA. Email: tersep@mail.nih.gov. PY - 2014 SP - 75 EP - 85 VL - 33 IS - 2 KW - Antimetabolites KW - 0 KW - Antimetabolites, Antineoplastic KW - Tetrahydrouridine KW - 18771-50-1 KW - decitabine KW - 776B62CQ27 KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - combination therapy KW - hematopoietic tissue KW - lymphoid tissue KW - tetrahydrouridine KW - CD-1 mice KW - Eating -- drug effects KW - Bone Marrow Cells -- drug effects KW - Animals KW - Micronucleus Tests KW - Body Weight -- drug effects KW - Mice KW - Pharmacokinetics KW - Male KW - Female KW - Blood Cell Count KW - Antimetabolites -- toxicity KW - Azacitidine -- toxicity KW - Azacitidine -- analogs & derivatives KW - Tetrahydrouridine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1511820354?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+toxicology&rft.atitle=Subchronic+oral+toxicity+study+of+decitabine+in+combination+with+tetrahydrouridine+in+CD-1+mice.&rft.au=Terse%2C+Pramod%3BEngelke%2C+Kory%3BChan%2C+Kenneth%3BLing%2C+Yonghua%3BSharpnack%2C+Douglas%3BSaunthararajah%2C+Yogen%3BCovey%2C+Joseph+M&rft.aulast=Terse&rft.aufirst=Pramod&rft.date=2014-03-01&rft.volume=33&rft.issue=2&rft.spage=75&rft.isbn=&rft.btitle=&rft.title=International+journal+of+toxicology&rft.issn=1092-874X&rft_id=info:doi/10.1177%2F1091581814524994 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-18 N1 - Date created - 2014-03-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Chemother Pharmacol. 2008 Aug;62(3):457-64 [18008070] PLoS One. 2009;4(2):e4563 [19234609] Blood. 2012 Feb 2;119(5):1240-7 [22160381] Clin Cancer Res. 2008 Jun 1;14(11):3529-35 [18519786] Am J Hematol. 2007 Nov;82(11):981-5 [17696208] J Clin Oncol. 2007 Jan 1;25(1):32-42 [17194903] Rapid Commun Mass Spectrom. 2006;20(7):1117-26 [16523529] Exp Hematol. 2006 Mar;34(3):339-47 [16543068] Ann Hematol. 1995 Feb;70(2):91-5 [7880931] Cancer Res. 1986 Nov;46(11):5511-7 [2428479] Am J Hematol. 1985 Mar;18(3):283-8 [2579548] Drug Chem Toxicol. 1981;4(4):373-81 [6178576] Cancer Res. 1977 Jun;37(6):1636-9 [66984] Cancer Chemother Rep 3. 1974 Sep;5(1):15-6 [4213302] Pharmacogenomics J. 2004;4(5):307-14 [15224082] Blood. 2004 Jun 1;103(11):4102-10 [14976039] Blood. 2003 Dec 1;102(12):3865-70 [12907443] Clin Cancer Res. 2013 Feb 15;19(4):938-48 [23287564] Blood. 2000 Oct 1;96(7):2379-84 [11001887] Blood. 2002 Jun 1;99(11):3905-8 [12010787] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/1091581814524994 ER - TY - JOUR T1 - Injection parameters and virus dependent choice of promoters to improve neuron targeting in the nonhuman primate brain AN - 1508762158; 19387222 AB - We, like many others, wish to use modern molecular methods to alter neuronal functionality in primates. For us, this requires expression in a large proportion of the targeted cell population. Long generation times make germline modification of limited use. The size and intricate primate brain anatomy poses additional challenges. We surved methods using lentiviruses and serotypes of adeno-associated viruses (AAVs) to introduce active molecular material into cortical and subcortical regions of old-world monkey brains. Slow injections of AAV2 give well-defined expression of neurons in the cortex surrounding the injection site. Somewhat surprisingly we find that in the monkey the use of cytomegalovirus promoter in lentivirus primarily targets glial cells but few neurons. In contrast, with a synapsin promoter fragment the lentivirus expression is neuron specific at high transduction levels in all cortical layers. We also achieve specific targeting of tyrosine hydroxlase (TH)- rich neurons in the locus coeruleus and substantia nigra with a lentvirus carrying a fragment of the TH promoter. Lentiviruses carrying neuron specific promoters are suitable for both cortical and subcortical injections even when injected quickly. JF - Gene Therapy AU - Lerchner, W AU - Corgiat, B AU - Der Minassian, V AU - Saunders, R C AU - Richmond, B J AD - Laboratory of Neuropsychology, National Institute of Mental Health/NIMH/DHHS, Bethesda, MD, USA Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 233 EP - 241 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 21 IS - 3 SN - 0969-7128, 0969-7128 KW - CSA Neurosciences Abstracts; Virology & AIDS Abstracts; Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Synapsin KW - Substantia nigra KW - Serotypes KW - Gene therapy KW - Locus coeruleus KW - Glial cells KW - Brain KW - Tyrosine KW - Cytomegalovirus KW - Primates KW - Adeno-associated virus KW - Promoters KW - Cortex KW - Lentivirus KW - Neurons KW - W 30905:Medical Applications KW - N3 11023:Neurogenetics KW - G 07730:Development & Cell Cycle KW - V 22310:Genetics, Taxonomy & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1508762158?accountid=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=Injection+parameters+and+virus+dependent+choice+of+promoters+to+improve+neuron+targeting+in+the+nonhuman+primate+brain&rft.au=Lerchner%2C+W%3BCorgiat%2C+B%3BDer+Minassian%2C+V%3BSaunders%2C+R+C%3BRichmond%2C+B+J&rft.aulast=Lerchner&rft.aufirst=W&rft.date=2014-03-01&rft.volume=21&rft.issue=3&rft.spage=233&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2013.75 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Last updated - 2014-07-10 N1 - SubjectsTermNotLitGenreText - Synapsin; Substantia nigra; Promoters; Cortex; Serotypes; Gene therapy; Locus coeruleus; Glial cells; Neurons; Brain; Tyrosine; Lentivirus; Primates; Cytomegalovirus; Adeno-associated virus DO - http://dx.doi.org/10.1038/gt.2013.75 ER - TY - JOUR T1 - Segmentation of PET Images for Computer-Aided Functional Quantification of Tuberculosis in Small Animal Models AN - 1508757671; 19399848 AB - Pulmonary infections often cause spatially diffuse and multi-focal radiotracer uptake in positron emission tomography (PET) images, which makes accurate quantification of the disease extent challenging. Image segmentation plays a vital role in quantifying uptake due to the distributed nature of immuno-pathology and associated metabolic activities in pulmonary infection, specifically tuberculosis (TB). For this task, thresholding-based segmentation methods may be better suited over other methods; however, performance of the thresholding-based methods depend on the selection of thresholding parameters, which are often suboptimal. Several optimal thresholding techniques have been proposed in the literature, but there is currently no consensus on how to determine the optimal threshold for precise identification of spatially diffuse and multi-focal radiotracer uptake. In this study, we propose a method to select optimal thresholding levels by utilizing a novel intensity affinity metric within the affinity propagation clustering framework. We tested the proposed method against 70 longitudinal PET images of rabbits infected with TB. The overall dice similarity coefficient between the segmentation from the proposed method and two expert segmentations was found to be syntax error at token \\ with a sensitivity of syntax error at token \\ and a specificity of syntax error at token \\ . High accuracy and heightened efficiency of our proposed method, as compared to other PET image segmentation methods, were reported with various quantification metrics. JF - IEEE Transactions on Biomedical Engineering AU - Foster, Brent AU - Bagci, Ulas AU - Xu, Ziyue AU - Dey, Bappaditya AU - Luna, Brian AU - Bishai, William AU - Jain, Sanjay AU - Mollura, Daniel J AD - Center for Infectious Disease Imaging (CIDI), Department of Radiology and Imaging Sciences, National Institutes of Health, Bethesda, USA Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 711 EP - 724 PB - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States VL - 61 IS - 3 SN - 0018-9294, 0018-9294 KW - Microbiology Abstracts B: Bacteriology; Biotechnology and Bioengineering Abstracts KW - Mycobacterium KW - Lung KW - Segmentation KW - Positron emission tomography KW - Animal models KW - Image processing KW - Tuberculosis KW - Infection KW - J 02410:Animal Diseases KW - W 30905:Medical Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1508757671?accountid=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=IEEE+Transactions+on+Biomedical+Engineering&rft.atitle=Segmentation+of+PET+Images+for+Computer-Aided+Functional+Quantification+of+Tuberculosis+in+Small+Animal+Models&rft.au=Foster%2C+Brent%3BBagci%2C+Ulas%3BXu%2C+Ziyue%3BDey%2C+Bappaditya%3BLuna%2C+Brian%3BBishai%2C+William%3BJain%2C+Sanjay%3BMollura%2C+Daniel+J&rft.aulast=Foster&rft.aufirst=Brent&rft.date=2014-03-01&rft.volume=61&rft.issue=3&rft.spage=711&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Biomedical+Engineering&rft.issn=00189294&rft_id=info:doi/10.1109%2FTBME.2013.2288258 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Lung; Animal models; Positron emission tomography; Segmentation; Image processing; Tuberculosis; Infection; Mycobacterium DO - http://dx.doi.org/10.1109/TBME.2013.2288258 ER - TY - JOUR T1 - Global fold of human cannabinoid type 2 receptor probed by solid-state super(13)C-, super(15)N-MAS NMR and molecular dynamics simulations AN - 1505345092; 19318207 AB - The global fold of human cannabinoid type 2 (CB sub(2)) receptor in the agonist-bound active state in lipid bilayers was investigated by solid-state super(13)C- and super(15)N magic-angle spinning (MAS) NMR, in combination with chemical-shift prediction from a structural model of the receptor obtained by microsecond-long molecular dynamics (MD) simulations. Uniformly super(13)C- and super(15)N-labeled CB sub(2) receptor was expressed in milligram quantities by bacterial fermentation, purified, and functionally reconstituted into liposomes. super(13)C MAS NMR spectra were recorded without sensitivity enhancement for direct comparison of C sub([alpha]), C sub([beta]), and C==O bands of superimposed resonances with predictions from protein structures generated by MD. The experimental NMR spectra matched the calculated spectra reasonably well indicating agreement of the global fold of the protein between experiment and simulations. In particular, the super(13)C chemical shift distribution of C sub([alpha]) resonances was shown to be very sensitive to both the primary amino acid sequence and the secondary structure of CB sub(2). Thus the shape of the C sub([alpha]) band can be used as an indicator of CB sub(2) global fold. The prediction from MD simulations indicated that upon receptor activation a rather limited number of amino acid residues, mainly located in the extracellular Loop 2 and the second half of intracellular Loop 3, change their chemical shifts significantly ( greater than or equal to 1.5 ppm for carbons and greater than or equal to 5.0 ppm for nitrogens). Simulated two-dimensional super(13)C sub([alpha])(i)-- super(13)C[double horizonal line]O(i) and super(13)C[double horizonal line]O(i)-- super(15)NH(i + 1) dipolar-interaction correlation spectra provide guidance for selective amino acid labeling and signal assignment schemes to study the molecular mechanism of activation of CB sub(2) by solid-state MAS NMR. Proteins 2014; 82:452-465. copyright 2013 Wiley Periodicals, Inc. JF - Proteins: Structure, Function and Bioinformatics AU - Kimura, Tomohiro AU - Vukoti, Krishna AU - Lynch, Diane L AU - Hurst, Dow P AU - Grossfield, Alan AU - Pitman, Michael C AU - Reggio, Patricia H AU - Yeliseev, Alexei A AU - Gawrisch, Klaus AD - Laboratory of Membrane Biochemistry and Biophysics, NIAAA, NIH, Bethesda, Maryland, 20892. Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 452 EP - 465 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States VL - 82 IS - 3 SN - 0887-3585, 0887-3585 KW - Biotechnology and Bioengineering Abstracts KW - cannabinoid receptor KW - CB sub(2) KW - GPCR KW - G protein-coupled receptor KW - solid-state NMR KW - molecular dynamics simulation KW - Molecular modelling KW - Lipid bilayers KW - Receptor mechanisms KW - Fermentation KW - Secondary structure KW - Liposomes KW - Spinning KW - Protein structure KW - Carbon KW - Cannabinoid CB2 receptors KW - N.M.R. KW - Bioinformatics KW - Amino acid sequence KW - Nitrogen KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1505345092?accountid=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=Global+fold+of+human+cannabinoid+type+2+receptor+probed+by+solid-state+super%2813%29C-%2C+super%2815%29N-MAS+NMR+and+molecular+dynamics+simulations&rft.au=Kimura%2C+Tomohiro%3BVukoti%2C+Krishna%3BLynch%2C+Diane+L%3BHurst%2C+Dow+P%3BGrossfield%2C+Alan%3BPitman%2C+Michael+C%3BReggio%2C+Patricia+H%3BYeliseev%2C+Alexei+A%3BGawrisch%2C+Klaus&rft.aulast=Kimura&rft.aufirst=Tomohiro&rft.date=2014-03-01&rft.volume=82&rft.issue=3&rft.spage=452&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24411 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Last updated - 2016-06-22 N1 - SubjectsTermNotLitGenreText - Molecular modelling; Lipid bilayers; Receptor mechanisms; Fermentation; Secondary structure; Liposomes; Spinning; Protein structure; Carbon; Cannabinoid CB2 receptors; N.M.R.; Bioinformatics; Nitrogen; Amino acid sequence DO - http://dx.doi.org/10.1002/prot.24411 ER - TY - JOUR T1 - Dynamic and inherent B sub(0) correction for DTI using stimulated echo spiral imaging AN - 1505339627; 19338247 AB - Purpose To present a novel technique for high-resolution stimulated echo diffusion tensor imaging with self-navigated interleaved spirals readout trajectories that can inherently and dynamically correct for image artifacts due to spatial and temporal variations in the static magnetic field (B sub(0)) resulting from eddy currents, tissue susceptibilities, subject/physiological motion, and hardware instabilities. Methods The Hahn spin echo formed by the first two 90 degree radiofrequency pulses is balanced to consecutively acquire two additional images with different echo times and generate an inherent field map, while the diffusion-prepared stimulated echo signal remains unaffected. For every diffusion-encoding direction, an intrinsically registered field map is estimated dynamically and used to effectively and inherently correct for off-resonance artifacts in the reconstruction of the corresponding diffusion-weighted image. Results After correction with the dynamically acquired field maps, local blurring artifacts are specifically removed from individual stimulated echo diffusion-weighted images and the estimated diffusion tensors have significantly improved spatial accuracy and larger fractional anisotropy. Conclusion Combined with the self-navigated interleaved spirals acquisition scheme, our new method provides an integrated high-resolution short-echo time diffusion tensor imaging solution with inherent and dynamic correction for both motion-induced phase errors and off-resonance effects. Magn Reson Med 71:1044-1053, 2014. copyright 2013 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Avram, Alexandru V AU - Guidon, Arnaud AU - Truong, Trong-Kha AU - Liu, Chunlei AU - Song, Allen W AD - Section on Tissue Biophysics and Biomimetics, NICHD, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 1044 EP - 1053 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 71 IS - 3 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Anisotropy KW - Magnetic resonance imaging KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1505339627?accountid=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=Dynamic+and+inherent+B+sub%280%29+correction+for+DTI+using+stimulated+echo+spiral+imaging&rft.au=Avram%2C+Alexandru+V%3BGuidon%2C+Arnaud%3BTruong%2C+Trong-Kha%3BLiu%2C+Chunlei%3BSong%2C+Allen+W&rft.aulast=Avram&rft.aufirst=Alexandru&rft.date=2014-03-01&rft.volume=71&rft.issue=3&rft.spage=1044&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.24767 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Last updated - 2014-04-03 N1 - SubjectsTermNotLitGenreText - Magnetic resonance imaging DO - http://dx.doi.org/10.1002/mrm.24767 ER - TY - JOUR T1 - The Association between Parity and Birthweight in a Longitudinal Consecutive Pregnancy Cohort AN - 1505338677; 19285518 AB - Nulliparity is associated with lower birthweight, but few studies have examined how within-mother changes in risk factors impact this association. We used longitudinal electronic medical record data from a hospital-based cohort of consecutive singleton live births from 2002-2010 in Utah. To reduce bias from unobserved pregnancies, primary analyses were limited to 9484 women who entered nulliparous from 2002-2004, with 23 380 pregnancies up to parity 3. Unrestricted secondary analyses used 101 225 pregnancies from 45 212 women with pregnancies up to parity 7. We calculated gestational age and sex-specific birthweight z-scores with nulliparas as the reference. Using linear mixed models, we estimated birthweight z-score by parity adjusting for pregnancy-specific sociodemographics, smoking, alcohol, prepregnancy body mass index, gestational weight gain, and medical conditions. Compared with nulliparas', infants of primiparas were larger by 0.20 unadjusted z-score units [95% confidence interval (CI) 0.18, 0.22]; the adjusted increase was similar at 0.18 z-score units [95% CI 0.15, 0.20]. Birthweight continued to increase up to parity 3, but with a smaller difference (parity 3 vs. 0 beta = 0.27 [95% CI 0.20, 0.34]). In the unrestricted secondary sample, there was significant departure in linearity from parity 1 to 7 (P < 0.001); birthweight increased only up to parity 4 (parity 4 vs. 0 beta = 0.34 [95% CI 0.31, 0.37]). The association between parity and birthweight was non-linear with the greatest increase observed between first- and second-born infants of the same mother. Adjustment for changes in weight or chronic diseases did not change the relationship between parity and birthweight. JF - Paediatric and Perinatal Epidemiology AU - Hinkle, Stefanie N AU - Albert, Paul S AU - Mendola, Pauline AU - Sjaarda, Lindsey A AU - Yeung, Edwina AU - Boghossian, Nansi S AU - Laughon, SKatherine AD - Epidemiology Branch Division of Intramural Population Health Research Eunice Kennedy Shriver National Institute of Child Health and Human Development. National Institutes of Health Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 106 EP - 115 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 28 IS - 2 SN - 0269-5022, 0269-5022 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Age KW - USA, Utah KW - Parity 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/1505338677?accountid=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=Paediatric+and+Perinatal+Epidemiology&rft.atitle=The+Association+between+Parity+and+Birthweight+in+a+Longitudinal+Consecutive+Pregnancy+Cohort&rft.au=Hinkle%2C+Stefanie+N%3BAlbert%2C+Paul+S%3BMendola%2C+Pauline%3BSjaarda%2C+Lindsey+A%3BYeung%2C+Edwina%3BBoghossian%2C+Nansi+S%3BLaughon%2C+SKatherine&rft.aulast=Hinkle&rft.aufirst=Stefanie&rft.date=2014-03-01&rft.volume=28&rft.issue=2&rft.spage=106&rft.isbn=&rft.btitle=&rft.title=Paediatric+and+Perinatal+Epidemiology&rft.issn=02695022&rft_id=info:doi/10.1111%2Fppe.12099 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Last updated - 2014-03-20 N1 - SubjectsTermNotLitGenreText - Parity; USA, Utah DO - http://dx.doi.org/10.1111/ppe.12099 ER - TY - JOUR T1 - Using Weighted Entropy to Rank Chemicals in Quantitative High-Throughput Screening Experiments AN - 1505336144; 19295923 AB - Quantitative high-throughput screening (qHTS) experiments can simultaneously produce concentration-response profiles for thousands of chemicals. In a typical qHTS study, a large chemical library is subjected to a primary screen to identify candidate hits for secondary screening, validation studies, or prediction modeling. Different algorithms, usually based on the Hill equation logistic model, have been used to classify compounds as active or inactive (or inconclusive). However, observed concentration-response activity relationships may not adequately fit a sigmoidal curve. Furthermore, it is unclear how to prioritize chemicals for follow-up studies given the large uncertainties that often accompany parameter estimates from nonlinear models. Weighted Shannon entropy can address these concerns by ranking compounds according to profile-specific statistics derived from estimates of the probability mass distribution of response at the tested concentration levels. This strategy can be used to rank all tested chemicals in the absence of a prespecified model structure, or the approach can complement existing activity call algorithms by ranking the returned candidate hits. The weighted entropy approach was evaluated here using data simulated from the Hill equation model. The procedure was then applied to a chemical genomics profiling data set interrogating compounds for androgen receptor agonist activity. JF - Journal of Biomolecular Screening AU - Shockley, Keith R AD - The National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 344 EP - 353 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 19 IS - 3 SN - 1087-0571, 1087-0571 KW - Biotechnology and Bioengineering Abstracts KW - Algorithms KW - Entropy KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1505336144?accountid=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=Using+Weighted+Entropy+to+Rank+Chemicals+in+Quantitative+High-Throughput+Screening+Experiments&rft.au=Shockley%2C+Keith+R&rft.aulast=Shockley&rft.aufirst=Keith&rft.date=2014-03-01&rft.volume=19&rft.issue=3&rft.spage=344&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Screening&rft.issn=10870571&rft_id=info:doi/10.1177%2F1087057113505325 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Number of references - 1 N1 - Last updated - 2014-03-20 N1 - SubjectsTermNotLitGenreText - Entropy DO - http://dx.doi.org/10.1177/1087057113505325 ER - TY - JOUR T1 - No evidence for synergy between human papillomavirus genotypes for the risk of high-grade squamous intraepithelial lesions in a large population-based study. AN - 1503542489; 24179110 AB - Multiple human papillomavirus (HPV) genotypes may be independently or synergistically associated with risk of high-grade squamous intraepithelial lesions (HSILs). We evaluated the risk of HSIL in women concomitantly infected with multiple HPV genotypes. A population-based stratified sample of 59 664 cervical cytology specimens from women residing in New Mexico were evaluated for cytologic abnormalities and HPV genotypes. We calculated the risk of HSIL in women infected with a single HPV genotype and the risk in those infected with multiple HPV genotypes. The highest risk of HSIL was observed for HPV-16 (0.036), followed by HPV-33 (0.028), HPV-58 (0.024), and HPV-18 (0.022). For most types, we observed a greater risk of HSIL in women infected with multiple carcinogenic HPV types. In contrast, the risk of HSIL was similar in women infected with HPV-16 and other types, compared with women infected with HPV-16 only. We observed an increased but plateauing risk of HSIL in women infected with multiple types, compared with those infected with a single type, with risk ratios of 1.5 (95% confidence interval [CI], 1.2-1.8), 1.7 (95% CI, 1.3-2.4), and 1.4 (95% CI, 0.83-2.5) for women infected with 2, 3, and ≥4 genotypes, respectively. In the largest population-based study of HPV genotypes and cytologic outcomes so far, we did not see more than additive effects of HPV types on the risk of HSIL in women infected with multiple types. JF - The Journal of infectious diseases AU - Wentzensen, Nicolas AU - Nason, Martha AU - Schiffman, Mark AU - Dodd, Lori AU - Hunt, William C AU - Wheeler, Cosette M AU - New Mexico HPV Pap Registry Steering Committee AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute. ; New Mexico HPV Pap Registry Steering Committee Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 855 EP - 864 VL - 209 IS - 6 KW - Abridged Index Medicus KW - Index Medicus KW - human papillomavirus (HPV) KW - cytology KW - cervical cancer screening KW - multiple Infections KW - New Mexico -- epidemiology KW - Cross-Sectional Studies KW - Logistic Models KW - Humans KW - Adult KW - Early Detection of Cancer KW - Coinfection -- virology KW - Cervix Uteri -- virology KW - Coinfection -- epidemiology KW - Female KW - Papillomavirus Infections -- epidemiology KW - Uterine Cervical Neoplasms -- epidemiology KW - Papillomaviridae -- isolation & purification KW - Papillomavirus Infections -- virology KW - Cervical Intraepithelial Neoplasia -- virology KW - Papillomaviridae -- genetics KW - Uterine Cervical Neoplasms -- virology KW - Cervical Intraepithelial Neoplasia -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1503542489?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=No+evidence+for+synergy+between+human+papillomavirus+genotypes+for+the+risk+of+high-grade+squamous+intraepithelial+lesions+in+a+large+population-based+study.&rft.au=Wentzensen%2C+Nicolas%3BNason%2C+Martha%3BSchiffman%2C+Mark%3BDodd%2C+Lori%3BHunt%2C+William+C%3BWheeler%2C+Cosette+M%3BNew+Mexico+HPV+Pap+Registry+Steering+Committee&rft.aulast=Wentzensen&rft.aufirst=Nicolas&rft.date=2014-03-01&rft.volume=209&rft.issue=6&rft.spage=855&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjit577 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-24 N1 - Date created - 2014-02-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 2011 Sep 21;103(18):1387-96 [21900119] Cancer Epidemiol Biomarkers Prev. 2011 Jul;20(7):1398-409 [21602310] Int J Cancer. 2012 Sep 15;131(6):E946-53 [22419273] Int J Cancer. 2013 Jan 1;132(1):198-207 [22532127] Obstet Gynecol. 1998 Jun;91(6):973-6 [9611007] Vaccine. 2006 Mar 30;24 Suppl 1:S1-15 [16406226] Cancer Epidemiol Biomarkers Prev. 2006 Jul;15(7):1274-80 [16835323] Cancer Res. 2006 Oct 15;66(20):10112-9 [17047075] Cancer Res. 2006 Nov 1;66(21):10630-6 [17062559] Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):863-5 [19273486] J Natl Cancer Inst. 2009 Apr 1;101(7):475-87 [19318628] Int J Cancer. 2009 Nov 1;125(9):2151-8 [19585494] Cancer Res. 2010 Nov 1;70(21):8578-86 [20959485] Int J Cancer. 2011 Feb 15;128(4):927-35 [20473886] J Natl Cancer Inst. 2011 Mar 2;103(5):368-83 [21282563] J Infect Dis. 2011 Apr 1;203(7):910-20 [21402543] J Pathol. 2012 May;227(1):62-71 [22127961] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/infdis/jit577 ER - TY - JOUR T1 - Opposing effects of prednisolone treatment on T/NKT cell- and hepatotoxin-mediated hepatitis in mice. AN - 1503541712; 24115096 AB - Prednisolone is a corticosteroid that has been used to treat inflammatory liver diseases such as autoimmune hepatitis and alcoholic hepatitis. However, the results have been controversial, and how prednisolone affects liver disease progression remains unknown. In the current study we examined the effect of prednisolone treatment on several models of liver injury, including T/NKT cell hepatitis induced by concanavalin A (ConA) and α-galactosylceramide (α-GalCer), and hepatotoxin-mediated hepatitis induced by carbon tetrachloride (CCl4 ) and/or ethanol. Prednisolone administration attenuated ConA- and α-GalCer-induced hepatitis and systemic inflammatory responses. Treating mice with prednisolone also suppressed inflammatory responses in a model of hepatotoxin (CCl4 )-induced hepatitis, but surprisingly exacerbated liver injury and delayed liver repair. In addition, administration of prednisolone also enhanced acetaminophen-, ethanol-, or ethanol plus CCl4 -induced liver injury. Immunohistochemical and flow cytometric analyses demonstrated that prednisolone treatment inhibited hepatic macrophage and neutrophil infiltration in CCl4 -induced hepatitis and suppressed their phagocytic activities in vivo and in vitro. Macrophage and/or neutrophil depletion aggravated CCl4 -induced liver injury and impeded liver regeneration. Finally, conditional disruption of glucocorticoid receptor in macrophages and neutrophils abolished prednisolone-mediated exacerbation of hepatotoxin-induced liver injury. Prednisolone treatment prevents T/NKT cell hepatitis but exacerbates hepatotoxin-induced liver injury by inhibiting macrophage- and neutrophil-mediated phagocytic and hepatic regenerative functions. These findings may not only increase our understanding of the steroid treatment mechanism but also help us to better manage steroid therapy in liver diseases. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - Hepatology (Baltimore, Md.) AU - Kwon, Hyo-Jung AU - Won, Young-Suk AU - Park, Ogyi AU - Feng, Dechun AU - Gao, Bin AD - Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA; College of Veterinary Medicine, Chungnam National University, Yuseong-gu, Daejeon, South Korea. Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 1094 EP - 1106 VL - 59 IS - 3 KW - Galactosylceramides KW - 0 KW - Glucocorticoids KW - Mitogens KW - alpha-galactosylceramide KW - Concanavalin A KW - 11028-71-0 KW - Prednisolone KW - 9PHQ9Y1OLM KW - Carbon Tetrachloride KW - CL2T97X0V0 KW - Index Medicus KW - Animals KW - Liver Regeneration -- drug effects KW - Neutrophils -- pathology KW - Concanavalin A -- toxicity KW - Macrophages -- immunology KW - Neutrophils -- immunology KW - Galactosylceramides -- toxicity KW - Mitogens -- toxicity KW - Disease Models, Animal KW - Mice KW - Liver Regeneration -- immunology KW - Macrophages -- drug effects KW - Carbon Tetrachloride -- toxicity KW - Glucocorticoids -- pharmacology KW - Mice, Knockout KW - Neutrophils -- drug effects KW - Macrophages -- pathology KW - Mice, Inbred C57BL KW - Male KW - Chemical and Drug Induced Liver Injury -- pathology KW - Prednisolone -- pharmacology KW - T-Lymphocytes -- drug effects KW - Killer Cells, Natural -- pathology KW - T-Lymphocytes -- pathology KW - Chemical and Drug Induced Liver Injury -- drug therapy KW - T-Lymphocytes -- immunology KW - Killer Cells, Natural -- immunology KW - Killer Cells, Natural -- drug effects KW - Chemical and Drug Induced Liver Injury -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1503541712?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Opposing+effects+of+prednisolone+treatment+on+T%2FNKT+cell-+and+hepatotoxin-mediated+hepatitis+in+mice.&rft.au=Kwon%2C+Hyo-Jung%3BWon%2C+Young-Suk%3BPark%2C+Ogyi%3BFeng%2C+Dechun%3BGao%2C+Bin&rft.aulast=Kwon&rft.aufirst=Hyo-Jung&rft.date=2014-03-01&rft.volume=59&rft.issue=3&rft.spage=1094&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.26748 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-28 N1 - Date created - 2014-02-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hepatology. 2012 Aug;56(2):668-76 [22334246] Liver Int. 2006 Oct;26(8):912-9 [16953830] J Hepatol. 2012 Sep;57(3):642-54 [22634126] Expert Rev Gastroenterol Hepatol. 2012 Sep;6(5):603-15 [23061711] Gastroenterology. 2012 Nov;143(5):1158-72 [22982943] Nat Protoc. 2013 Mar;8(3):627-37 [23449255] Hepatology. 2013 Jul;58(1):314-24 [23424168] Hepatology. 2013 Aug;58(2):718-28 [23475565] J Hepatol. 2013 Sep;59(3):583-94 [23567086] Hepatology. 2013 Nov;58(5):1814-23 [23532958] Gastroenterol Clin North Am. 2011 Sep;40(3):611-39 [21893277] Alcohol. 2002 May;27(1):23-7 [12062633] Alcohol. 2002 May;27(1):43-6 [12062636] Z Gastroenterol. 2007 Jan;45(1):63-70 [17236122] Crit Rev Immunol. 2006;26(5):453-73 [17341188] Blood. 2007 May 15;109(10):4313-9 [17255352] Clin Liver Dis. 2007 Aug;11(3):525-48, vi [17723918] J Cell Physiol. 2007 Nov;213(2):286-300 [17559071] Toxicol Pathol. 2007 Oct;35(6):757-66 [17943649] Gastroenterology. 2008 Jan;134(1):248-58 [18166357] Hepatology. 2009 Feb;49(2):676-88 [19177577] N Engl J Med. 2009 Jun 25;360(26):2758-69 [19553649] Gastroenterology. 2009 Aug;137(2):541-8 [19445945] Am J Pathol. 2010 Jan;176(1):2-13 [20019184] World J Gastroenterol. 2010 Apr 21;16(15):1811-9 [20397256] J Hepatol. 2010 Aug;53(2):390-1 [20466448] Gastroenterology. 2010 Jul;139(1):58-72.e4 [20451521] Hepatology. 2010 Nov;52(5):1836-46 [21038418] Gut. 2011 Feb;60(2):255-60 [20940288] Hepatology. 2011 Apr;53(4):1316-22 [21400552] Trends Immunol. 2011 Oct;32(10):461-9 [21839681] Gastroenterology. 2011 Nov;141(5):1572-85 [21920463] N Engl J Med. 2011 Nov 10;365(19):1781-9 [22070475] Annu Rev Immunol. 2012;30:459-89 [22224774] Hepatology. 2012 Apr;55(4):1282-91 [22234976] Annu Rev Nutr. 2012 Aug 21;32:343-68 [22524187] Toxicology. 2003 Jul 15;189(1-2):113-27 [12821287] Gut. 1979 Dec;20(12):1109-24 [393573] J Clin Invest. 1992 Jul;90(1):196-203 [1634608] J Immunol. 2005 Aug 1;175(3):1540-50 [16034092] N Engl J Med. 2005 Oct 20;353(16):1711-23 [16236742] Hepatology. 2012 Aug;56(2):735-46 [22334567] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/hep.26748 ER - TY - JOUR T1 - Intestinal CYP3A4 protects against lithocholic acid-induced hepatotoxicity in intestine-specific VDR-deficient mice. AN - 1502996715; 24343899 AB - Vitamin D receptor (VDR) mediates vitamin D signaling involved in bone metabolism, cellular growth and differentiation, cardiovascular function, and bile acid regulation. Mice with an intestine-specific disruption of VDR (Vdr(ΔIEpC)) have abnormal body size, colon structure, and imbalance of bile acid metabolism. Lithocholic acid (LCA), a secondary bile acid that activates VDR, is among the most toxic of the bile acids that when overaccumulated in the liver causes hepatotoxicity. Because cytochrome P450 3A4 (CYP3A4) is a target gene of VDR-involved bile acid metabolism, the role of CYP3A4 in VDR biology and bile acid metabolism was investigated. The CYP3A4 gene was inserted into Vdr(ΔIEpC) mice to produce the Vdr(ΔIEpC)/3A4 line. LCA was administered to control, transgenic-CYP3A4, Vdr(ΔIEpC), and Vdr(ΔIEpC)/3A4 mice, and hepatic toxicity and bile acid levels in the liver, intestine, bile, and urine were measured. VDR deficiency in the intestine of the Vdr(ΔIEpC) mice exacerbates LCA-induced hepatotoxicity manifested by increased necrosis and inflammation, due in part to over-accumulation of hepatic bile acids including taurocholic acid and taurodeoxycholic acid. Intestinal expression of CYP3A4 in the Vdr(ΔIEpC)/3A4 mouse line reduces LCA-induced hepatotoxicity through elevation of LCA metabolism and detoxification, and suppression of bile acid transporter expression in the small intestine. This study reveals that intestinal CYP3A4 protects against LCA hepatotoxicity. JF - Journal of lipid research AU - Cheng, Jie AU - Fang, Zhong-Ze AU - Kim, Jung-Hwan AU - Krausz, Kristopher W AU - Tanaka, Naoki AU - Chiang, John Y L AU - Gonzalez, Frank J AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 455 EP - 465 VL - 55 IS - 3 KW - Bile Acids and Salts KW - 0 KW - Receptors, Calcitriol KW - Lithocholic Acid KW - 5QU0I8393U KW - Cholesterol KW - 97C5T2UQ7J KW - Cytochrome P-450 CYP3A KW - EC 1.14.14.1 KW - cytochrome P450 3A4, mouse KW - Index Medicus KW - vitamin D receptor KW - metabolomics KW - bile acids KW - Animals KW - Metabolomics -- methods KW - Liver -- pathology KW - Liver -- metabolism KW - Mice KW - Bile -- metabolism KW - Reverse Transcriptase Polymerase Chain Reaction KW - Mice, Transgenic KW - Bile Acids and Salts -- metabolism KW - Mice, Knockout KW - Cholesterol -- blood KW - Blotting, Western KW - Cholesterol -- metabolism KW - Gallbladder -- metabolism KW - Male KW - Receptors, Calcitriol -- deficiency KW - Chemical and Drug Induced Liver Injury -- etiology KW - Receptors, Calcitriol -- genetics KW - Cytochrome P-450 CYP3A -- metabolism KW - Chemical and Drug Induced Liver Injury -- genetics KW - Intestines -- metabolism KW - Cytochrome P-450 CYP3A -- genetics KW - Cytochrome P-450 CYP3A -- urine KW - Chemical and Drug Induced Liver Injury -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1502996715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+lipid+research&rft.atitle=Intestinal+CYP3A4+protects+against+lithocholic+acid-induced+hepatotoxicity+in+intestine-specific+VDR-deficient+mice.&rft.au=Cheng%2C+Jie%3BFang%2C+Zhong-Ze%3BKim%2C+Jung-Hwan%3BKrausz%2C+Kristopher+W%3BTanaka%2C+Naoki%3BChiang%2C+John+Y+L%3BGonzalez%2C+Frank+J&rft.aulast=Cheng&rft.aufirst=Jie&rft.date=2014-03-01&rft.volume=55&rft.issue=3&rft.spage=455&rft.isbn=&rft.btitle=&rft.title=Journal+of+lipid+research&rft.issn=1539-7262&rft_id=info:doi/10.1194%2Fjlr.M044420 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-28 N1 - Date created - 2014-02-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Chim Acta. 1996 Jul 30;251(2):173-86 [8862472] Annu Rev Nutr. 1995;15:35-55 [8527224] Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9831-5 [9275211] J Endocrinol. 1997 Sep;154 Suppl:S57-73 [9379138] J Biol Chem. 2004 Nov 19;279(47):49517-22 [15358766] Drug Metab Rev. 2004 Oct;36(3-4):703-22 [15554243] J Cell Biochem. 2005 Apr 1;94(5):917-43 [15578590] Endocrinology. 2005 Jul;146(7):2911-9 [15817670] J Biol Chem. 2005 Jun 17;280(24):23232-42 [15824121] Pharm Res. 2007 Oct;24(10):1803-23 [17404808] Curr Opin Clin Nutr Metab Care. 2007 Sep;10(5):632-8 [17693749] Cell. 2006 Aug 25;126(4):789-99 [16923397] Endocr Rev. 2008 Oct;29(6):726-76 [18694980] J Pharmacol Exp Ther. 2009 Feb;328(2):564-70 [18988769] Drug Metab Dispos. 2009 Mar;37(3):469-78 [19106115] Steroids. 2009 Nov;74(12):963-70 [19646460] Mol Endocrinol. 2010 Jun;24(6):1151-64 [20371703] Curr Mol Med. 2010 Aug;10(6):579-95 [20642438] Biopharm Drug Dispos. 2011 Mar;32(2):112-25 [21341280] Toxicol Sci. 2011 Dec;124(2):251-60 [21914718] Annu Rev Pharmacol Toxicol. 2012;52:37-56 [21819238] J Clin Invest. 2012 May;122(5):1803-15 [22523068] Biochim Biophys Acta. 2013 Jan;1830(1):2118-28 [23041070] Am J Physiol Gastrointest Liver Physiol. 2013 Feb 1;304(3):G227-34 [23203158] Science. 2002 May 17;296(5571):1313-6 [12016314] J Clin Invest. 2002 Jul;110(2):229-38 [12122115] Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13801-6 [12370413] Mol Pharmacol. 2004 Mar;65(3):720-9 [14978251] J Clin Invest. 1966 Aug;45(8):1255-67 [5923701] Br J Pharmacol. 1977 Sep;61(1):133P-134P [912184] Histochemistry. 1991;95(4):319-28 [1708749] Nat Genet. 1997 Aug;16(4):391-6 [9241280] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1194/jlr.M044420 ER - TY - JOUR T1 - Phase I trial of a recombinant yeast-CEA vaccine (GI-6207) in adults with metastatic CEA-expressing carcinoma. AN - 1500689076; 24327292 AB - Yeast-CEA (GI-6207) is a therapeutic cancer vaccine genetically modified to express recombinant carcinoembryonic antigen (CEA) protein, using heat-killed yeast (Saccharomyces cerevisiae) as a vector. In preclinical studies, yeast-CEA induced a strong immune response to CEA and antitumor responses. Patients received subcutaneous vaccines every 2 weeks for 3 months and then monthly. Patients were enrolled at 3 sequential dose levels: 4, 16, and 40 yeast units (10(7) yeast particles/unit). Eligible patients were required to have serum CEA > 5 ng/mL or > 20 % CEA(+) tumor block, ECOG PS 0-2, and no history of autoimmunity. Restaging scans were performed at 3 months and then bimonthly. Peripheral blood was collected for the analysis of immune response (e.g., by ELISPOT assay). Twenty-five patients with metastatic CEA-expressing carcinomas were enrolled. Median patient age was 52 (range 39-81). A total of 135 vaccines were administered. The vaccine was well tolerated, and the most common adverse event was grade 1/2 injection-site reaction. Five patients had stable disease beyond 3 months (range 3.5-18 months), and each had CEA stabilization while on-study. Some patients showed evidence post-vaccination of increases in antigen-specific CD8(+) T cells and CD4(+) T lymphocytes and decreases in regulatory T cells. Of note, a patient with medullary thyroid cancer had substantial T cell responses and a vigorous inflammatory reaction at sites of metastatic disease. Yeast-CEA vaccination had minimal toxicity and induced some antigen-specific T cell responses and CEA stabilization in a heterogeneous, heavily pre-treated patient population. Further studies are required to determine the clinical benefit of yeast-CEA vaccination. JF - Cancer immunology, immunotherapy : CII AU - Bilusic, Marijo AU - Heery, Christopher R AU - Arlen, Philip M AU - Rauckhorst, Myrna AU - Apelian, David AU - Tsang, Kwong Y AU - Tucker, Jo A AU - Jochems, Caroline AU - Schlom, Jeffrey AU - Gulley, James L AU - Madan, Ravi A AD - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 225 EP - 234 VL - 63 IS - 3 KW - Cancer Vaccines KW - 0 KW - Carcinoembryonic Antigen KW - Cytokines KW - Vaccines, DNA KW - yeast-CEA vaccine KW - Index Medicus KW - Genetic Engineering KW - Enzyme-Linked Immunospot Assay KW - Humans KW - Aged KW - Cytokines -- metabolism KW - Aged, 80 and over KW - Cells, Cultured KW - Genetic Vectors KW - Adult KW - Treatment Outcome KW - Neoplasm Metastasis KW - Injections, Subcutaneous KW - Middle Aged KW - Follow-Up Studies KW - Male KW - Female KW - Carcinoembryonic Antigen -- immunology KW - Vaccines, DNA -- therapeutic use KW - Cancer Vaccines -- therapeutic use KW - CD4-Positive T-Lymphocytes -- immunology KW - Adenocarcinoma -- immunology KW - Adenocarcinoma -- therapy KW - Carcinoembryonic Antigen -- therapeutic use KW - Colonic Neoplasms -- immunology KW - Saccharomyces cerevisiae -- genetics KW - Colonic Neoplasms -- therapy KW - CD8-Positive T-Lymphocytes -- immunology KW - Carcinoembryonic Antigen -- genetics KW - T-Lymphocytes, Regulatory -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500689076?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+I+trial+of+a+recombinant+yeast-CEA+vaccine+%28GI-6207%29+in+adults+with+metastatic+CEA-expressing+carcinoma.&rft.au=Bilusic%2C+Marijo%3BHeery%2C+Christopher+R%3BArlen%2C+Philip+M%3BRauckhorst%2C+Myrna%3BApelian%2C+David%3BTsang%2C+Kwong+Y%3BTucker%2C+Jo+A%3BJochems%2C+Caroline%3BSchlom%2C+Jeffrey%3BGulley%2C+James+L%3BMadan%2C+Ravi+A&rft.aulast=Bilusic&rft.aufirst=Marijo&rft.date=2014-03-01&rft.volume=63&rft.issue=3&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Cancer+immunology%2C+immunotherapy+%3A+CII&rft.issn=1432-0851&rft_id=info:doi/10.1007%2Fs00262-013-1505-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-29 N1 - Date created - 2014-02-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Curr Cancer Drug Targets. 2007 Feb;7(1):31-40 [17305476] Vaccine. 2007 Feb 9;25(8):1452-63 [17098335] Clin Cancer Res. 2007 Nov 1;13(21):6247-51 [17975134] Ann Pharmacother. 2008 Jan;42(1):91-8 [18094343] Vaccine. 2008 Jan 24;26(4):509-21 [18155327] Clin Cancer Res. 2008 May 15;14(10):3060-9 [18483372] Clin Cancer Res. 2008 Jul 1;14(13):4316-25 [18594015] Vaccine. 2009 Feb 11;27(7):987-94 [19110021] N Engl J Med. 2010 Aug 19;363(8):711-23 [20525992] N Engl J Med. 2010 Jul 29;363(5):411-22 [20818862] N Engl J Med. 2010 Jul 29;363(5):479-81 [20818868] Anticancer Res. 2010 Dec;30(12):5091-7 [21187495] Cancer Immunol Immunother. 2011 Feb;60(2):197-206 [20976449] Immunol Lett. 2011 Mar 30;135(1-2):124-8 [21073899] PLoS One. 2011;6(6):e21146 [21731662] Clin Cancer Res. 2011 Nov 15;17(22):7164-73 [22068656] Semin Oncol. 2012 Jun;39(3):296-304 [22595052] Gastroenterology. 2012 Jul;143(1):155-65.e8 [22465431] Int J Cancer. 2012 Dec 15;131(12):2839-51 [22495743] Cancer Res. 1999 Nov 15;59(22):5800-7 [10582702] J Biol Chem. 2000 Sep 1;275(35):26935-43 [10864933] Nat Med. 2001 May;7(5):625-9 [11329066] Clin Cancer Res. 2001 May;7(5):1181-91 [11350882] Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8809-14 [11427731] J Immunol Methods. 2002 Jan 1;259(1-2):95-110 [11730845] Curr Opin Mol Ther. 2002 Feb;4(1):35-40 [11883693] Cancer Res. 2002 Sep 1;62(17):5049-57 [12208760] J Clin Immunol. 2004 Sep;24(5):571-8 [15359116] Proc Natl Acad Sci U S A. 1989 Sep;86(18):7159-63 [2674949] Jpn J Cancer Res. 1990 Sep;81(9):884-9 [2121689] J Clin Lab Anal. 1991;5(5):344-66 [1941355] Int J Cancer. 1993 Apr 1;53(6):892-7 [8386136] J Natl Cancer Inst. 1995 Jul 5;87(13):982-90 [7629885] Int J Cancer. 1997 Sep 17;72(6):949-54 [9378556] J Clin Oncol. 2005 Feb 1;23(4):720-31 [15613691] Clin Cancer Res. 2005 Mar 15;11(6):2416-26 [15788693] Clin Cancer Res. 2005 May 1;11(9):3353-62 [15867235] Expert Opin Biol Ther. 2005 Apr;5(4):565-75 [15934834] Cancer Invest. 2005;23(4):338-51 [16100946] Clin Cancer Res. 2006 Feb 15;12(4):1260-9 [16489082] Breast Cancer Res. 2006;8(4):R37 [16846534] Clin Cancer Res. 2007 Apr 15;13(8):2471-8 [17438107] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00262-013-1505-8 ER - TY - JOUR T1 - SALL4 expression in germ cell and non-germ cell tumors: a systematic immunohistochemical study of 3215 cases. AN - 1499157317; 24525512 AB - The SALL4 transcription factor is associated with embryonic cell pluripotency and has been shown as a useful immunohistochemical marker for germ cell tumors. However, information of SALL4 distribution in normal human tissues and non-germ cell tumors is limited. In this study we examined normal human tissues and 3215 tumors for SALL4 expression using a monoclonal antibody 6E3 and automated immunohistochemistry. In a 10-week embryo, SALL4 was expressed in ovocytes, intestine, kidney, and some hepatocytes. In adult tissues, it was only detected in germ cells. SALL4 was consistently expressed in all germ cell tumors except some trophoblastic tumors and mature components of teratomas, in which it was selectively expressed in intestinal-like and some squamous epithelia. In non-germ cell carcinomas, SALL4 was detected in 20% of cases or more of serous carcinoma of the ovary, urothelial high-grade carcinoma, and gastric adenocarcinoma (especially the intestinal type). SALL4 was only rarely (≤ 5%) expressed in mammary, colorectal, prostatic, and squamous cell carcinomas. Many SALL4-positive carcinomas showed poorly differentiated patterns, and some showed positivity in most tumor cells mimicking the expression in germ cell tumors. SALL4 was commonly expressed in rhabdoid tumors of the kidney and extrarenal sites and in the Wilms tumor. Expression of SALL4 was rare in other mesenchymal and neuroendocrine tumors but was occasionally detected in melanoma, desmoplastic small round cell tumor, epithelioid sarcoma, and rhabdomyosarcoma. All hematopoietic tumors were negative. SALL4 is an excellent marker of nonteratomatous germ cell tumors, but it is also expressed in other tumors, sometimes extensively. Such expression may reflect stem cell-like differentiation and must be considered when using SALL4 as a marker for germ cell tumors. Observed lack of other pluripotency factors, OCT4 and NANOG, in SALL4-positive non-germ cell tumors can also be diagnostically helpful. JF - The American journal of surgical pathology AU - Miettinen, Markku AU - Wang, Zengfeng AU - McCue, Peter A AU - Sarlomo-Rikala, Maarit AU - Rys, Janusz AU - Biernat, Wojciech AU - Lasota, Jerzy AU - Lee, Yi-Shan AD - *Laboratory of Pathology, National Cancer Institute, Bethesda, MD †Department of Pathology, Cell Biology and Anatomy, Jefferson Medical College of Thomas Jefferson University and University Hospital, Philadelphia, PA ‡Department of Pathology/Haartman Institute and HusLab, Helsinki University Hospital, Helsinki, Finland §Department of Tumor Pathology, Centre of Oncology, Maria Sklodowska-Curie Memorial Institute, Krakow ∥Department of Pathomorphology, Medical University of Gdansk, Gdansk, Poland. Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 410 EP - 420 VL - 38 IS - 3 KW - Biomarkers, Tumor KW - 0 KW - SALL4 protein, human KW - Transcription Factors KW - Index Medicus KW - Humans KW - Adult KW - Neoplasm Grading KW - Cell Differentiation KW - Predictive Value of Tests KW - Biopsy KW - Male KW - Female KW - Carcinoma -- pathology KW - Carcinoma -- chemistry KW - Neoplasms, Germ Cell and Embryonal -- chemistry KW - Biomarkers, Tumor -- analysis KW - Transcription Factors -- analysis KW - Neoplasms, Germ Cell and Embryonal -- pathology KW - Immunohistochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499157317?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+surgical+pathology&rft.atitle=SALL4+expression+in+germ+cell+and+non-germ+cell+tumors%3A+a+systematic+immunohistochemical+study+of+3215+cases.&rft.au=Miettinen%2C+Markku%3BWang%2C+Zengfeng%3BMcCue%2C+Peter+A%3BSarlomo-Rikala%2C+Maarit%3BRys%2C+Janusz%3BBiernat%2C+Wojciech%3BLasota%2C+Jerzy%3BLee%2C+Yi-Shan&rft.aulast=Miettinen&rft.aufirst=Markku&rft.date=2014-03-01&rft.volume=38&rft.issue=3&rft.spage=410&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+surgical+pathology&rft.issn=1532-0979&rft_id=info:doi/10.1097%2FPAS.0000000000000116 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-10 N1 - Date created - 2014-02-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mod Pathol. 2006 Dec;19(12):1585-92 [16998462] Blood. 2006 Oct 15;108(8):2726-35 [16763212] Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16438-43 [17940043] Am J Surg Pathol. 2008 Apr;32(4):600-7 [18277882] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19756-61 [19060217] Am J Surg Pathol. 2009 Jun;33(6):894-904 [19295406] Mod Pathol. 2009 Jun;22(6):824-32 [19329941] Cancer. 2009 Jun 15;115(12):2640-51 [19365862] Am J Surg Pathol. 2009 Jul;33(7):1065-77 [19390421] Am J Surg Pathol. 2009 Oct;33(10):1529-39 [19574883] Am J Surg Pathol. 2010 Apr;34(4):533-40 [20182341] Am J Surg Pathol. 2010 May;34(5):697-706 [20410807] Int J Oncol. 2011 Apr;38(4):933-9 [21274508] Oncol Rep. 2011 Oct;26(4):965-70 [21725617] Pathol Oncol Res. 2011 Sep;17(3):639-44 [21258884] Am J Surg Pathol. 2011 Oct;35(10):1463-72 [21921784] Pediatr Dev Pathol. 2011 Sep-Oct;14(5):353-9 [21417895] Appl Immunohistochem Mol Morphol. 2012 Jul;20(4):410-2 [22495380] Hum Pathol. 2012 Nov;43(11):1955-63 [22516245] J Biomed Sci. 2013;20:6 [23363002] Cancer Res. 2013 Jun 15;73(12):3489-93 [23740771] Hum Pathol. 2013 Jul;44(7):1293-9 [23347651] Cytogenet Genome Res. 2002;98(4):274-7 [12826753] J Med Genet. 2003 Jul;40(7):473-8 [12843316] J Biol Chem. 2006 Aug 25;281(34):24090-4 [16840789] Nat Cell Biol. 2006 Oct;8(10):1114-23 [16980957] Genesis. 2007 Jan;45(1):51-8 [17216607] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/PAS.0000000000000116 ER - TY - JOUR T1 - Genome-wide association study identifies multiple loci associated with bladder cancer risk. AN - 1499133164; 24163127 AB - Candidate gene and genome-wide association studies (GWAS) have identified 11 independent susceptibility loci associated with bladder cancer risk. To discover additional risk variants, we conducted a new GWAS of 2422 bladder cancer cases and 5751 controls, followed by a meta-analysis with two independently published bladder cancer GWAS, resulting in a combined analysis of 6911 cases and 11 814 controls of European descent. TaqMan genotyping of 13 promising single nucleotide polymorphisms with P < 1 × 10(-5) was pursued in a follow-up set of 801 cases and 1307 controls. Two new loci achieved genome-wide statistical significance: rs10936599 on 3q26.2 (P = 4.53 × 10(-9)) and rs907611 on 11p15.5 (P = 4.11 × 10(-8)). Two notable loci were also identified that approached genome-wide statistical significance: rs6104690 on 20p12.2 (P = 7.13 × 10(-7)) and rs4510656 on 6p22.3 (P = 6.98 × 10(-7)); these require further studies for confirmation. In conclusion, our study has identified new susceptibility alleles for bladder cancer risk that require fine-mapping and laboratory investigation, which could further understanding into the biological underpinnings of bladder carcinogenesis. JF - Human molecular genetics AU - Figueroa, Jonine D AU - Ye, Yuanqing AU - Siddiq, Afshan AU - Garcia-Closas, Montserrat AU - Chatterjee, Nilanjan AU - Prokunina-Olsson, Ludmila AU - Cortessis, Victoria K AU - Kooperberg, Charles AU - Cussenot, Olivier AU - Benhamou, Simone AU - Prescott, Jennifer AU - Porru, Stefano AU - Dinney, Colin P AU - Malats, Núria AU - Baris, Dalsu AU - Purdue, Mark AU - Jacobs, Eric J AU - Albanes, Demetrius AU - Wang, Zhaoming AU - Deng, Xiang AU - Chung, Charles C AU - Tang, Wei AU - Bas Bueno-de-Mesquita, H AU - Trichopoulos, Dimitrios AU - Ljungberg, Börje AU - Clavel-Chapelon, Françoise AU - Weiderpass, Elisabete AU - Krogh, Vittorio AU - Dorronsoro, Miren AU - Travis, Ruth AU - Tjønneland, Anne AU - Brenan, Paul AU - Chang-Claude, Jenny AU - Riboli, Elio AU - Conti, David AU - Gago-Dominguez, Manuela AU - Stern, Mariana C AU - Pike, Malcolm C AU - Van Den Berg, David AU - Yuan, Jian-Min AU - Hohensee, Chancellor AU - Rodabough, Rebecca AU - Cancel-Tassin, Geraldine AU - Roupret, Morgan AU - Comperat, Eva AU - Chen, Constance AU - De Vivo, Immaculata AU - Giovannucci, Edward AU - Hunter, David J AU - Kraft, Peter AU - Lindstrom, Sara AU - Carta, Angela AU - Pavanello, Sofia AU - Arici, Cecilia AU - Mastrangelo, Giuseppe AU - Kamat, Ashish M AU - Lerner, Seth P AU - Barton Grossman, H AU - Lin, Jie AU - Gu, Jian AU - Pu, Xia AU - Hutchinson, Amy AU - Burdette, Laurie AU - Wheeler, William AU - Kogevinas, Manolis AU - Tardón, Adonina AU - Serra, Consol AU - Carrato, Alfredo AU - García-Closas, Reina AU - Lloreta, Josep AU - Schwenn, Molly AU - Karagas, Margaret R AU - Johnson, Alison AU - Schned, Alan AU - Armenti, Karla R AU - Hosain, G M AU - Andriole, Gerald AU - Grubb, Robert AU - Black, Amanda AU - Ryan Diver, W AU - Gapstur, Susan M AU - Weinstein, Stephanie J AU - Virtamo, Jarmo AU - Haiman, Chris A AU - Landi, Maria T AU - Caporaso, Neil AU - Fraumeni, Joseph F AU - Vineis, Paolo AU - Wu, Xifeng AU - Silverman, Debra T AU - Chanock, Stephen AU - Rothman, Nathaniel AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA. Y1 - 2014/03/01/ PY - 2014 DA - 2014 Mar 01 SP - 1387 EP - 1398 VL - 23 IS - 5 KW - Index Medicus KW - Genotype KW - Risk KW - Polymorphism, Single Nucleotide KW - Humans KW - Case-Control Studies KW - Genetic Predisposition to Disease KW - Meta-Analysis as Topic KW - Linkage Disequilibrium KW - Urinary Bladder Neoplasms -- pathology KW - Genetic Loci KW - Urinary Bladder Neoplasms -- genetics KW - Genome-Wide Association Study UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499133164?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=Genome-wide+association+study+identifies+multiple+loci+associated+with+bladder+cancer+risk.&rft.au=Figueroa%2C+Jonine+D%3BYe%2C+Yuanqing%3BSiddiq%2C+Afshan%3BGarcia-Closas%2C+Montserrat%3BChatterjee%2C+Nilanjan%3BProkunina-Olsson%2C+Ludmila%3BCortessis%2C+Victoria+K%3BKooperberg%2C+Charles%3BCussenot%2C+Olivier%3BBenhamou%2C+Simone%3BPrescott%2C+Jennifer%3BPorru%2C+Stefano%3BDinney%2C+Colin+P%3BMalats%2C+N%C3%BAria%3BBaris%2C+Dalsu%3BPurdue%2C+Mark%3BJacobs%2C+Eric+J%3BAlbanes%2C+Demetrius%3BWang%2C+Zhaoming%3BDeng%2C+Xiang%3BChung%2C+Charles+C%3BTang%2C+Wei%3BBas+Bueno-de-Mesquita%2C+H%3BTrichopoulos%2C+Dimitrios%3BLjungberg%2C+B%C3%B6rje%3BClavel-Chapelon%2C+Fran%C3%A7oise%3BWeiderpass%2C+Elisabete%3BKrogh%2C+Vittorio%3BDorronsoro%2C+Miren%3BTravis%2C+Ruth%3BTj%C3%B8nneland%2C+Anne%3BBrenan%2C+Paul%3BChang-Claude%2C+Jenny%3BRiboli%2C+Elio%3BConti%2C+David%3BGago-Dominguez%2C+Manuela%3BStern%2C+Mariana+C%3BPike%2C+Malcolm+C%3BVan+Den+Berg%2C+David%3BYuan%2C+Jian-Min%3BHohensee%2C+Chancellor%3BRodabough%2C+Rebecca%3BCancel-Tassin%2C+Geraldine%3BRoupret%2C+Morgan%3BComperat%2C+Eva%3BChen%2C+Constance%3BDe+Vivo%2C+Immaculata%3BGiovannucci%2C+Edward%3BHunter%2C+David+J%3BKraft%2C+Peter%3BLindstrom%2C+Sara%3BCarta%2C+Angela%3BPavanello%2C+Sofia%3BArici%2C+Cecilia%3BMastrangelo%2C+Giuseppe%3BKamat%2C+Ashish+M%3BLerner%2C+Seth+P%3BBarton+Grossman%2C+H%3BLin%2C+Jie%3BGu%2C+Jian%3BPu%2C+Xia%3BHutchinson%2C+Amy%3BBurdette%2C+Laurie%3BWheeler%2C+William%3BKogevinas%2C+Manolis%3BTard%C3%B3n%2C+Adonina%3BSerra%2C+Consol%3BCarrato%2C+Alfredo%3BGarc%C3%ADa-Closas%2C+Reina%3BLloreta%2C+Josep%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BJohnson%2C+Alison%3BSchned%2C+Alan%3BArmenti%2C+Karla+R%3BHosain%2C+G+M%3BAndriole%2C+Gerald%3BGrubb%2C+Robert%3BBlack%2C+Amanda%3BRyan+Diver%2C+W%3BGapstur%2C+Susan+M%3BWeinstein%2C+Stephanie+J%3BVirtamo%2C+Jarmo%3BHaiman%2C+Chris+A%3BLandi%2C+Maria+T%3BCaporaso%2C+Neil%3BFraumeni%2C+Joseph+F%3BVineis%2C+Paolo%3BWu%2C+Xifeng%3BSilverman%2C+Debra+T%3BChanock%2C+Stephen%3BRothman%2C+Nathaniel&rft.aulast=Figueroa&rft.aufirst=Jonine&rft.date=2014-03-01&rft.volume=23&rft.issue=5&rft.spage=1387&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=1460-2083&rft_id=info:doi/10.1093%2Fhmg%2Fddt519 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-15 N1 - Date created - 2014-02-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Lancet. 2005 Aug 20-26;366(9486):649-59 [16112301] Hum Mol Genet. 2011 Nov 1;20(21):4282-9 [21824976] Genetics. 2004 Aug;167(4):2067-81 [15342541] Int J Cancer. 1985 Jun 15;35(6):703-6 [4008097] Nat Genet. 2006 Aug;38(8):904-9 [16862161] Cancer Res. 2006 Aug 1;66(15):7390-4 [16885332] Immunol Res. 2006;35(1-2):65-74 [17003510] Bioinformatics. 2006 Dec 15;22(24):3061-6 [17060358] Nucleic Acids Res. 2012 Jan;40(Database issue):D930-4 [22064851] Gut. 2012 Feb;61(2):248-54 [21708826] Cancer Epidemiol Biomarkers Prev. 2012 Mar;21(3):537-46 [22147365] Proc Natl Acad Sci U S A. 2012 Mar 27;109(13):4974-9 [22416122] Genome Res. 2012 Sep;22(9):1790-7 [22955989] Nature. 2012 Sep 6;489(7414):91-100 [22955619] PLoS One. 2012;7(10):e47454 [23077621] Am J Epidemiol. 2012 Dec 1;176(11):1060-7 [23118105] Nat Genet. 2012 Dec;44(12):1330-5 [23143601] Hum Mol Genet. 2012 Dec 15;21(24):5373-84 [22976474] PLoS Genet. 2012;8(12):e1003098 [23284291] Cancer Res. 2013 Apr 1;73(7):2211-20 [23536561] Nat Genet. 2013 Jul;45(7):799-803 [23727862] Nat Genet. 2013 Aug;45(8):868-76 [23770605] Int J Urol. 2006 Apr;13(4):401-8 [16734859] Nat Genet. 2007 Jun;39(6):770-5 [17460697] Nat Genet. 2007 Jul;39(7):870-4 [17529973] Nature. 2007 Jun 28;447(7148):1087-93 [17529967] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1595-600 [17684133] PLoS Genet. 2006 Dec;2(12):e190 [17194218] Nature. 2007 Oct 18;449(7164):851-61 [17943122] Diabetes. 2007 Dec;56(12):3101-4 [17804762] PLoS One. 2008;3(7):e2551 [18596976] BMC Public Health. 2008;8:203 [18538025] Nat Genet. 2008 Aug;40(8):955-62 [18587394] Biostatistics. 2008 Oct;9(4):593-600 [18441336] Biometrics. 2008 Sep;64(3):685-94 [18162111] Hum Mol Genet. 2008 Oct 15;17(R2):R122-8 [18852200] Nat Genet. 2008 Nov;40(11):1307-12 [18794855] Nat Genet. 2009 Feb;41(2):221-7 [19151717] Carcinogenesis. 2009 May;30(5):763-8 [19237606] PLoS Genet. 2009 Jun;5(6):e1000529 [19543373] Nat Genet. 2009 Sep;41(9):991-5 [19648920] Am J Hum Genet. 2009 Nov;85(5):679-91 [19836008] Nat Genet. 2010 May;42(5):415-9 [20348956] Nat Genet. 2010 Jul;42(7):570-5 [20562874] Hum Mutat. 2010 Sep;31(9):1050-8 [20597107] Nat Chem Biol. 2007 Oct;3(10):640-9 [17876321] Nat Genet. 2010 Nov;42(11):978-84 [20972438] Nat Genet. 2010 Nov;42(11):973-7 [20972440] Nat Genet. 2010 Dec;42(12):1118-25 [21102463] Carcinogenesis. 2011 Feb;32(2):182-9 [21037224] Int J Cancer. 2010 Dec 15;127(12):2893-917 [21351269] Nat Genet. 2011 Mar;43(3):246-52 [21297633] Nature. 2011 Aug 11;476(7359):214-9 [21833088] Hum Mol Genet. 2011 Oct 1;20(19):3867-75 [21743057] Hum Mol Genet. 2011 Nov 1;20(21):4268-81 [21750109] Hum Mol Genet. 2012 Apr 15;21(8):1918-30 [22228101] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/hmg/ddt519 ER - TY - JOUR T1 - Structural basis for HIV-1 neutralization by 2F5-like antibodies m66 and m66.6. AN - 1499131128; 24335316 AB - Antibodies m66.6 and 2F5 are the only effective human HIV-1-neutralizing antibodies reported thus far to recognize the N-terminal region of the membrane-proximal external region (MPER) of the gp41 subunit of the HIV-1 envelope glycoprotein. Although 2F5 has been extensively characterized, much less is known about antibody m66.6 or antibody m66, a closely related light-chain variant. Here, we report the crystal structure of m66 in complex with its gp41 epitope, along with unbound structures of m66 and m66.6. We used mutational and binding analyses to decipher antibody elements critical for their recognition of gp41 and determined the molecular basis that underlies their neutralization of HIV-1. When bound by m66, the N-terminal region of the gp41 MPER adopts a conformation comprising a helix, followed by an extended loop. Comparison of gp41-bound m66 to unbound m66.6 identified three light-chain residues of m66.6 that were confirmed through mutagenesis to underlie the greater breadth of m66.6-mediated virus neutralization. Recognition of gp41 by m66 also revealed similarities to antibody 2F5 both in the conformation of crucial epitope residues as well as in the angle of antibody approach. Aromatic residues at the tip of the m66.6 heavy-chain third complementarity-determining region, as in the case of 2F5, were determined to be critical for virus neutralization in a manner that correlated with antibody recognition of the MPER in a lipid context. Antibodies m66, m66.6, and 2F5 thus utilize similar mechanistic elements to recognize a common gp41-MPER epitope and to neutralize HIV-1. JF - Journal of virology AU - Ofek, Gilad AU - Zirkle, Brett AU - Yang, Yongping AU - Zhu, Zhongyu AU - McKee, Krisha AU - Zhang, Baoshan AU - Chuang, Gwo-Yu AU - Georgiev, Ivelin S AU - O'Dell, Sijy AU - Doria-Rose, Nicole AU - Mascola, John R AU - Dimitrov, Dimiter S AU - Kwong, Peter D AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 2426 EP - 2441 VL - 88 IS - 5 KW - Antibodies, Neutralizing KW - 0 KW - Antigen-Antibody Complex KW - Complementarity Determining Regions KW - Epitopes KW - HIV Antibodies KW - HIV Envelope Protein gp41 KW - Peptides KW - Index Medicus KW - Models, Molecular KW - Humans KW - Complementarity Determining Regions -- chemistry KW - HIV Envelope Protein gp41 -- metabolism KW - Antigen-Antibody Complex -- chemistry KW - Peptides -- immunology KW - HIV Envelope Protein gp41 -- immunology KW - Protein Interaction Domains and Motifs -- immunology KW - Amino Acid Sequence KW - Protein Binding -- immunology KW - Complementarity Determining Regions -- metabolism KW - Molecular Docking Simulation KW - Complementarity Determining Regions -- genetics KW - Neutralization Tests KW - Molecular Sequence Data KW - Peptides -- chemistry KW - Epitopes -- chemistry KW - Epitopes -- immunology KW - Mutation KW - HIV Envelope Protein gp41 -- chemistry KW - Protein Conformation KW - HIV-1 -- metabolism KW - HIV-1 -- immunology KW - HIV Antibodies -- metabolism KW - HIV Antibodies -- immunology KW - Antibodies, Neutralizing -- chemistry KW - Antibodies, Neutralizing -- immunology KW - HIV Antibodies -- chemistry KW - Antibodies, Neutralizing -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499131128?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Structural+basis+for+HIV-1+neutralization+by+2F5-like+antibodies+m66+and+m66.6.&rft.au=Ofek%2C+Gilad%3BZirkle%2C+Brett%3BYang%2C+Yongping%3BZhu%2C+Zhongyu%3BMcKee%2C+Krisha%3BZhang%2C+Baoshan%3BChuang%2C+Gwo-Yu%3BGeorgiev%2C+Ivelin+S%3BO%27Dell%2C+Sijy%3BDoria-Rose%2C+Nicole%3BMascola%2C+John+R%3BDimitrov%2C+Dimiter+S%3BKwong%2C+Peter+D&rft.aulast=Ofek&rft.aufirst=Gilad&rft.date=2014-03-01&rft.volume=88&rft.issue=5&rft.spage=2426&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.02837-13 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-08 N1 - Date created - 2014-02-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Virol. 2000 Sep;74(17):8038-47 [10933713] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3739-44 [18322015] J Virol. 2001 Nov;75(22):10892-905 [11602729] J Virol. 2002 Jul;76(13):6780-90 [12050391] Acta Crystallogr D Biol Crystallogr. 2002 Nov;58(Pt 11):1948-54 [12393927] J Virol. 2004 Mar;78(5):2627-31 [14963170] J Virol. 2008 Jun;82(11):5417-28 [18353944] J Mol Biol. 2008 Dec 12;384(2):377-92 [18824005] J Virol. 2009 Apr;83(8):3617-25 [19193787] J Virol. 2009 Sep;83(17):8451-62 [19515770] J Virol. 2009 Sep;83(17):8925-37 [19553335] Protein Sci. 2009 Dec;18(12):2624-8 [19785006] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702] J Virol. 2010 Mar;84(6):2955-62 [20042512] J Virol. 2010 May;84(9):4136-47 [20147404] Proc Natl Acad Sci U S A. 2010 Oct 19;107(42):17880-7 [20876137] Nat Struct Mol Biol. 2010 Dec;17(12):1492-4 [21076400] Acta Crystallogr D Biol Crystallogr. 2011 Apr;67(Pt 4):235-42 [21460441] J Virol. 2011 Nov;85(21):11401-8 [21880764] PLoS One. 2011;6(9):e23532 [21980336] Nat Struct Mol Biol. 2011 Nov;18(11):1235-43 [22002224] J Virol. 2012 Aug;86(15):8319-23 [22623764] Immunity. 2012 Sep 21;37(3):412-25 [22999947] Nature. 2012 Nov 15;491(7424):406-12 [23151583] Science. 2013 May 10;340(6133):751-6 [23661761] J Virol. 2013 Sep;87(18):10047-58 [23843642] J Virol. 2004 Oct;78(19):10724-37 [15367639] J Virol. 1993 Nov;67(11):6642-7 [7692082] J Mol Biol. 1994 May 20;238(5):777-93 [8182748] Nat Struct Biol. 1996 Oct;3(10):842-8 [8836100] Electrophoresis. 1997 Dec;18(15):2714-23 [9504803] J Virol. 1999 Mar;73(3):2469-80 [9971832] J Virol. 1999 Jul;73(7):6089-92 [10364363] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] Immunity. 2005 Feb;22(2):163-73 [15723805] Science. 2005 Jun 24;308(5730):1906-8 [15860590] J Virol. 2005 Aug;79(16):10108-25 [16051804] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2641-6 [16481622] J Virol. 2007 Apr;81(8):4033-43 [17287272] Nucleic Acids Res. 2007 Jul;35(Web Server issue):W375-83 [17452350] J Mol Biol. 2007 Sep 21;372(3):774-97 [17681537] Immunity. 2008 Jan;28(1):52-63 [18191596] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10037-41 [11517324] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/JVI.02837-13 ER - TY - JOUR T1 - Pre-exposure prophylaxis for conception (Prep-C) as a risk reduction strategy in HIV- positive men and HIV-negative women in the UK AN - 1499081050; 4528511 AB - Couples wishing to have biological children when one partner is HIV positive and the other is HIV negative present clinicians with complex clinical, social and ethical considerations. We established two multidisciplinary pre-conception services for HIV- positive individuals and their partners. We report the first UK use of pre-exposure prophylaxis for conception (PrEP-C) as part of an overall risk reduction strategy. Couples were counselled and written informed consent for PrEP-C was obtained. Patient demographics, HIV and medical histories were recorded. Males underwent baseline semen analysis and seminal HIV viral load testing. Females had full fertility screens. Both partners were screened for sexually transmitted infections. All couples used timed ovulatory intercourse (TOI). Tenofovir±emtricitabine was taken by the female at protocol designated times before±after TOI. Thirty-two male positive/female negative couples used the services. Thirteen couples have used PrEP-C (median age of male 41 years (range 32-56), female 31 (28-43); median CD4 533 (236-1194); all male plasma and seminal HIV viral loads were undetectable). Eleven pregnancies in 10 couples have resulted in 7 live births, 1 ongoing pregnancy and 4 miscarriages (5/40, 6/40, 10/40 and 1 twin 17/40) after a median of 2.5 attempts (range 1-5). PrEP-C was well tolerated with no discontinuations and no HIV transmissions. These data suggest that PrEP-C is a safe and effective option for serodiscordant couples wishing to conceive; a standardised protocol has been developed; data collection via a central database is under way. Reprinted by permission of Routledge, Taylor & Francis Ltd. JF - AIDS care AU - Whetham, J AU - Taylor, S AU - Charlwood, L AU - Keith, T AU - Howell, R AU - McInnes, C AU - Payne, E AU - Home, J AU - White, D AU - Gilleece, Y AD - Brighton and Sussex University Hospitals NHS Trust ; National Institutes of Health, United Kingdom Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 332 EP - 336 VL - 26 IS - 3 SN - 0954-0121, 0954-0121 KW - Sociology KW - Gender KW - Children KW - HIV KW - United Kingdom KW - Sexually transmitted diseases KW - Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499081050?accountid=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=AIDS+care&rft.atitle=Pre-exposure+prophylaxis+for+conception+%28Prep-C%29+as+a+risk+reduction+strategy+in+HIV-+positive+men+and+HIV-negative+women+in+the+UK&rft.au=Whetham%2C+J%3BTaylor%2C+S%3BCharlwood%2C+L%3BKeith%2C+T%3BHowell%2C+R%3BMcInnes%2C+C%3BPayne%2C+E%3BHome%2C+J%3BWhite%2C+D%3BGilleece%2C+Y&rft.aulast=Whetham&rft.aufirst=J&rft.date=2014-03-01&rft.volume=26&rft.issue=3&rft.spage=332&rft.isbn=&rft.btitle=&rft.title=AIDS+care&rft.issn=09540121&rft_id=info:doi/10.1080%2F09540121.2013.819406 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-02-10 N1 - Last updated - 2014-02-18 N1 - SubjectsTermNotLitGenreText - 3458 2991 9429 9416 2153; 5703 3617 6220; 5421 6091; 2212; 11581 3617 6220; 438 462 129 302 DO - http://dx.doi.org/10.1080/09540121.2013.819406 ER - TY - JOUR T1 - Differences in testing, stigma, and perceived consequences of stigmatization among heterosexual men and women living with HIV in Bengaluru, India AN - 1499080718; 4528514 AB - Approximately 2.4 million people in India are living with HIV. Gender inequality affects HIV prevention, detection, and management. The purpose of this paper was to describe gender differences in the experience of living with HIV in Bengaluru, India. A subsample of n = 313 (159 men and 154 women) from a larger cohort was used for these analyses. Participants were recruited through AIDS service organizations. They completed an interviewer-administered survey assessing HIV testing experience, types of stigma, and perceived consequences of stigmatization. The majority of men (67%) reported getting HIV tested because of illness, while women were more likely to be tested after learning their spouse's HIV-positive status (42%). More men (59%) than women (45%, p<0.05) were tested in private care settings. Men reported significantly higher mean levels of internalized stigma (men: M=0.71, SD = 0.63; women: M=0.46, SD = 0.55; p<0.001), whereas the women reported significantly higher scores for enacted stigma (men: M=1.30, SD = 1.69; women: M=2.10, SD = 2.17; p<0.001). These differences remained significant after controlling for potential socio-demographic covariates. Following their diagnosis, more women reported moving out of their homes (men: 16%; women: 26%; p<0.05). More men (89%) than women (66%; p<0.001) reported to have modified their sexual behavior after being diagnosed. These findings suggest that the experience of living with HIV and HIV stigma varies by gender in this population. Suggestions for a gender-based approach to HIV prevention and stigma reduction are provided. Reprinted by permission of Routledge, Taylor & Francis Ltd. JF - AIDS care AU - Malavé, S AU - Ramakrishna, J AU - Heylen, E AU - Bharat, S AU - Ekstrand, M L AD - University of California, San Francisco ; National Institute of Mental Health and Neuroscience ; Tata Institute of Social Sciences Y1 - 2014/03// PY - 2014 DA - Mar 2014 SP - 396 EP - 403 VL - 26 IS - 3 SN - 0954-0121, 0954-0121 KW - Sociology KW - Prevention KW - Karnataka KW - Gender differentiation KW - HIV KW - Health services KW - Stigma KW - India UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499080718?accountid=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=AIDS+care&rft.atitle=Differences+in+testing%2C+stigma%2C+and+perceived+consequences+of+stigmatization+among+heterosexual+men+and+women+living+with+HIV+in+Bengaluru%2C+India&rft.au=Malav%C3%A9%2C+S%3BRamakrishna%2C+J%3BHeylen%2C+E%3BBharat%2C+S%3BEkstrand%2C+M+L&rft.aulast=Malav%C3%A9&rft.aufirst=S&rft.date=2014-03-01&rft.volume=26&rft.issue=3&rft.spage=396&rft.isbn=&rft.btitle=&rft.title=AIDS+care&rft.issn=09540121&rft_id=info:doi/10.1080%2F09540121.2013.819409 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-02-10 N1 - Last updated - 2014-02-18 N1 - SubjectsTermNotLitGenreText - 5423 3549 2688 2449 10404; 5703 3617 6220; 12258 11762 11859 11856; 10072; 5792 10484; 175 387 30; 197 175 387 30 DO - http://dx.doi.org/10.1080/09540121.2013.819409 ER - TY - JOUR T1 - Sphingolipid signaling reduces basal P-glycoprotein activity in renal proximal tubule. AN - 1492699913; 24385389 AB - P-glycoprotein is an ATP-driven xenobiotic export pump that is highly expressed in barrier and excretory tissues, where it greatly influences drug pharmacokinetics. Recent studies in the blood-brain and spinal cord barriers identified a sphingolipid-based signaling pathway that regulates basal activity of P-glycoprotein. Here we use an established comparative renal model that permits direct measurement of P-glycoprotein activity to determine whether such signaling occurs in another tissue, killifish renal proximal tubule. Isolated killifish tubules exposed to 0.01-1.0 μM sphingosine-1-phosphate (S1P) exhibited a profound decrease in P-glycoprotein transport activity, measured as specific accumulation of a fluorescent cyclosporine A derivative in the tubule lumen. Loss of activity had a rapid onset and was fully reversible when the S1P was removed. Transport mediated by multidrug resistance-associated protein 2 (Mrp2) or a teleost fish organic anion transporter (Oat) was not affected. S1P effects were blocked by a specific S1P receptor 1 (S1PR1) antagonist and mimicked by a S1PR agonist. Sphingosine also reduced P-glycoprotein transport activity and those effects were blocked by an inhibitor of sphingosine kinase and by the S1PR1 antagonist. These results for a comparative renal model suggest that sphingolipid signaling to P-glycoprotein is not just restricted to the blood-brain and blood-spinal cord barriers, but occurs in other excretory and barrier tissues. JF - The Journal of pharmacology and experimental therapeutics 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; and Mount Desert Island Biological Laboratory, Salsbury Cove, Maine. Y1 - 2014/03// PY - 2014 DA - March 2014 SP - 459 EP - 464 VL - 348 IS - 3 KW - Lysophospholipids KW - 0 KW - P-Glycoprotein KW - Receptors, Lysosphingolipid KW - sphingosine 1-phosphate KW - 26993-30-6 KW - Sphingosine KW - NGZ37HRE42 KW - Index Medicus KW - Animals KW - Receptors, Lysosphingolipid -- agonists KW - Receptors, Lysosphingolipid -- metabolism KW - In Vitro Techniques KW - Fundulidae KW - Biological Transport KW - Signal Transduction KW - Receptors, Lysosphingolipid -- antagonists & inhibitors KW - Sphingosine -- metabolism KW - P-Glycoprotein -- metabolism KW - Kidney Tubules, Proximal -- metabolism KW - Lysophospholipids -- pharmacology KW - Lysophospholipids -- metabolism KW - Sphingosine -- pharmacology KW - Kidney Tubules, Proximal -- drug effects KW - Sphingosine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492699913?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sphingolipid+signaling+reduces+basal+P-glycoprotein+activity+in+renal+proximal+tubule.&rft.au=Miller%2C+David+S&rft.aulast=Miller&rft.aufirst=David&rft.date=2014-03-01&rft.volume=348&rft.issue=3&rft.spage=459&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.113.210641 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-02 N1 - Date created - 2014-01-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Pharmacol. 2000 Jan;57(1):59-67 [10617679] Curr Pharm Des. 2014;20(10):1463-71 [23789954] Am J Physiol Renal Physiol. 2002 Mar;282(3):F458-64 [11832426] J Biochem Mol Toxicol. 2002;16(3):121-7 [12112711] Am J Physiol Renal Physiol. 2004 Jul;287(1):F33-8 [14970002] Semin Cell Dev Biol. 2004 Oct;15(5):529-40 [15271298] Fortschr Zool. 1975;23(2-3):222-31 [765247] Fed Proc. 1980 Dec;39(14):3207-12 [7002623] Environ Health Perspect. 1987 Apr;71:59-68 [3297665] Am J Physiol. 1995 Jan;268(1 Pt 2):F46-52 [7840247] Am J Physiol. 1996 Dec;271(6 Pt 2):F1173-82 [8997391] J Exp Zool. 1997 Dec 1;279(5):462-70 [9392867] Biochim Biophys Acta. 2006 Dec;1758(12):2037-48 [16890187] Am J Physiol Regul Integr Comp Physiol. 2007 Dec;293(6):R2382-9 [17855498] Kidney Int. 2008 Jun;73(11):1220-30 [18322542] Kidney Int. 2009 Jan;75(2):167-75 [18971925] J Cereb Blood Flow Metab. 2010 Sep;30(9):1593-7 [20628400] J Neurochem. 2010 Oct;115(1):200-8 [20649844] J Pharmacol Exp Ther. 2011 Jul;338(1):362-71 [21515814] Arterioscler Thromb Vasc Biol. 2012 Sep;32(9):e104-16 [22837470] Proc Natl Acad Sci U S A. 2012 Sep 25;109(39):15930-5 [22949658] J Biol Chem. 2013 Jan 25;288(4):2143-56 [23229546] J Cereb Blood Flow Metab. 2013 Mar;33(3):381-8 [23168528] Cell Physiol Biochem. 2013;31(6):745-60 [23736205] Mol Pharmacol. 2000 Dec;58(6):1357-67 [11093774] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/jpet.113.210641 ER - TY - CPAPER T1 - Epitope Mapping Of An Anti-Bla g 1 ScFv Used For Cockroach Allergen Quantitation T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AN - 1518614275; 6283841 JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AU - Mueller, Geoffrey AU - Ankney, John AU - Pedersen, Lars AU - Khurana, Taruna AU - Slater, Jay AU - Glesner, Jill AU - Pomes, Anna AU - London, Robert Y1 - 2014/02/28/ PY - 2014 DA - 2014 Feb 28 KW - Allergens KW - Epitope mapping KW - Quantitation KW - Fv UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518614275?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.atitle=Epitope+Mapping+Of+An+Anti-Bla+g+1+ScFv+Used+For+Cockroach+Allergen+Quantitation&rft.au=Mueller%2C+Geoffrey%3BAnkney%2C+John%3BPedersen%2C+Lars%3BKhurana%2C+Taruna%3BSlater%2C+Jay%3BGlesner%2C+Jill%3BPomes%2C+Anna%3BLondon%2C+Robert&rft.aulast=Mueller&rft.aufirst=Geoffrey&rft.date=2014-02-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Estradiol Has a Negative Impact On The Anaphylactic Response In Mice, Independent From Mast Cell Degranulation T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AN - 1518613859; 6283715 JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AU - Hox, Valerie AU - Desai, Avanti AU - Bandara, Geethani AU - Gilfillan, Alasdair AU - Beaven, Michael AU - Olivera, Ana AU - Metcalfe, Dean Y1 - 2014/02/28/ PY - 2014 DA - 2014 Feb 28 KW - Anaphylaxis KW - Degranulation KW - Mast cells KW - Mice KW - Estradiol UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518613859?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.atitle=Estradiol+Has+a+Negative+Impact+On+The+Anaphylactic+Response+In+Mice%2C+Independent+From+Mast+Cell+Degranulation&rft.au=Hox%2C+Valerie%3BDesai%2C+Avanti%3BBandara%2C+Geethani%3BGilfillan%2C+Alasdair%3BBeaven%2C+Michael%3BOlivera%2C+Ana%3BMetcalfe%2C+Dean&rft.aulast=Hox&rft.aufirst=Valerie&rft.date=2014-02-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Human EMR1, An Eosinophil-Specific Surface Receptor Of Unknown Function, Is Modulated In Vivo and In Vitro T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AN - 1518612949; 6283723 JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AU - Legrand, Fanny AU - Tomasevic, Nenad AU - Makiya, Michelle AU - Bebbington, Christopher AU - Klion, Amy Y1 - 2014/02/28/ PY - 2014 DA - 2014 Feb 28 KW - Receptor mechanisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518612949?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.atitle=Human+EMR1%2C+An+Eosinophil-Specific+Surface+Receptor+Of+Unknown+Function%2C+Is+Modulated+In+Vivo+and+In+Vitro&rft.au=Legrand%2C+Fanny%3BTomasevic%2C+Nenad%3BMakiya%2C+Michelle%3BBebbington%2C+Christopher%3BKlion%2C+Amy&rft.aulast=Legrand&rft.aufirst=Fanny&rft.date=2014-02-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Outcome Measures Of Challenge Testing In Patients With Physically Induced-Urticaria T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AN - 1518612717; 6283901 JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AU - Metcalfe, Dean AU - Arceo, Sarah AU - Young, Michael AU - Nelson, Celeste AU - Komarow, Hirsh Y1 - 2014/02/28/ PY - 2014 DA - 2014 Feb 28 KW - Hypersensitivity KW - Epidemiology KW - Lung KW - Immunology KW - Asthma KW - Respiratory diseases KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518612717?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.atitle=Outcome+Measures+Of+Challenge+Testing+In+Patients+With+Physically+Induced-Urticaria&rft.au=Metcalfe%2C+Dean%3BArceo%2C+Sarah%3BYoung%2C+Michael%3BNelson%2C+Celeste%3BKomarow%2C+Hirsh&rft.aulast=Metcalfe&rft.aufirst=Dean&rft.date=2014-02-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Gene Expression Profiling Of Food-Induced Anaphylaxis Associated With Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AN - 1518612445; 6283613 JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AU - Munoz-Cano, Rosa AU - Bartra, Joan AU - Scheffel, Jorg AU - Pascal, Mariona AU - Dema, Barbara AU - Valero, Antonio AU - Olivera, Ana AU - Picado, Cesar AU - Rivera, Juan Y1 - 2014/02/28/ PY - 2014 DA - 2014 Feb 28 KW - Gene expression KW - Anaphylaxis KW - Food KW - Profiling KW - Drugs KW - Antiinflammatory agents KW - Nonsteroidal antiinflammatory drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518612445?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.atitle=Gene+Expression+Profiling+Of+Food-Induced+Anaphylaxis+Associated+With+Non-Steroidal+Anti-Inflammatory+Drugs+%28NSAIDs%29&rft.au=Munoz-Cano%2C+Rosa%3BBartra%2C+Joan%3BScheffel%2C+Jorg%3BPascal%2C+Mariona%3BDema%2C+Barbara%3BValero%2C+Antonio%3BOlivera%2C+Ana%3BPicado%2C+Cesar%3BRivera%2C+Juan&rft.aulast=Munoz-Cano&rft.aufirst=Rosa&rft.date=2014-02-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Teasing and Bullying Among Adolescents With Food Allergy T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AN - 1518611622; 6284081 JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AU - Lin, Adora AU - Sharma, Hemant Y1 - 2014/02/28/ PY - 2014 DA - 2014 Feb 28 KW - Food hypersensitivity KW - Bullying KW - Adolescents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611622?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.atitle=Teasing+and+Bullying+Among+Adolescents+With+Food+Allergy&rft.au=Lin%2C+Adora%3BSharma%2C+Hemant&rft.aulast=Lin&rft.aufirst=Adora&rft.date=2014-02-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - CPAPER T1 - Worldwide Impact Of LAD2 Mast Cell Line On Mast Cell Biology Research T2 - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AN - 1518610944; 6283709 JF - 2014 Annual Meeting of the American Academy of Allergy, Asthma and Immunology (AAAAI 2014) AU - Kirshenbaum, Arnold AU - Petrik, Amy AU - Walsh, Rosemary AU - Vepa, Sury AU - Metcalfe, Dean Y1 - 2014/02/28/ PY - 2014 DA - 2014 Feb 28 KW - Mast cells KW - Cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518610944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.atitle=Worldwide+Impact+Of+LAD2+Mast+Cell+Line+On+Mast+Cell+Biology+Research&rft.au=Kirshenbaum%2C+Arnold%3BPetrik%2C+Amy%3BWalsh%2C+Rosemary%3BVepa%2C+Sury%3BMetcalfe%2C+Dean&rft.aulast=Kirshenbaum&rft.aufirst=Arnold&rft.date=2014-02-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Academy+of+Allergy%2C+Asthma+and+Immunology+%28AAAAI+2014%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aaaai.org/Aaaai/media/MediaLibrary/PDF%20Documents/Announcements/am14-final-prog.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - JOUR T1 - Evaluating the additivity of perfluoroalkyl acids in binary combinations on peroxisome proliferator-activated receptor-α activation. AN - 1499137621; 24374136 AB - Perfluoroalkyl acids (PFAAs) are found globally in the environment, detected in humans and wildlife, and are typically present as mixtures of PFAA congeners. Mechanistic studies have found that responses to PFAAs are mediated in part by PPARα. Our previous studies showed that individual PFAAs activate PPARα transfected into COS-1 cells. The goal of the current study was to determine if binary combinations of perfluorooctanoic acid (PFOA) and another PFAA act in an additive fashion to activate PPARα in the mouse one-hybrid in vitro model. COS-1 cells were transiently transfected with mouse PPARα luciferase reporter construct and exposed to either vehicle control (0.1% DMSO or water), PPARα agonist (WY14643, 10 μM), PFOA at 1-128μM, perfluorononanoic acid (PFNA) at 1-128 μM, perfluorohexanoic acid (PFHxA) at 8-1024 μM, perfluorooctane sulfonate (PFOS) at 4-384 μM or perfluorohexane sulfonate (PFHxS) at 8-2048 μM to generate sigmoidal concentration-response curves. In addition, cells were exposed to binary combinations of PFOA+either PFNA, PFHxA, PFOS or PFHxS in an 8×8 factorial design. The concentration-response data for individual chemicals were fit to sigmoidal curves and analyzed with nonlinear regression to generate EC₅₀s and Hillslopes, which were used in response-addition and concentration-addition models to calculate predicted responses for mixtures in the same plate. All PFOA+PFAA combinations produced concentration-response curves that were closely aligned with the predicted curves for both response addition and concentration addition at low concentrations. However, at higher concentrations of all chemicals, the observed response curves deviated from the predicted models of additivity. We conclude that binary combinations of PFAAs behave additively at the lower concentration ranges in activating PPARα in this in vitro system. Published by Elsevier Ireland Ltd. JF - Toxicology AU - Wolf, Cynthia J AU - Rider, Cynthia V AU - Lau, Christopher AU - Abbott, Barbara D AD - Developmental Toxicology Branch, Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, ORD, U.S. EPA, Research Triangle Park, NC 27711, United States. Electronic address: wolf.cynthiaj@epa.gov. ; National Toxicology Program, NIEHS, Research Triangle Park, NC 27709, United States. ; Developmental Toxicology Branch, Toxicity Assessment Division, National Health and Environmental Effects Research Laboratory, ORD, U.S. EPA, Research Triangle Park, NC 27711, United States. Y1 - 2014/02/28/ PY - 2014 DA - 2014 Feb 28 SP - 43 EP - 54 VL - 316 KW - Alkanesulfonic Acids KW - 0 KW - Caprylates KW - Environmental Pollutants KW - Fluorocarbons KW - PPAR alpha KW - Pyrimidines KW - pirinixic acid KW - 86C4MRT55A KW - perfluorooctanoic acid KW - 947VD76D3L KW - Index Medicus KW - Additivity KW - PFOA KW - Mixtures KW - Perfluoroalkyl acids KW - PPARα KW - Regression Analysis KW - Animals KW - Alkanesulfonic Acids -- administration & dosage KW - COS Cells KW - Transfection KW - Dose-Response Relationship, Drug KW - Alkanesulfonic Acids -- toxicity KW - Cercopithecus aethiops KW - Pyrimidines -- pharmacology KW - Alkanesulfonic Acids -- chemistry KW - Mice KW - Fluorocarbons -- chemistry KW - Caprylates -- administration & dosage KW - PPAR alpha -- drug effects KW - Caprylates -- chemistry KW - Environmental Pollutants -- toxicity KW - Fluorocarbons -- administration & dosage KW - Fluorocarbons -- toxicity KW - Environmental Pollutants -- chemistry KW - Caprylates -- toxicity KW - PPAR alpha -- metabolism KW - Environmental Pollutants -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499137621?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evaluating+the+additivity+of+perfluoroalkyl+acids+in+binary+combinations+on+peroxisome+proliferator-activated+receptor-%CE%B1+activation.&rft.au=Wolf%2C+Cynthia+J%3BRider%2C+Cynthia+V%3BLau%2C+Christopher%3BAbbott%2C+Barbara+D&rft.aulast=Wolf&rft.aufirst=Cynthia&rft.date=2014-02-28&rft.volume=316&rft.issue=&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=1879-3185&rft_id=info:doi/10.1016%2Fj.tox.2013.12.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-15 N1 - Date created - 2014-02-11 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.tox.2013.12.002 ER - TY - JOUR T1 - A bacterial homolog of a eukaryotic inositol phosphate signaling enzyme mediates cross-kingdom dialog in the mammalian gut. AN - 1504152424; 24529702 AB - Dietary InsP6 can modulate eukaryotic cell proliferation and has complex nutritive consequences, but its metabolism in the mammalian gastrointestinal tract is poorly understood. Therefore, we performed phylogenetic analyses of the gastrointestinal microbiome in order to search for candidate InsP6 phosphatases. We determined that prominent gut bacteria express homologs of the mammalian InsP6 phosphatase (MINPP) and characterized the enzyme from Bacteroides thetaiotaomicron (BtMinpp). We show that BtMinpp has exceptionally high catalytic activity, which we rationalize on the basis of mutagenesis studies and by determining its crystal structure at 1.9 Å resolution. We demonstrate that BtMinpp is packaged inside outer membrane vesicles (OMVs) protecting the enzyme from degradation by gastrointestinal proteases. Moreover, we uncover an example of cross-kingdom cell-to-cell signaling, showing that the BtMinpp-OMVs interact with intestinal epithelial cells to promote intracellular Ca(2+) signaling. Our characterization of BtMinpp offers several directions for understanding how the microbiome serves human gastrointestinal physiology. Copyright © 2014 The Authors. Published by Elsevier Inc. All rights reserved. JF - Cell reports AU - Stentz, Régis AU - Osborne, Samantha AU - Horn, Nikki AU - Li, Arthur W H AU - Hautefort, Isabelle AU - Bongaerts, Roy AU - Rouyer, Marine AU - Bailey, Paul AU - Shears, Stephen B AU - Hemmings, Andrew M AU - Brearley, Charles A AU - Carding, Simon R AD - Gut Health and Food Safety Programme, Institute of Food Research, Norwich NR4 7UA, UK. ; School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK. ; Department of Computational and Systems Biology, John Innes Centre, Norwich NR4 7UH, UK. ; Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK; School of Chemistry, University of East Anglia, Norwich NR4 7TJ, UK. ; School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK. Electronic address: c.brearley@uea.ac.uk. ; Gut Health and Food Safety Programme, Institute of Food Research, Norwich NR4 7UA, UK; Norwich Medical School, University of East Anglia, Norwich NR4 7TJ, UK. Electronic address: simon.carding@ifr.ac.uk. Y1 - 2014/02/27/ PY - 2014 DA - 2014 Feb 27 SP - 646 EP - 656 VL - 6 IS - 4 KW - Bacterial Proteins KW - 0 KW - Phosphoric Monoester Hydrolases KW - EC 3.1.3.2 KW - multiple inositol-polyphosphate phosphatase KW - EC 3.1.3.62 KW - Index Medicus KW - Proteolysis KW - Phylogeny KW - Humans KW - Molecular Sequence Data KW - Intestinal Mucosa -- microbiology KW - Catalytic Domain KW - Intestinal Mucosa -- metabolism KW - HT29 Cells KW - Amino Acid Sequence KW - Mutation KW - Calcium Signaling KW - Host-Pathogen Interactions KW - Phosphoric Monoester Hydrolases -- chemistry KW - Bacteroides -- genetics KW - Bacterial Proteins -- genetics KW - Bacterial Proteins -- chemistry KW - Bacteroides -- enzymology KW - Bacterial Proteins -- metabolism KW - Phosphoric Monoester Hydrolases -- genetics KW - Bacteroides -- chemistry KW - Phosphoric Monoester Hydrolases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504152424?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+reports&rft.atitle=A+bacterial+homolog+of+a+eukaryotic+inositol+phosphate+signaling+enzyme+mediates+cross-kingdom+dialog+in+the+mammalian+gut.&rft.au=Stentz%2C+R%C3%A9gis%3BOsborne%2C+Samantha%3BHorn%2C+Nikki%3BLi%2C+Arthur+W+H%3BHautefort%2C+Isabelle%3BBongaerts%2C+Roy%3BRouyer%2C+Marine%3BBailey%2C+Paul%3BShears%2C+Stephen+B%3BHemmings%2C+Andrew+M%3BBrearley%2C+Charles+A%3BCarding%2C+Simon+R&rft.aulast=Stentz&rft.aufirst=R%C3%A9gis&rft.date=2014-02-27&rft.volume=6&rft.issue=4&rft.spage=646&rft.isbn=&rft.btitle=&rft.title=Cell+reports&rft.issn=2211-1247&rft_id=info:doi/10.1016%2Fj.celrep.2014.01.021 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-07 N1 - Date created - 2014-03-03 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4FDT; PDB; 4FDU N1 - SuppNotes - Cited By: Dan Med Bull. 1999 Jun;46(3):183-96 [10421978] Biochem J. 2013 Feb 15;450(1):115-25 [23186306] Appl Microbiol Biotechnol. 2005 Sep;68(5):588-97 [16041577] Science. 2006 Mar 3;311(5765):1283-7 [16513982] J Biotechnol. 2006 Nov 1;126(2):248-59 [16759730] Plant Biotechnol J. 2007 Mar;5(2):325-38 [17309687] Int J Food Microbiol. 2007 Jun 10;117(1):76-84 [17462768] Biochem J. 2008 Jan 15;409(2):333-48 [18092946] Nat Rev Mol Cell Biol. 2008 Feb;9(2):151-61 [18216771] Nat Rev Genet. 2008 Aug;9(8):605-18 [18591983] Microbiol Mol Biol Rev. 2010 Mar;74(1):81-94 [20197500] Biochem Biophys Res Commun. 2010 Jul 9;397(4):745-9 [20541524] Cell. 2010 Dec 10;143(6):897-910 [21145457] Nat Immunol. 2011 Aug;12(8):752-60 [21685907] Mol Cell Biol. 2000 Sep;20(17):6496-507 [10938126] Pflugers Arch. 2001 Jan;441(4):529-37 [11212217] Mol Biol Evol. 2001 May;18(5):691-9 [11319253] Complement Ther Med. 2002 Dec;10(4):229-34 [12594974] Science. 2003 Mar 28;299(5615):2074-6 [12663928] J Nutr. 2003 Nov;133(11 Suppl 1):3778S-3784S [14608114] J Biol Chem. 2003 Nov 21;278(47):46210-8 [12963730] Curr Issues Intest Microbiol. 2004 Sep;5(2):23-39 [15460064] J Biol Chem. 1972 Jun 25;247(12):3962-72 [4555955] J Biol Chem. 1991 Sep 5;266(25):16499-506 [1653239] Biochem J. 1995 Jan 15;305 ( Pt 2):557-61 [7832774] Microb Pathog. 1996 Apr;20(4):191-202 [8737489] Nat Struct Biol. 1997 Mar;4(3):185-90 [9164457] Biochem J. 1997 Nov 15;328 ( Pt 1):75-81 [9359836] J Cell Sci. 1998 Mar;111 ( Pt 6):803-13 [9472008] FEBS Lett. 1999 Jan 8;442(1):99-104 [9923613] Mol Biol Evol. 2011 Oct;28(10):2731-9 [21546353] Science. 2011 Nov 11;334(6057):802-5 [22076377] Appl Environ Microbiol. 2012 Jul;78(14):5013-5 [22582052] Nature. 2012 Sep 13;489(7415):242-9 [22972297] Cell Host Microbe. 2012 Oct 18;12(4):509-20 [22999859] Nucleic Acids Res. 2005 Jul 1;33(Web Server issue):W299-302 [15980475] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.celrep.2014.01.021 ER - TY - JOUR T1 - Washing older blood units before transfusion reduces plasma iron and improves outcomes in experimental canine pneumonia. AN - 1503555845; 24366359 AB - In a randomized controlled blinded trial, 2-year-old purpose-bred beagles (n = 24), with Staphylococcus aureus pneumonia, were exchanged-transfused with either 7- or 42-day-old washed or unwashed canine universal donor blood (80 mL/kg in 4 divided doses). Washing red cells (RBC) before transfusion had a significantly different effect on canine survival, multiple organ injury, plasma iron, and cell-free hemoglobin (CFH) levels depending on the age of stored blood (all, P < .05 for interactions). Washing older units of blood improved survival rates, shock score, lung injury, cardiac performance and liver function, and reduced levels of non-transferrin bound iron and plasma labile iron. In contrast, washing fresh blood worsened all these same clinical parameters and increased CFH levels. Our data indicate that transfusion of fresh blood, which results in less hemolysis, CFH, and iron release, is less toxic than transfusion of older blood in critically ill infected subjects. However, washing older blood prevented elevations in plasma circulating iron and improved survival and multiple organ injury in animals with an established pulmonary infection. Our data suggest that fresh blood should not be washed routinely because, in a setting of established infection, washed RBC are prone to release CFH and result in worsened clinical outcomes. JF - Blood AU - Cortés-Puch, Irene AU - Wang, Dong AU - Sun, Junfeng AU - Solomon, Steven B AU - Remy, Kenneth E AU - Fernandez, Melinda AU - Feng, Jing AU - Kanias, Tamir AU - Bellavia, Landon AU - Sinchar, Derek AU - Perlegas, Andreas AU - Solomon, Michael A AU - Kelley, Walter E AU - Popovsky, Mark A AU - Gladwin, Mark T AU - Kim-Shapiro, Daniel B AU - Klein, Harvey G AU - Natanson, Charles AD - Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD; Y1 - 2014/02/27/ PY - 2014 DA - 2014 Feb 27 SP - 1403 EP - 1411 VL - 123 IS - 9 KW - Iron KW - E1UOL152H7 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Down-Regulation KW - Treatment Outcome KW - Dogs KW - Disease Models, Animal KW - Acute Lung Injury -- mortality KW - Acute Lung Injury -- etiology KW - Blood Preservation KW - Blood Specimen Collection -- methods KW - Erythrocyte Transfusion -- adverse effects KW - Pneumonia, Staphylococcal -- mortality KW - Erythrocyte Transfusion -- methods KW - Pneumonia, Staphylococcal -- therapy KW - Iron -- isolation & purification KW - Erythrocytes -- cytology KW - Iron -- blood KW - Plasma -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1503555845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Washing+older+blood+units+before+transfusion+reduces+plasma+iron+and+improves+outcomes+in+experimental+canine+pneumonia.&rft.au=Cort%C3%A9s-Puch%2C+Irene%3BWang%2C+Dong%3BSun%2C+Junfeng%3BSolomon%2C+Steven+B%3BRemy%2C+Kenneth+E%3BFernandez%2C+Melinda%3BFeng%2C+Jing%3BKanias%2C+Tamir%3BBellavia%2C+Landon%3BSinchar%2C+Derek%3BPerlegas%2C+Andreas%3BSolomon%2C+Michael+A%3BKelley%2C+Walter+E%3BPopovsky%2C+Mark+A%3BGladwin%2C+Mark+T%3BKim-Shapiro%2C+Daniel+B%3BKlein%2C+Harvey+G%3BNatanson%2C+Charles&rft.aulast=Cort%C3%A9s-Puch&rft.aufirst=Irene&rft.date=2014-02-27&rft.volume=123&rft.issue=9&rft.spage=1403&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=1528-0020&rft_id=info:doi/10.1182%2Fblood-2013-11-539353 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-05-06 N1 - Date created - 2014-02-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Vox Sang. 2004 Jul;87(1):19-26 [15260818] Transfus Med. 2002 Jun;12(3):173-9 [12071873] N Engl J Med. 2005 Mar 10;352(10):1011-23 [15758012] J Extra Corpor Technol. 2005 Mar;37(1):58-9 [15804159] Vox Sang. 2006 Jan;90(1):40-4 [16359354] Vox Sang. 2006 Jul;91(1):13-9 [16756596] Transfusion. 2006 Nov;46(11):2014-27 [17076859] Vox Sang. 2007 Feb;92(2):130-5 [17298575] Transfusion. 2007 Feb;47(2):248-50 [17302770] Transfus Med. 2007 Apr;17(2):89-95 [17430464] Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2487-500 [17644570] J Proteomics. 2010 Jan 3;73(3):368-73 [19914410] Clin Chem Lab Med. 2010 May;48(5):677-83 [20158444] Blood. 2010 May 27;115(21):4284-92 [20299509] Transfus Apher Sci. 2010 Aug;43(1):107-16 [20655807] Sci Transl Med. 2010 Sep 29;2(51):51ra71 [20881280] Nephrol Dial Transplant. 2011 Mar;26(3):977-87 [20826742] Eur J Clin Invest. 2011 May;41(5):479-86 [21128934] Transfus Med Rev. 2011 Jul;25(3):197-205 [21550205] Circulation. 2011 Jul 26;124(4):465-76 [21747051] Blood. 2011 Dec 15;118(25):6675-82 [22021369] Crit Care Med. 2012 Jan;40(1):199-207 [21926575] J Am Soc Nephrol. 1998 Apr;9(4):655-63 [9555668] Transfus Med. 2012 Jun;22(3):181-5 [22188550] Transfusion. 2012 Jun;52(6):1184-95 [22188419] Transfusion. 2012 Jun;52(6):1203-12 [22257314] J Trauma Acute Care Surg. 2012 Aug;73(2 Suppl 1):S128-33 [22847082] Intensive Care Med. 2012 Dec;38(12):2063-71 [23111805] Transfusion. 2012 Jan;52(1):34-8 [21682733] Crit Care Med. 2013 Mar;41(3):784-90 [23314583] Blood. 2013 Feb 28;121(9):1663-72 [23255558] Transfusion. 2013 May;53(5):1001-9 [22897672] Blood Transfus. 2013 Jul;11(3):419-25 [23058860] Transfusion. 2013 Aug;53(8):1772-9 [23521180] J Trauma. 2001 Mar;50(3):426-31; discussion 432 [11265021] Vox Sang. 2002 Apr;82(3):122-6 [11952985] Comment In: Blood. 2014 Feb 27;123(9):1287-9 [24578494] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1182/blood-2013-11-539353 ER - TY - JOUR T1 - Characterizing the genetic basis of methylome diversity in histologically normal human lung tissue. AN - 1503551301; 24572595 AB - The genetic regulation of the human epigenome is not fully appreciated. Here we describe the effects of genetic variants on the DNA methylome in human lung based on methylation-quantitative trait loci (meQTL) analyses. We report 34,304 cis- and 585 trans-meQTLs, a genetic-epigenetic interaction of surprising magnitude, including a regulatory hotspot. These findings are replicated in both breast and kidney tissues and show distinct patterns: cis-meQTLs mostly localize to CpG sites outside of genes, promoters and CpG islands (CGIs), while trans-meQTLs are over-represented in promoter CGIs. meQTL SNPs are enriched in CTCF-binding sites, DNaseI hypersensitivity regions and histone marks. Importantly, four of the five established lung cancer risk loci in European ancestry are cis-meQTLs and, in aggregate, cis-meQTLs are enriched for lung cancer risk in a genome-wide analysis of 11,587 subjects. Thus, inherited genetic variation may affect lung carcinogenesis by regulating the human methylome. JF - Nature communications AU - Shi, Jianxin AU - Marconett, Crystal N AU - Duan, Jubao AU - Hyland, Paula L AU - Li, Peng AU - Wang, Zhaoming AU - Wheeler, William AU - Zhou, Beiyun AU - Campan, Mihaela AU - Lee, Diane S AU - Huang, Jing AU - Zhou, Weiyin AU - Triche, Tim AU - Amundadottir, Laufey AU - Warner, Andrew AU - Hutchinson, Amy AU - Chen, Po-Han AU - Chung, Brian S I AU - Pesatori, Angela C AU - Consonni, Dario AU - Bertazzi, Pier Alberto AU - Bergen, Andrew W AU - Freedman, Mathew AU - Siegmund, Kimberly D AU - Berman, Benjamin P AU - Borok, Zea AU - Chatterjee, Nilanjan AU - Tucker, Margaret A AU - Caporaso, Neil E AU - Chanock, Stephen J AU - Laird-Offringa, Ite A AU - Landi, Maria Teresa AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892, USA. ; 1] Department of Surgery, USC/Norris Comprehensive Cancer Center, Keck School of Medicine, Los Angeles, California 90089, USA [2] Department of Biochemistry and Molecular Biology, USC/Norris Comprehensive Cancer Center, Keck School of Medicine, Los Angeles, California 90089, USA. ; Center for Psychiatric Genetics, Department of Psychiatry and Behavioral Sciences, North Shore University Health System Research Institute, University of Chicago Pritzker School of Medicine, Evanston, Illinois 60201, USA. ; Information Management Services Inc., Rockville, Maryland 20852, USA. ; Will Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care and Sleep Medicine, USC Keck School of Medicine, Los Angeles, California 90089, USA. ; Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892, USA. ; Bioinformatics Division, Department of Preventive Medicine, University of Southern California, Los Angeles, California 90089, USA. ; Pathology/Histotechnology Laboratory, Laboratory Animal Sciences Program, Frederick National Laboratory for Cancer Research, Frederick, Maryland 21702, USA. ; Unit of Epidemiology, IRCCS Fondazione Ca' Granda Ospedale Maggiore Policlinico, Department of Clinical Sciences and Community Health, University of Milan, Milan 20122, Italy. ; Molecular Genetics Program, Center for Health Sciences, SRI, Menlo Park, California 94025, USA. ; 1] Program in Medical and Population Genetics, The Broad Institute, Cambridge, Massachusetts 02142, USA [2] Department of Medical Oncology, The Center for Functional Cancer Epigenetics, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA. ; 1] Bioinformatics Division, Department of Preventive Medicine, University of Southern California, Los Angeles, California 90089, USA [2] USC Epigenome Center and USC/Norris Comprehensive Cancer Center, Los Angeles, California 90089, USA. ; 1] Department of Biochemistry and Molecular Biology, USC/Norris Comprehensive Cancer Center, Keck School of Medicine, Los Angeles, California 90089, USA [2] Will Rogers Institute Pulmonary Research Center, Division of Pulmonary, Critical Care and Sleep Medicine, USC Keck School of Medicine, Los Angeles, California 90089, USA. Y1 - 2014/02/27/ PY - 2014 DA - 2014 Feb 27 SP - 3365 VL - 5 KW - Index Medicus KW - Polymorphism, Single Nucleotide KW - Kidney -- metabolism KW - Humans KW - European Continental Ancestry Group -- genetics KW - Epistasis, Genetic KW - Lung Neoplasms -- ethnology KW - Genome-Wide Association Study KW - Genotype KW - Genetic Predisposition to Disease -- ethnology KW - Genetic Predisposition to Disease -- genetics KW - Risk Factors KW - CpG Islands -- genetics KW - Lung Neoplasms -- genetics KW - Promoter Regions, Genetic -- genetics KW - Breast -- metabolism KW - Genetic Variation KW - DNA Methylation KW - Quantitative Trait Loci -- genetics KW - Lung -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1503551301?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=Characterizing+the+genetic+basis+of+methylome+diversity+in+histologically+normal+human+lung+tissue.&rft.au=Shi%2C+Jianxin%3BMarconett%2C+Crystal+N%3BDuan%2C+Jubao%3BHyland%2C+Paula+L%3BLi%2C+Peng%3BWang%2C+Zhaoming%3BWheeler%2C+William%3BZhou%2C+Beiyun%3BCampan%2C+Mihaela%3BLee%2C+Diane+S%3BHuang%2C+Jing%3BZhou%2C+Weiyin%3BTriche%2C+Tim%3BAmundadottir%2C+Laufey%3BWarner%2C+Andrew%3BHutchinson%2C+Amy%3BChen%2C+Po-Han%3BChung%2C+Brian+S+I%3BPesatori%2C+Angela+C%3BConsonni%2C+Dario%3BBertazzi%2C+Pier+Alberto%3BBergen%2C+Andrew+W%3BFreedman%2C+Mathew%3BSiegmund%2C+Kimberly+D%3BBerman%2C+Benjamin+P%3BBorok%2C+Zea%3BChatterjee%2C+Nilanjan%3BTucker%2C+Margaret+A%3BCaporaso%2C+Neil+E%3BChanock%2C+Stephen+J%3BLaird-Offringa%2C+Ite+A%3BLandi%2C+Maria+Teresa&rft.aulast=Shi&rft.aufirst=Jianxin&rft.date=2014-02-27&rft.volume=5&rft.issue=&rft.spage=3365&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms4365 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-03 N1 - Date created - 2014-02-27 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - PHS000093; dbGaP; GSE52401 N1 - SuppNotes - Cited By: Nat Genet. 2011 Jul;43(7):630-8 [21685913] Biometrics. 1999 Dec;55(4):997-1004 [11315092] Nature. 2011 Nov 3;479(7371):74-9 [21964334] Nat Genet. 2012 May;44(5):502-10 [22446964] Cancer Discov. 2012 Feb;2(2):131-9 [22585858] Nat Rev Genet. 2012 Jul;13(7):484-92 [22641018] Genome Biol. 2012;13(1):R7 [22293038] Vital Health Stat 10. 2012 Jan;(252):1-207 [22834228] Genome Res. 2012 Sep;22(9):1680-8 [22955980] Nature. 2012 Sep 6;489(7414):75-82 [22955617] Science. 2012 Sep 7;337(6099):1190-5 [22955828] Nat Genet. 2012 Oct;44(10):1084-9 [22941192] PLoS Genet. 2012 Sep;8(9):e1002956 [23028363] Hum Mol Genet. 2012 Nov 15;21(22):4980-95 [22899653] J Biol Chem. 2012 Nov 16;287(47):40003-11 [23027861] Nat Rev Genet. 2013 Jan;14(1):62-75 [23247436] Int J Cancer. 2013 Apr 15;132(8):1811-20 [23011884] PLoS One. 2013;8(2):e55923 [23431366] Mol Cell. 2013 Mar 7;49(5):783-94 [23473599] Cell. 2013 Mar 28;153(1):38-55 [23540689] Nucleic Acids Res. 2013 Apr;41(7):e90 [23476028] PLoS Genet. 2013 May;9(5):e1003486 [23671422] Carcinogenesis. 2013 Jun;34(6):1281-5 [23430818] PLoS Genet. 2013 Jun;9(6):e1003513 [23818859] Nature. 2013 Aug 22;500(7463):415-21 [23945592] Am J Hum Genet. 2013 Nov 7;93(5):876-90 [24183450] Genome Biol. 2012;13(10):R84 [23034185] BMC Public Health. 2008;8:203 [18538025] Nature. 2008 Oct 23;455(7216):1061-8 [18772890] J Biol Chem. 2000 Sep 22;275(38):29915-21 [10906122] Am J Hum Genet. 2010 Mar 12;86(3):411-9 [20215007] Genome Biol. 2003;4(5):P3 [12734009] Science. 1990 Sep 14;249(4974):1288-90 [1697983] Trends Genet. 1997 Aug;13(8):335-40 [9260521] Cell. 1999 Aug 6;98(3):387-96 [10458613] EMBO J. 2005 Jan 26;24(2):336-46 [15616584] Mol Biol Evol. 2006 May;23(5):1068-75 [16510556] Hum Mol Genet. 2007 Mar 1;16(5):547-54 [17339271] Nucleic Acids Res. 2008 Jan;36(Database issue):D83-7 [17981843] Nature. 2008 Apr 3;452(7187):633-7 [18385738] Nature. 2008 Apr 3;452(7187):638-42 [18385739] Nat Genet. 2008 May;40(5):616-22 [18385676] PLoS Genet. 2010 May;6(5):e1000952 [20485568] Nature. 2010 Jul 8;466(7303):253-7 [20613842] Nature. 2010 Sep 23;467(7314):460-4 [20827270] Nature. 2010 Oct 28;467(7319):1061-73 [20981092] Nat Rev Genet. 2011 Apr;12(4):277-82 [21386863] PLoS Biol. 2011 Apr;9(4):e1001046 [21526222] Nat Genet. 2011 Jun;43(6):561-4 [21572415] Nat Genet. 2011 Jun;43(6):513-8 [21614091] Nat Genet. 2008 Dec;40(12):1407-9 [18978787] Nat Genet. 2008 Dec;40(12):1404-6 [18978790] Nat Genet. 2009 Feb;41(2):178-86 [19151715] Nat Genet. 2009 Feb;41(2):240-5 [19151718] PLoS Genet. 2009 Jun;5(6):e1000529 [19543373] Cell. 2009 Jun 26;137(7):1194-211 [19563753] Am J Hum Genet. 2009 Nov;85(5):679-91 [19836008] Nature. 2010 Jan 14;463(7278):184-90 [20016488] Cold Spring Harb Perspect Biol. 2010 Jan;2(1):a001008 [20182602] Genome Res. 2010 Mar;20(3):320-31 [20133333] Genome Biol. 2011;12(1):R10 [21251332] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncomms4365 ER - TY - JOUR T1 - The immunological and clinical effects of mutated ras peptide vaccine in combination with IL-2, GM-CSF, or both in patients with solid tumors. AN - 1504452341; 24565030 AB - Mutant Ras oncogenes produce proteins that are unique to cancer cells and represent attractive targets for vaccine therapy. We have shown previously that vaccinating cancer patients with mutant ras peptides is feasible and capable of inducing a specific immune response against the relevant mutant proteins. Here, we tested the mutant ras peptide vaccine administered in combination with low dose interleukin-2 (IL-2) or/and granulocyte-macrophage colony-stimulating factor (GM-CSF) in order to enhance the vaccine immune response. 5000 μg of the corresponding mutant ras peptide was given subcutaneously (SQ) along with IL-2 (Arm A), GM-CSF (Arm B) or both (Arm C). IL-2 was given SQ at 6.0 million IU/m²/day starting at day 5, 5 days/week for 2 weeks. GM-CSF was given SQ in a dose of 100 μg/day one day prior to each ras peptide vaccination for 4 days. Vaccines were repeated every 5 weeks on arm A and C, and every 4 weeks on arm B, for a maximum of 15 cycles or until disease progression. We treated 53 advanced cancer patients (38 with colorectal, 11 with pancreatic, 1 with common bile duct and 3 with lung) on 3 different arms (16 on arm A, 18 on arm B, and 19 on arm C). The median progression free survival (PFS) and overall survival (OS) was 3.6 and 16.9 months, respectively, for all patients evaluable for clinical response (n = 48). There was no difference in PFS or OS between the three arms (P = 0.73 and 0.99, respectively). Most adverse events were grade 1-2 toxicities and resolved spontaneously. The vaccine induced an immune response to the relevant ras peptide in a total of 20 out of 37 evaluable patients (54%) by ELISPOT, proliferative assay, or both. While 92.3% of patients on arm B had a positive immune response, only 31% of patients on arm A and 36% of patients on arm C had positive immune responses (P = 0.003, Fisher's exact test). The reported data showed that IL-2 might have a negative effect on the specific immune response induced by the relevant mutant ras vaccine in patients with advanced cancer. This observation deserves further investigations. NCI97C0141. JF - Journal of translational medicine AU - Rahma, Osama E AU - Hamilton, J Michael AU - Wojtowicz, Malgorzata AU - Dakheel, Omar AU - Bernstein, Sarah AU - Liewehr, David J AU - Steinberg, Seth M AU - Khleif, Samir N AD - Cancer Vaccine Branch, CCR, NCI, 10 Center Drive, Bethesda, MD 20892, USA. skhleif@gru.edu. Y1 - 2014/02/24/ PY - 2014 DA - 2014 Feb 24 SP - 55 VL - 12 KW - Cancer Vaccines KW - 0 KW - Interleukin-2 KW - Vaccines, Subunit KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - ras Proteins KW - EC 3.6.5.2 KW - Index Medicus KW - Immunity -- immunology KW - Humans KW - Enzyme-Linked Immunospot Assay KW - Adult KW - Treatment Outcome KW - Molecular Sequence Data KW - Aged KW - Middle Aged KW - Amino Acid Sequence KW - T-Lymphocytes, Regulatory -- immunology KW - ras Proteins -- genetics KW - Neoplasms -- drug therapy KW - Cancer Vaccines -- adverse effects KW - Vaccines, Subunit -- therapeutic use KW - Vaccines, Subunit -- chemistry KW - Interleukin-2 -- therapeutic use KW - Cancer Vaccines -- therapeutic use KW - Neoplasms -- prevention & control KW - Granulocyte-Macrophage Colony-Stimulating Factor -- therapeutic use KW - Vaccines, Subunit -- adverse effects KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504452341?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+translational+medicine&rft.atitle=The+immunological+and+clinical+effects+of+mutated+ras+peptide+vaccine+in+combination+with+IL-2%2C+GM-CSF%2C+or+both+in+patients+with+solid+tumors.&rft.au=Rahma%2C+Osama+E%3BHamilton%2C+J+Michael%3BWojtowicz%2C+Malgorzata%3BDakheel%2C+Omar%3BBernstein%2C+Sarah%3BLiewehr%2C+David+J%3BSteinberg%2C+Seth+M%3BKhleif%2C+Samir+N&rft.aulast=Rahma&rft.aufirst=Osama&rft.date=2014-02-24&rft.volume=12&rft.issue=&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Journal+of+translational+medicine&rft.issn=1479-5876&rft_id=info:doi/10.1186%2F1479-5876-12-55 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-05 N1 - Date created - 2014-03-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Cancer Res. 2009 Feb 15;15(4):1443-51 [19228745] Cancer Immunol Immunother. 2012 Mar;61(3):373-84 [21927947] Clin Cancer Res. 2009 Dec 1;15(23):7412-20 [19934295] Curr Med Chem. 2010;17(29):3297-302 [20712575] J Exp Med. 1999 Nov 1;190(9):1297-308 [10544201] Int J Cancer. 2001 May 1;92(3):441-50 [11291084] Exp Dermatol. 2001 Jun;10(3):161-7 [11380611] Cancer. 2003 Jan 1;97(1):186-200 [12491520] Nat Rev Cancer. 2003 Jun;3(6):459-65 [12778136] Br J Cancer. 2004 Feb 23;90(4):773-80 [14970852] Nature. 1982 Nov 11;300(5888):149-52 [7133135] Cancer Res. 1989 Sep 1;49(17):4682-9 [2547513] N Engl J Med. 1990 Aug 30;323(9):561-5 [2199829] Cell. 1991 Feb 22;64(4):767-76 [1847667] Nature. 1991 Sep 26;353(6342):326-9 [1922338] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3539-43 [8097319] Am J Pathol. 1993 Aug;143(2):545-54 [8342602] Int J Cancer. 1996 Feb 8;65(4):450-3 [8621226] Blood. 1996 Jul 1;88(1):202-10 [8704175] Nat Med. 1998 Mar;4(3):321-7 [9500606] Cell Immunol. 1997 Dec 15;182(2):137-51 [9514698] J Immunother. 1999 Mar;22(2):155-65 [10093040] J Clin Oncol. 2005 Aug 1;23(22):5099-107 [15983396] J Clin Oncol. 2007 Apr 20;25(12):1539-44 [17442997] Vaccine. 2007 Aug 1;25(31):5882-91 [17602804] Lung Cancer. 2007 Oct;58(1):88-94 [17599645] Cancer Immunol Immunother. 2008 Sep;57(9):1413-20 [18297281] J Clin Oncol. 2008 Oct 20;26(30):4973-80 [18809608] Clin Cancer Res. 2011 Feb 15;17(4):907-17 [21106727] Cancer Immunol Immunother. 2011 Mar;60(3):433-42 [21221967] Genes Chromosomes Cancer. 2011 May;50(5):307-12 [21305640] Int J Oncol. 2009 Sep;35(3):569-81 [19639177] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/1479-5876-12-55 ER - TY - JOUR T1 - Association between Maternal Serum Perfluoroalkyl Substances during Pregnancy and Maternal and Cord Thyroid Hormones: Taiwan Maternal and Infant Cohort Study AN - 1534851235; 20047042 AB - Background: Perfluoroalkyl substances (PFASs) are synthetic compounds that are widely used in industry and are often detectable in humans. In pregnant rats and their pups, PFASs can interfere with thyroid hormone homeostasis. In humans, maternal thyroid hormones supply the fetus throughout pregnancy, and thyroid hormones play a critical role in fetal growth and neurodevelopment. Objectives: We investigated the association between maternal PFAS exposure and thyroid hormone status in pregnant women and neonates. Methods: In a study of environmental exposure and health in Taiwan, we measured serum concentrations of nine PFASs and four thyroid hormones for 285 pregnant women in their third trimester, and also measured cord serum thyroid hormones for 116 neonates. Associations between maternal PFASs and maternal and cord thyroid hormones were examined in multiple linear regression models. Results: Perfluorohexanesulfonic acid concentrations were positively associated with maternal thyroid-stimulating hormone (TSH) levels. Pregnant women with higher levels of perfluorononanoic acid (PFNA), perfluoroundecanoic acid (PFUnDA), and perfluorododecanoic acid (PFDoDA) had lower free thyroxine (T4) and total T4 levels. For example, we estimated that maternal free T4 levels decreased 0.019 ng/dL (95% CI: -0.028, -0.009) with each nanogram per milliliter increase in maternal PFNA. Finally, maternal PFNA, PFUnDA, and PFDoDA levels were associated with lower cord total triiodothyronine (T3) and total T4 levels, and maternal perfluorodecanoic acid (PFDeA) was associated with lower cord total T3. Conclusions: Our results suggest that exposure to some PFASs during pregnancy may interfere with thyroid hormone homeostasis in pregnant women and fetuses. Citation: Wang Y, Rogan WJ, Chen PC, Lien GW, Chen HY, Tseng YC, Longnecker MP, Wang SL. 2014. Association between maternal serum perfluoroalkyl substances during pregnancy and maternal and cord thyroid hormones: Taiwan Maternal and Infant Cohort Study. Environ Health Perspect 122:529-534; http://dx.doi.org/10.1289/ehp.1306925 JF - Environmental Health Perspectives AU - Wang, Yan AU - Rogan, Walter J AU - Chen, Pau-Chung AU - Lien, Guang-Wen AU - Chen, Hsiao-Yen AU - Tseng, Ying-Chih AU - Longnecker, Matthew P AU - Wang, Shu-Li 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 - 2014/02/21/ PY - 2014 DA - 2014 Feb 21 SP - 529 EP - 534 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 122 IS - 5 SN - 0091-6765, 0091-6765 KW - Environment Abstracts; Health & Safety Science Abstracts KW - Rats KW - Taiwan KW - Thyroid KW - Neonates KW - Hormones KW - Fetuses KW - Pregnancy KW - Infants KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534851235?accountid=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=Association+between+Maternal+Serum+Perfluoroalkyl+Substances+during+Pregnancy+and+Maternal+and+Cord+Thyroid+Hormones%3A+Taiwan+Maternal+and+Infant+Cohort+Study&rft.au=Wang%2C+Yan%3BRogan%2C+Walter+J%3BChen%2C+Pau-Chung%3BLien%2C+Guang-Wen%3BChen%2C+Hsiao-Yen%3BTseng%2C+Ying-Chih%3BLongnecker%2C+Matthew+P%3BWang%2C+Shu-Li&rft.aulast=Wang&rft.aufirst=Yan&rft.date=2014-02-21&rft.volume=122&rft.issue=5&rft.spage=529&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1306925 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Rats; Thyroid; Neonates; Hormones; Fetuses; Infants; Pregnancy; Taiwan DO - http://dx.doi.org/10.1289/ehp.1306925 ER - TY - JOUR T1 - Introduction to thematic minireview series: Development of human therapeutics based on induced pluripotent stem cell (iPSC) technology. AN - 1501835497; 24362035 AB - With the advent of human induced pluripotent stem cell (hiPSC) technology, it is now possible to derive patient-specific cell lines that are of great potential in both basic research and the development of new therapeutics for human diseases. Not only do hiPSCs offer unprecedented opportunities to study cellular differentiation and model human diseases, but the differentiated cell types obtained from iPSCs may become therapeutics themselves. These cells can also be used in the screening of therapeutics and in toxicology assays for potential liabilities of therapeutic agents. The remarkable achievement of transcription factor reprogramming to generate iPSCs was recognized by the award of the Nobel Prize in Medicine to Shinya Yamanaka in 2012, just 6 years after the first publication of reprogramming methods to generate hiPSCs (Takahashi, K., Tanabe, K., Ohnuki, M., Narita, M., Ichisaka, T., Tomoda, K., and Yamanaka, S. (2007) Cell 131, 861-872). This minireview series highlights both the promises and challenges of using iPSC technology for disease modeling, drug screening, and the development of stem cell therapeutics. JF - The Journal of biological chemistry AU - Rao, Mahendra AU - Gottesfeld, Joel M AD - From the Center for Regenerative Medicine, National Institutes of Health, Bethesda, Maryland 20892 and. Y1 - 2014/02/21/ PY - 2014 DA - 2014 Feb 21 SP - 4553 EP - 4554 VL - 289 IS - 8 KW - Index Medicus KW - Genomic Instability KW - Immunogenicity KW - Gene Correction KW - Stem Cells KW - Regenerative Medicine KW - Toxicology KW - Induced Pluripotent Stem Cells KW - Humans KW - Drug Evaluation, Preclinical KW - Induced Pluripotent Stem Cells -- cytology KW - Stem Cell Transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1501835497?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Introduction+to+thematic+minireview+series%3A+Development+of+human+therapeutics+based+on+induced+pluripotent+stem+cell+%28iPSC%29+technology.&rft.au=Rao%2C+Mahendra%3BGottesfeld%2C+Joel+M&rft.aulast=Rao&rft.aufirst=Mahendra&rft.date=2014-02-21&rft.volume=289&rft.issue=8&rft.spage=4553&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.R113.543652 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-22 N1 - Date created - 2014-02-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2014 Feb 21;289(8):4585-93 [24362021] J Biol Chem. 2014 Feb 21;289(8):4555-61 [24362027] J Biol Chem. 2014 Feb 21;289(8):4578-84 [24362040] J Biol Chem. 2014 Feb 21;289(8):4562-70 [24362033] J Biol Chem. 2014 Feb 21;289(8):4571-7 [24362036] J Biol Chem. 2014 Feb 21;289(8):4594-9 [24362028] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.R113.543652 ER - TY - JOUR T1 - International Myeloma Working Group consensus statement for the management, treatment, and supportive care of patients with myeloma not eligible for standard autologous stem-cell transplantation. AN - 1499148888; 24419113 AB - To provide an update on recent advances in the management of patients with multiple myeloma who are not eligible for autologous stem-cell transplantation. A comprehensive review of the literature on diagnostic criteria is provided, and treatment options and management of adverse events are summarized. Patients with symptomatic disease and organ damage (ie, hypercalcemia, renal failure, anemia, or bone lesions) require immediate treatment. The International Staging System and chromosomal abnormalities identify high- and standard-risk patients. Proteasome inhibitors, immunomodulatory drugs, corticosteroids, and alkylating agents are the most active agents. The presence of concomitant diseases, frailty, or disability should be assessed and, if present, treated with reduced-dose approaches. Bone disease, renal damage, hematologic toxicities, infections, thromboembolism, and peripheral neuropathy are the most frequent disabling events requiring prompt and active supportive care. These recommendations will help clinicians ensure the most appropriate care for patients with myeloma in everyday clinical practice. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Palumbo, Antonio AU - Rajkumar, S Vincent AU - San Miguel, Jesus F AU - Larocca, Alessandra AU - Niesvizky, Ruben AU - Morgan, Gareth AU - Landgren, Ola AU - Hajek, Roman AU - Einsele, Hermann AU - Anderson, Kenneth C AU - Dimopoulos, Meletios A AU - Richardson, Paul G AU - Cavo, Michele AU - Spencer, Andrew AU - Stewart, A Keith AU - Shimizu, Kazuyuki AU - Lonial, Sagar AU - Sonneveld, Pieter AU - Durie, Brian G M AU - Moreau, Philippe AU - Orlowski, Robert Z AD - Antonio Palumbo and Alessandra Larocca, University of Torino, Torino; Michele Cavo, Seràgnoli Institute of Hematology, Bologna University School of Medicine, Bologna, Italy; S. Vincent Rajkumar, Mayo Clinic, Rochester, MN; Jesus F. San Miguel, University Hospital of Salamanca, Salamanca, Spain; Ruben Niesvizky, Weill Cornell Medical College, New York, NY; Gareth Morgan, Royal Marsden Hospital, London, United Kingdom; Ola Landgren, National Cancer Institute, Bethesda, MD; Roman Hajek, University of Ostrava School of Medicine and University Hospital Ostrava, Ostrava, Czech Republic; Hermann Einsele, University of Wurzburg, Wurzburg, Germany; Kenneth C. Anderson and Paul G. Richardson, Dana-Farber Cancer Institute, Boston, MA; Meletios A. Dimopoulos, University of Athens School of Medicine, Athens, Greece; Andrew Spencer, Alfred Hospital, Melbourne, Victoria, Australia; A. Keith Stewart, Mayo Clinic, Scottsdale, AZ; Kazuyuki Shimizu, Aichi Gakuin Hospital, Nagoya, Japan; Sagar Lonial, Emory University, Atlanta, GA; Pieter Sonneveld, Erasmus Medical Centre, Rotterdam, the Netherlands; Brian G.M. Durie, Cedars-Sinai Comprehensive Cancer Center, Los Angeles, CA; Philippe Moreau, University Hospital, Nantes, France; and Robert Z. Orlowski, MD Anderson Cancer Center, Houston, TX. Y1 - 2014/02/20/ PY - 2014 DA - 2014 Feb 20 SP - 587 EP - 600 VL - 32 IS - 6 KW - Index Medicus KW - Humans KW - Prognosis KW - Hematopoietic Stem Cell Transplantation KW - Palliative Care KW - Multiple Myeloma -- diagnosis KW - Multiple Myeloma -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499148888?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=International+Myeloma+Working+Group+consensus+statement+for+the+management%2C+treatment%2C+and+supportive+care+of+patients+with+myeloma+not+eligible+for+standard+autologous+stem-cell+transplantation.&rft.au=Palumbo%2C+Antonio%3BRajkumar%2C+S+Vincent%3BSan+Miguel%2C+Jesus+F%3BLarocca%2C+Alessandra%3BNiesvizky%2C+Ruben%3BMorgan%2C+Gareth%3BLandgren%2C+Ola%3BHajek%2C+Roman%3BEinsele%2C+Hermann%3BAnderson%2C+Kenneth+C%3BDimopoulos%2C+Meletios+A%3BRichardson%2C+Paul+G%3BCavo%2C+Michele%3BSpencer%2C+Andrew%3BStewart%2C+A+Keith%3BShimizu%2C+Kazuyuki%3BLonial%2C+Sagar%3BSonneveld%2C+Pieter%3BDurie%2C+Brian+G+M%3BMoreau%2C+Philippe%3BOrlowski%2C+Robert+Z&rft.aulast=Palumbo&rft.aufirst=Antonio&rft.date=2014-02-20&rft.volume=32&rft.issue=6&rft.spage=587&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2013.48.7934 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-14 N1 - Date created - 2014-02-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Haematologica. 2013 Jan;98(1):87-94 [22875621] Am J Health Syst Pharm. 2001 Nov 15;58 Suppl 3:S16-20 [11757204] Lancet. 2003 Feb 8;361(9356):489-91 [12583950] Cancer. 2003 Oct 15;98(8):1735-44 [14534891] J Pharm Pharmacol. 2003 Dec;55(12):1701-6 [14738599] BMJ. 2004 Jun 19;328(7454):1490 [15205295] Eur J Haematol. 2004 Aug;73(2):98-103 [15245508] J Clin Oncol. 2004 Jul 15;22(14):2909-17 [15254060] Cancer. 2004 Aug 1;101(3):558-66 [15274069] Expert Opin Drug Saf. 2004 Nov;3(6):535-46 [15500413] N Engl J Med. 2004 Oct 28;351(18):1860-73 [15509819] J Chronic Dis. 1987;40(5):373-83 [3558716] Blood. 1992 Aug 15;80(4):887-90 [1498331] Br J Haematol. 1998 Sep;102(5):1115-23 [9753033] Blood. 2004 Nov 15;104(10):3052-7 [15265788] Cancer. 2005 Mar 15;103(6):1195-200 [15690325] J Clin Oncol. 2005 May 20;23(15):3412-20 [15809451] N Engl J Med. 2005 Jun 16;352(24):2487-98 [15958804] Ann Oncol. 2005 Aug;16(8):1223-31 [15928069] J Clin Oncol. 2005 Dec 20;23(36):9219-26 [16275935] J Clin Oncol. 2006 Jan 20;24(3):431-6 [16365178] Lancet. 2006 Mar 11;367(9513):825-31 [16530576] Blood. 2006 Jul 1;108(1):403; author reply 404 [16790586] J Clin Oncol. 2006 Jul 1;24(19):3113-20 [16754936] Mayo Clin Proc. 2006 Aug;81(8):1047-53 [16901028] Leukemia. 2006 Sep;20(9):1467-73 [16855634] Eur J Haematol. 2006 Nov;77(5):378-86 [17044835] Blood. 2006 Nov 15;108(10):3458-64 [16840727] Leuk Lymphoma. 2006 Nov;47(11):2276-9 [17107897] Haematologica. 2007 Jan;92(1):50-5 [17229635] Blood. 2007 Mar 15;109(6):2276-84 [17105813] Blood. 2007 Apr 15;109(8):3177-88 [17185464] J Clin Oncol. 2007 Jun 10;25(17):2464-72 [17515569] J Pain Symptom Manage. 2007 Aug;34(2):183-9 [17604592] J Clin Oncol. 2007 Sep 1;25(25):3892-901 [17679727] Lancet. 2007 Oct 6;370(9594):1209-18 [17920916] N Engl J Med. 2007 Nov 22;357(21):2123-32 [18032762] N Engl J Med. 2007 Nov 22;357(21):2133-42 [18032763] Leukemia. 2008 Feb;22(2):414-23 [18094721] Leukemia. 2008 Apr;22(4):842-9 [18200040] J Clin Oncol. 2008 May 1;26(13):2171-7 [18362366] Curr Opin Support Palliat Care. 2007 Apr;1(1):3-5 [18660716] N Engl J Med. 2008 Aug 28;359(9):906-17 [18753647] Leukemia. 2008 Oct;22(10):1933-7 [18596742] Blood. 2008 Dec 1;112(12):4445-51 [18799726] Pain. 2009 Jan;141(1-2):19-24 [19013718] Leukemia. 2013 Mar;27(3):711-7 [23032723] Leukemia. 2009 Jan;23(1):3-9 [18971951] Leukemia. 2009 Feb;23(2):215-24 [19020545] Blood. 2009 Apr 9;113(15):3435-42 [18955563] Cochrane Database Syst Rev. 2009;(3):CD007303 [19588423] Leukemia. 2009 Jul;23(7):1337-41 [19225538] J Clin Oncol. 2009 Aug 1;27(22):3664-70 [19451428] Ann Oncol. 2009 Aug;20(8):1303-17 [19465418] Clin Infect Dis. 2009 Oct 15;49(8):1211-25 [19769539] Leukemia. 2009 Oct;23(10):1716-30 [19494840] Leukemia. 2009 Dec;23(12):2210-21 [19798094] J Clin Oncol. 2009 Dec 20;27(36):6086-93 [19858394] Lancet Oncol. 2010 Jan;11(1):29-37 [19853510] J Clin Oncol. 2010 Feb 10;28(5):800-7 [20048187] Blood. 2010 Apr 22;115(16):3416-7 [20413666] Nat Rev Clin Oncol. 2010 May;7(5):289-94 [20351701] J Clin Oncol. 2010 May 1;28(13):2259-66 [20368561] Lancet. 2010 May 15;375(9727):1721-8 [20472173] J Clin Oncol. 2010 Jul 1;28(19):3160-6 [20516439] Blood. 2010 Aug 5;116(5):679-86 [20385792] Cancer. 2010 Aug 15;116(16):3807-14 [20564094] Haematologica. 2010 Sep;95(9):1548-54 [20418244] Blood. 2010 Sep 2;116(9):1405-12 [20448107] Lancet Oncol. 2010 Oct;11(10):934-41 [20739218] Lancet Oncol. 2010 Oct;11(10):973-82 [20863761] Leukemia. 2010 Oct;24(10):1769-78 [20739955] J Clin Oncol. 2010 Nov 20;28(33):4976-84 [20956629] J Clin Oncol. 2010 Nov 20;28(33):4996-5010 [20975064] J Clin Oncol. 2010 Dec 1;28(34):5101-9 [20940200] Blood. 2010 Dec 2;116(23):4745-53 [20807892] Lancet. 2010 Dec 11;376(9757):1989-99 [21131037] Eur J Haematol. 2011 Jan;86(1):16-22 [20942865] Blood Rev. 2011 Mar;25(2):65-73 [21295387] J Clin Oncol. 2011 Mar 10;29(8):986-93 [21282540] Blood. 2011 Mar 17;117(11):3025-31 [21228328] Lancet Oncol. 2011 May;12(5):431-40 [21507715] Blood. 2011 May 5;117(18):4691-5 [21292775] Blood. 2011 May 5;117(18):4696-700 [21292777] Blood. 2011 May 5;117(18):4701-5 [21292778] Br J Haematol. 2011 Jul;154(1):76-103 [21517805] Br J Haematol. 2011 Jul;154(1):32-75 [21569004] Blood. 2011 Jun 9;117(23):6063-73 [21447828] Blood. 2011 Jul 21;118(3):529-34 [21482708] Lancet Oncol. 2011 Aug;12(8):743-52 [21771568] N Engl J Med. 2011 Aug 4;365(5):474-5 [21812699] Blood. 2011 Aug 4;118(5):1231-8 [21652683] Blood. 2011 Aug 4;118(5):1239-47 [21670471] Blood. 2011 Oct 27;118(17):4519-29 [21841166] Blood. 2011 Nov 24;118(22):5759-66 [21951682] Blood. 2011 Dec 1;118(23):5989-95 [21900189] Am J Hematol. 2012 Jan;87(1):78-88 [22180161] Blood. 2012 Jan 5;119(1):7-15 [22021371] Leukemia. 2012 Jan;26(1):149-57 [21799510] Leukemia. 2012 Jan;26(1):73-85 [22024721] Blood. 2012 Jan 26;119(4):933-9; quiz 1093 [21835953] Chest. 2012 Feb;141(2 Suppl):e419S-94S [22315268] Clin Lymphoma Myeloma Leuk. 2012 Feb;12(1):5-11 [22178143] Blood. 2012 Mar 29;119(13):3003-15 [22271445] Leukemia. 2012 Apr;26(4):595-608 [22193964] N Engl J Med. 2012 May 10;366(19):1759-69 [22571200] Leuk Lymphoma. 2012 Jul;53(7):1318-20 [22211836] Haematologica. 2012 Aug;97(8):1272-7 [22371180] Blood. 2012 Sep 27;120(13):2581-8 [22889759] Blood. 2012 Oct 4;120(14):2817-25 [22833546] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2013.48.7934 ER - TY - JOUR T1 - Nomogram to predict cycle-one serious drug-related toxicity in phase I oncology trials. AN - 1499146793; 24419130 AB - All patients in phase I trials do not have equivalent susceptibility to serious drug-related toxicity (SDRT). Our goal was to develop a nomogram to predict the risk of cycle-one SDRT to better select appropriate patients for phase I trials. The prospectively maintained database of patients with solid tumor enrolled onto Cancer Therapeutics Evaluation Program-sponsored phase I trials activated between 2000 and 2010 was used. SDRT was defined as a grade ≥ 4 hematologic or grade ≥ 3 nonhematologic toxicity attributed, at least possibly, to study drug(s). Logistic regression was used to test the association of candidate factors to cycle-one SDRT. A final model, or nomogram, was chosen based on both clinical and statistical significance and validated internally using a bootstrapping technique and externally in an independent data set. Data from 3,104 patients enrolled onto 127 trials were analyzed to build the nomogram. In a model with multiple covariates, Eastern Cooperative Oncology Group performance status, WBC count, creatinine clearance, albumin, AST, number of study drugs, biologic study drug (yes v no), and dose (relative to maximum administered) were significant predictors of cycle-one SDRT. All significant factors except dose were included in the final nomogram. The model was validated both internally (bootstrap-adjusted concordance index, 0.60) and externally (concordance index, 0.64). This nomogram can be used to accurately predict a patient's risk for SDRT at the time of enrollment. Excluding patients at high risk for SDRT should improve the safety and efficiency of phase I trials. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Hyman, David M AU - Eaton, Anne A AU - Gounder, Mrinal M AU - Smith, Gary L AU - Pamer, Erika G AU - Hensley, Martee L AU - Spriggs, David R AU - Ivy, Percy AU - Iasonos, Alexia AD - David M. Hyman, Anne A. Eaton, Mrinal M. Gounder, Erika G. Pamer, Martee L. Hensley, David R. Spriggs, and Alexia Iasonos, Memorial Sloan-Kettering Cancer Center; David M. Hyman, Mrinal M. Gounder, Martee L. Hensley, David R. Spriggs, and Alexia Iasonos, Weill Cornell Medical College, New York, NY; and Gary L. Smith and Percy Ivy, National Cancer Institute, Bethesda, MD. Y1 - 2014/02/20/ PY - 2014 DA - 2014 Feb 20 SP - 519 EP - 526 VL - 32 IS - 6 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Young Adult KW - Prospective Studies KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Cohort Studies KW - Adult KW - Treatment Outcome KW - Prognosis KW - Databases, Factual KW - Aged KW - Middle Aged KW - Adolescent KW - Clinical Trials, Phase I as Topic -- methods KW - Clinical Trials, Phase I as Topic -- statistics & numerical data KW - Antineoplastic Agents -- administration & dosage KW - Nomograms KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499146793?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Nomogram+to+predict+cycle-one+serious+drug-related+toxicity+in+phase+I+oncology+trials.&rft.au=Hyman%2C+David+M%3BEaton%2C+Anne+A%3BGounder%2C+Mrinal+M%3BSmith%2C+Gary+L%3BPamer%2C+Erika+G%3BHensley%2C+Martee+L%3BSpriggs%2C+David+R%3BIvy%2C+Percy%3BIasonos%2C+Alexia&rft.aulast=Hyman&rft.aufirst=David&rft.date=2014-02-20&rft.volume=32&rft.issue=6&rft.spage=519&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2013.49.8808 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-14 N1 - Date created - 2014-02-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Eur J Cancer. 2008 Jul;44(11):1536-40 [18550361] Ann Oncol. 2012 Aug;23(8):1968-73 [22408187] Ann Oncol. 2012 Aug;23(8):1963-7 [22377564] Crit Rev Oncol Hematol. 2012 Aug;83(2):242-8 [22226569] Ann N Y Acad Sci. 2001 Dec;949:333-40 [11795372] Stat Med. 1996 Feb 28;15(4):361-87 [8668867] BMC Cancer. 2006;6:263 [17092349] J Clin Oncol. 2008 Mar 10;26(8):1364-70 [18323559] Eur J Cancer. 2008 May;44(7):978-82 [18362066] Br J Cancer. 2012 Sep 25;107(7):1025-30 [22910320] J Clin Oncol. 2009 Jun 1;27(16):2692-6 [19332724] Clin Cancer Res. 2010 Mar 15;16(6):1726-36 [20215542] Clin Cancer Res. 2010 Mar 15;16(6):1737-44 [20215555] Cancer. 2012 Mar 1;118(5):1422-8 [21823111] J Clin Oncol. 2012 Mar 20;30(9):996-1004 [22355064] Comment In: J Clin Oncol. 2014 Oct 1;32(28):3200 [25071106] J Clin Oncol. 2014 Feb 20;32(6):489-90 [24419111] J Clin Oncol. 2014 Oct 1;32(28):3199-200 [25071117] J Clin Oncol. 2014 Oct 1;32(28):3198-9 [25071142] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2013.49.8808 ER - TY - JOUR T1 - Microbial release from seeded beach sediments during wave conditions AN - 1656033858; 2015-012657 AB - Beach sands can sustain indigenous and introduced populations of enterococci. The objective of this study was to evaluate wave action in promoting the release of introduced bacteria. To accomplish this objective this study developed a method to assess attachment and identified conditions under which introduced bacteria are integrated into the sand. A new "shearing assay" showed that attachment of the introduced spike mimicked that of the natural sand when the spike was allowed to integrate into the sand for 24 h at room temperature at a sand moisture content of 20%. Experiments in a wave flume showed that waves were capable of releasing about 60% of the total bacteria added. This suggests that for the range of wave conditions evaluated (height: 1.9-10.5 cm, period:1-2.7 s), waves were incapable of releasing all of the bacteria. Further study is needed to evaluate bacteria attachment mechanisms. Abstract Copyright (2014) Elsevier, B.V. JF - Marine Pollution Bulletin AU - Phillips, Matthew C AU - Feng, Zhixuan AU - Vogel, Laura J AU - Reniers, Ad J H M AU - Haus, Brian K AU - Enns, Amber A AU - Zhang, Yifan AU - Hernandez, David B AU - Solo-Gabriele, Helena M Y1 - 2014/02/15/ PY - 2014 DA - 2014 Feb 15 SP - 114 EP - 122 PB - Elsevier, Oxford VL - 79 IS - 1-2 SN - 0025-326X, 0025-326X KW - sand KW - experimental studies KW - clastic sediments KW - waves KW - statistical analysis KW - dye tracers KW - pollution KW - flume studies KW - laboratory studies KW - beaches KW - Enterococcus KW - bacteria KW - sediments KW - pore water KW - microorganisms KW - 22:Environmental geology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1656033858?accountid=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=Marine+Pollution+Bulletin&rft.atitle=Microbial+release+from+seeded+beach+sediments+during+wave+conditions&rft.au=Phillips%2C+Matthew+C%3BFeng%2C+Zhixuan%3BVogel%2C+Laura+J%3BReniers%2C+Ad+J+H+M%3BHaus%2C+Brian+K%3BEnns%2C+Amber+A%3BZhang%2C+Yifan%3BHernandez%2C+David+B%3BSolo-Gabriele%2C+Helena+M&rft.aulast=Phillips&rft.aufirst=Matthew&rft.date=2014-02-15&rft.volume=79&rft.issue=1-2&rft.spage=114&rft.isbn=&rft.btitle=&rft.title=Marine+Pollution+Bulletin&rft.issn=0025326X&rft_id=info:doi/10.1016%2Fj.marpolbul.2013.12.029 L2 - http://www.sciencedirect.com/science/journal/0025326X LA - English DB - GeoRef N1 - Copyright - GeoRef, Copyright 2015, American Geosciences Institute. Reference includes data from CAPCAS, Elsevier Scientific Publishers, Amsterdam, Netherlands N1 - Date revised - 2015-01-01 N1 - Number of references - 58 N1 - Document feature - illus. N1 - Last updated - 2015-02-19 N1 - CODEN - MPNBAZ N1 - SubjectsTermNotLitGenreText - bacteria; beaches; clastic sediments; dye tracers; Enterococcus; experimental studies; flume studies; laboratory studies; microorganisms; pollution; pore water; sand; sediments; statistical analysis; waves DO - http://dx.doi.org/10.1016/j.marpolbul.2013.12.029 ER - TY - JOUR T1 - HTS navigator: freely accessible cheminformatics software for analyzing high-throughput screening data AN - 1534819235; 19360551 AB - Summary: We report on the development of the high-throughput screening (HTS) Navigator software to analyze and visualize the results of HTS of chemical libraries. The HTS Navigator processes output files from different plate readers' formats, computes the overall HTS matrix, automatically detects hits and has different types of baseline navigation and correction features. The software incorporates advanced cheminformatics capabilities such as chemical structure storage and visualization, fast similarity search and chemical neighborhood analysis for retrieved hits. The software is freely available for academic laboratories. JF - Bioinformatics AU - Fourches, Denis AU - Sassano, Maria F AU - Roth, Bryan L AU - Tropsha, Alexander AD - super(1)Division of Chemical Biology and Medicinal Chemistry, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill and super(2)Department of Pharmacology and the NIMH Psychoactive Drug Screening Program, School of Medicine, University of North Carolina Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA Y1 - 2014/02/15/ PY - 2014 DA - 2014 Feb 15 SP - 588 EP - 589 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 30 IS - 4 SN - 1367-4803, 1367-4803 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Computer programs KW - software KW - Data processing KW - Informatics KW - high-throughput screening KW - Bioinformatics KW - Internet KW - N 14810:Methods KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534819235?accountid=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=HTS+navigator%3A+freely+accessible+cheminformatics+software+for+analyzing+high-throughput+screening+data&rft.au=Fourches%2C+Denis%3BSassano%2C+Maria+F%3BRoth%2C+Bryan+L%3BTropsha%2C+Alexander&rft.aulast=Fourches&rft.aufirst=Denis&rft.date=2014-02-15&rft.volume=30&rft.issue=4&rft.spage=588&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt718 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Computer programs; software; Data processing; Informatics; high-throughput screening; Bioinformatics; Internet DO - http://dx.doi.org/10.1093/bioinformatics/btt718 ER - TY - JOUR T1 - EGFRvIII mCAR-modified T-cell therapy cures mice with established intracerebral glioma and generates host immunity against tumor-antigen loss. AN - 1500701886; 24352643 AB - Chimeric antigen receptor (CAR) transduced T cells represent a promising immune therapy that has been shown to successfully treat cancers in mice and humans. However, CARs targeting antigens expressed in both tumors and normal tissues have led to significant toxicity. Preclinical studies have been limited by the use of xenograft models that do not adequately recapitulate the immune system of a clinically relevant host. A constitutively activated mutant of the naturally occurring epidermal growth factor receptor (EGFRvIII) is antigenically identical in both human and mouse glioma, but is also completely absent from any normal tissues. We developed a third-generation, EGFRvIII-specific murine CAR (mCAR), and performed tests to determine its efficacy in a fully immunocompetent mouse model of malignant glioma. At elevated doses, infusion with EGFRvIII mCAR T cells led to cures in all mice with brain tumors. In addition, antitumor efficacy was found to be dependent on lymphodepletive host conditioning. Selective blockade with EGFRvIII soluble peptide significantly abrogated the activity of EGFRvIII mCAR T cells in vitro and in vivo, and may offer a novel strategy to enhance the safety profile for CAR-based therapy. Finally, mCAR-treated, cured mice were resistant to rechallenge with EGFRvIII(NEG) tumors, suggesting generation of host immunity against additional tumor antigens. All together, these data support that third-generation, EGFRvIII-specific mCARs are effective against gliomas in the brain and highlight the importance of syngeneic, immunocompetent models in the preclinical evaluation of tumor immunotherapies. ©2013 AACR JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Sampson, John H AU - Choi, Bryan D AU - Sanchez-Perez, Luis AU - Suryadevara, Carter M AU - Snyder, David J AU - Flores, Catherine T AU - Schmittling, Robert J AU - Nair, Smita K AU - Reap, Elizabeth A AU - Norberg, Pamela K AU - Herndon, James E AU - Kuan, Chien-Tsun AU - Morgan, Richard A AU - Rosenberg, Steven A AU - Johnson, Laura A AD - Authors' Affiliations: Duke Brain Tumor Immunotherapy Program, Division of Neurosurgery, Department of Surgery; Department of Pathology; The Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center; Department of Biostatistics and Bioinformatics, Duke University, Durham, North Carolina; and Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/02/15/ PY - 2014 DA - 2014 Feb 15 SP - 972 EP - 984 VL - 20 IS - 4 SN - 1078-0432, 1078-0432 KW - Receptors, Antigen, T-Cell KW - 0 KW - Single-Chain Antibodies KW - epidermal growth factor receptor VIII KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Neoplasm Transplantation KW - Animals KW - T-Lymphocytes -- transplantation KW - Humans KW - Mice KW - Cell Line, Tumor KW - T-Lymphocytes -- immunology KW - Single-Chain Antibodies -- metabolism KW - Brain Neoplasms -- therapy KW - Receptor, Epidermal Growth Factor -- metabolism KW - Adoptive Transfer KW - Brain Neoplasms -- immunology KW - Receptors, Antigen, T-Cell -- metabolism KW - Receptor, Epidermal Growth Factor -- immunology KW - Brain Neoplasms -- metabolism KW - Astrocytoma -- metabolism KW - Astrocytoma -- immunology KW - Astrocytoma -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500701886?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=EGFRvIII+mCAR-modified+T-cell+therapy+cures+mice+with+established+intracerebral+glioma+and+generates+host+immunity+against+tumor-antigen+loss.&rft.au=Sampson%2C+John+H%3BChoi%2C+Bryan+D%3BSanchez-Perez%2C+Luis%3BSuryadevara%2C+Carter+M%3BSnyder%2C+David+J%3BFlores%2C+Catherine+T%3BSchmittling%2C+Robert+J%3BNair%2C+Smita+K%3BReap%2C+Elizabeth+A%3BNorberg%2C+Pamela+K%3BHerndon%2C+James+E%3BKuan%2C+Chien-Tsun%3BMorgan%2C+Richard+A%3BRosenberg%2C+Steven+A%3BJohnson%2C+Laura+A&rft.aulast=Sampson&rft.aufirst=John&rft.date=2014-02-15&rft.volume=20&rft.issue=4&rft.spage=972&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-13-0709 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-14 N1 - Date created - 2014-02-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Neuroimmunol. 2000 Feb 1;103(1):16-25 [10674985] Curr Mol Med. 2013 Aug;13(7):1079-88 [23116267] J Clin Invest. 2002 Jul;110(2):185-92 [12122110] Science. 2002 Oct 25;298(5594):850-4 [12242449] J Immunol. 2003 Feb 1;170(3):1202-8 [12538677] J Immunother. 2003 Sep-Oct;26(5):385-93 [12973027] Mol Cell Neurosci. 2003 Dec;24(4):1116-30 [14697673] Clin Cancer Res. 2004 Oct 1;10(19):6732-43 [15475464] Acta Neuropathol. 1980;51(1):53-64 [7435141] Transplant Proc. 1989 Feb;21(1 Pt 1):127-30 [2784887] Cancer Res. 1995 Jul 15;55(14):3140-8 [7606735] Cancer. 1996 Apr 15;77(8):1551-5 [8608542] Neurosurgery. 1997 Dec;41(6):1365-72; discussion 1372-3 [9402588] Cancer Res. 2004 Dec 15;64(24):9160-6 [15604287] J Exp Med. 2005 Oct 3;202(7):907-12 [16203864] Cancer Res. 2006 Mar 15;66(6):3294-302 [16540683] J Clin Oncol. 2006 May 1;24(13):e20-2 [16648493] Science. 2006 Oct 6;314(5796):126-9 [16946036] J Clin Invest. 2007 Aug;117(8):2197-204 [17657310] Nat Rev Cancer. 2008 Apr;8(4):299-308 [18354418] J Clin Invest. 2008 Apr;118(4):1398-404 [18317595] Nat Cell Biol. 2008 May;10(5):619-24 [18425114] Nat Med. 2008 Nov;14(11):1264-70 [18978797] J Immunother. 2009 Feb-Mar;32(2):169-80 [19238016] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3360-5 [19211796] Nat Med. 2009 Mar;15(3):338-44 [19219023] Lancet Oncol. 2009 May;10(5):459-66 [19269895] Blood. 2009 Jul 16;114(3):535-46 [19451549] Mol Ther. 2009 Aug;17(8):1453-64 [19384291] J Neurooncol. 2009 Sep;94(3):373-82 [19387557] J Immunol. 2009 Nov 1;183(9):5563-74 [19843940] J Immunother. 2010 Jan;33(1):1-7 [19952961] Clin Cancer Res. 2010 Jan 15;16(2):474-85 [20068073] Mol Ther. 2010 Feb;18(2):413-20 [19773745] PLoS One. 2010;5(3):e9750 [20305783] Mol Ther. 2010 Apr;18(4):843-51 [20179677] Hum Gene Ther. 2009 Nov;20(11):1229-39 [19702437] Genes Dev. 2010 Aug 15;24(16):1731-45 [20713517] Clin Cancer Res. 2010 Oct 1;16(19):4892-8 [20719934] J Clin Oncol. 2010 Nov 1;28(31):4722-9 [20921459] J Clin Invest. 2010 Nov;120(11):3953-68 [20978347] Blood. 2010 Nov 11;116(19):3875-86 [20631379] Cancer Sci. 2010 Dec;101(12):2518-24 [20880333] Blood. 2010 Nov 18;116(20):4099-102 [20668228] Cancer Res. 2011 Feb 15;71(4):1253-62 [21216894] J Clin Oncol. 2011 Mar 1;29(7):917-24 [21282551] Mol Ther. 2011 Mar;19(3):620-6 [21157437] Science. 2011 Mar 25;331(6024):1565-70 [21436444] J Immunother. 2011 May;34(4):343-52 [21499127] N Engl J Med. 2011 Aug 25;365(8):725-33 [21830940] Nat Rev Clin Oncol. 2011 Oct;8(10):577-85 [21808266] Blood. 2011 Nov 3;118(18):4817-28 [21849486] Nat Rev Cancer. 2012 Apr;12(4):252-64 [22437870] Nat Rev Immunol. 2012 Apr;12(4):269-81 [22437939] Blood. 2012 Mar 22;119(12):2709-20 [22160384] Mol Ther. 2012 May;20(5):882-4 [22549804] Hum Gene Ther. 2012 Oct;23(10):1043-53 [22780919] Clin Vaccine Immunol. 2013 Mar;20(3):319-27 [23283640] N Engl J Med. 2013 Apr 18;368(16):1509-18 [23527958] Oncogene. 2013 May 23;32(21):2670-81 [22797070] J Exp Med. 2013 Jun 3;210(6):1125-35 [23712432] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7503-8 [10852962] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-13-0709 ER - TY - JOUR T1 - (R,R')-4'-methoxy-1-naphthylfenoterol targets GPR55-mediated ligand internalization and impairs cancer cell motility. AN - 1494310629; 24355564 AB - (R,R')-4'-Methoxy-1-naphthylfenoterol (MNF) promotes growth inhibition and apoptosis of human HepG2 hepatocarcinoma cells via cannabinoid receptor (CBR) activation. The synthetic CB1R inverse agonist, AM251, has been shown to block the anti-mitogenic effect of MNF in these cells; however, AM251 is also an agonist of the recently deorphanized, lipid-sensing receptor, GPR55, whose upregulation contributes to carcinogenesis. Here, we investigated the role of MNF in GPR55 signaling in human HepG2 and PANC-1 cancer cell lines in culture by focusing first on internalization of the fluorescent ligand Tocrifluor 1117 (T1117). Initial results indicated that cell pretreatment with GPR55 agonists, including the atypical cannabinoid O-1602 and l-α-lysophosphatidylinositol, dose-dependently reduced the rate of cellular T1117 uptake, a process that was sensitive to MNF inhibition. GPR55 internalization and signaling mediated by O-1602 was blocked by MNF in GPR55-expressing HEK293 cells. Pretreatment of HepG2 and PANC-1 cells with MNF significantly abrogated the induction of ERK1/2 phosphorylation in response to AM251 and O-1602. Moreover, MNF exerted a coordinated negative regulation of AM251 and O-1602 inducible processes, including changes in cellular morphology and cell migration using scratch wound healing assay. This study shows for the first time that MNF impairs GPR55-mediated signaling and, therefore, may have therapeutic potential in the management of cancer. Published by Elsevier Inc. JF - Biochemical pharmacology AU - Paul, Rajib K AU - Wnorowski, Artur AU - Gonzalez-Mariscal, Isabel AU - Nayak, Surendra K AU - Pajak, Karolina AU - Moaddel, Ruin AU - Indig, Fred E AU - Bernier, Michel AU - Wainer, Irving W AD - Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: paulrk@mail.nih.gov. ; Laboratory of Medicinal Chemistry and Neuroengineering, Department of Chemistry, Medical University of Lublin, 20-093 Lublin, Poland. Electronic address: artur.wnorowski@gmail.com. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: isabel.gonzalezmariscal@nih.gov. ; SRI International (S.K.N.), Harrisonburg, VA 22802, USA. Electronic address: surendra.nayak@sri.com. ; Laboratory of Medicinal Chemistry and Neuroengineering, Department of Chemistry, Medical University of Lublin, 20-093 Lublin, Poland. Electronic address: karolina.pajak@umlub.pl. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: moaddelru@grc.nia.nih.gov. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: indigfr@grc.nia.nih.gov. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: bernierm@mail.nih.gov. ; Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health (NIH), Baltimore, MD 21224, USA. Electronic address: wainerir@grc.nia.nih.gov. Y1 - 2014/02/15/ PY - 2014 DA - 2014 Feb 15 SP - 547 EP - 561 VL - 87 IS - 4 KW - GPR55 protein, human KW - 0 KW - Ligands KW - Piperidines KW - Pyrazoles KW - Receptor, Cannabinoid, CB1 KW - Receptors, G-Protein-Coupled KW - Fenoterol KW - 22M9P70OQ9 KW - AM 251 KW - 3I4FA44MAI KW - Index Medicus KW - Ligand internalization KW - GPR55 KW - G-protein coupled receptor KW - Cellular morphology KW - Cell motility KW - Pyrazoles -- metabolism KW - Pyrazoles -- administration & dosage KW - Receptor, Cannabinoid, CB1 -- agonists KW - Pyrazoles -- chemistry KW - Receptor, Cannabinoid, CB1 -- physiology KW - Piperidines -- chemistry KW - Hep G2 Cells KW - Humans KW - HEK293 Cells KW - Piperidines -- administration & dosage KW - Piperidines -- metabolism KW - Drug Inverse Agonism KW - Neoplasms -- drug therapy KW - Receptors, G-Protein-Coupled -- antagonists & inhibitors KW - Neoplasms -- pathology KW - Fenoterol -- administration & dosage KW - Cell Movement -- physiology KW - Receptors, G-Protein-Coupled -- metabolism KW - Fenoterol -- analogs & derivatives KW - Endocytosis -- drug effects KW - Cell Movement -- drug effects KW - Molecular Targeted Therapy -- methods KW - Endocytosis -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1494310629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=%28R%2CR%27%29-4%27-methoxy-1-naphthylfenoterol+targets+GPR55-mediated+ligand+internalization+and+impairs+cancer+cell+motility.&rft.au=Paul%2C+Rajib+K%3BWnorowski%2C+Artur%3BGonzalez-Mariscal%2C+Isabel%3BNayak%2C+Surendra+K%3BPajak%2C+Karolina%3BMoaddel%2C+Ruin%3BIndig%2C+Fred+E%3BBernier%2C+Michel%3BWainer%2C+Irving+W&rft.aulast=Paul&rft.aufirst=Rajib&rft.date=2014-02-15&rft.volume=87&rft.issue=4&rft.spage=547&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=1873-2968&rft_id=info:doi/10.1016%2Fj.bcp.2013.11.020 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-03-27 N1 - Date created - 2014-02-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Pharmacol. 2010 Feb;159(4):787-96 [20136833] J Med Chem. 2008 Oct 9;51(19):6128-37 [18783211] Pharmacol Ther. 2010 Jun;126(3):301-13 [20298715] Br J Pharmacol. 2010 Jun;160(3):627-42 [20590567] Br J Pharmacol. 2010 Jun;160(3):762-71 [20590578] Br J Pharmacol. 2010 Jun;160(3):604-14 [20136841] Br J Pharmacol. 2010 Aug;160(7):1583-94 [20649563] Oncogene. 2011 Jan 13;30(2):245-52 [20818416] Oncogene. 2011 Jan 13;30(2):142-52 [20838378] J Pharmacol Exp Ther. 2011 Feb;336(2):524-32 [21071556] Mol Cell. 2011 Mar 18;41(6):661-71 [21419341] Br J Pharmacol. 2011 Aug;163(7):1447-63 [21410463] Br J Pharmacol. 2011 Oct;164(3):1026-40 [21449913] Cell Res. 2011 Oct;21(10):1452-69 [21467997] Mol Pharmacol. 2011 Nov;80(5):760-8 [21836019] Cell Signal. 2012 Jan;24(1):333-41 [21964067] Cancer Metastasis Rev. 2011 Dec;30(3-4):599-612 [22038019] J Biol Chem. 2012 Jan 2;287(1):91-104 [22027819] Annu Rev Pharmacol Toxicol. 2012;52:153-78 [21910627] J Pharmacol Sci. 2008 Nov;108(3):308-19 [19008645] J Biol Chem. 2009 May 1;284(18):12328-38 [19286662] Endocrinology. 2009 Jun;150(6):2551-60 [19213840] FEBS Lett. 2009 Jun 18;583(12):2071-6 [19464294] Br J Pharmacol. 2009 Sep;158(1):5-14 [19309353] J Biol Chem. 2009 Oct 23;284(43):29817-27 [19723626] Bioorg Med Chem. 2010 Jan 15;18(2):728-36 [20036561] Zhonghua Gan Zang Bing Za Zhi. 2010 Mar;18(3):204-8 [20380798] Biochim Biophys Acta. 2012 Apr;1821(4):694-705 [22285325] J Biol Chem. 2012 Jun 15;287(25):20851-65 [22532560] J Pharmacol Exp Ther. 2012 Oct;343(1):157-66 [22776956] PLoS One. 2012;7(9):e41354 [22984397] J Biol Chem. 2012 Dec 28;287(53):44234-48 [23161546] Oncogene. 2013 May 16;32(20):2534-42 [22751111] J Biol Chem. 2000 Jan 28;275(4):2479-85 [10644702] J Neurochem. 2000 Aug;75(2):755-62 [10899952] J Cell Sci. 2002 Feb 1;115(Pt 3):455-65 [11861753] Biochemistry. 2004 May 25;43(20):6190-9 [15147203] J Pharmacobiodyn. 1980 Apr;3(4):183-90 [6110717] Eur J Clin Pharmacol. 1985;28 Suppl:55-63 [2865151] Am J Cardiol. 1991 Apr 22;67(10):8B-12B [1673583] Life Sci. 1995;56(23-24):1941-7 [7776817] Mol Pharmacol. 1995 Sep;48(3):443-50 [7565624] J Pharmacol Exp Ther. 1996 Sep;278(3):989-99 [8819477] Science. 1999 Jan 29;283(5402):655-61 [9924018] J Med Chem. 1999 Feb 25;42(4):769-76 [10052983] Br J Pharmacol. 1999 Feb;126(3):665-72 [10188977] EMBO Rep. 2005 Apr;6(4):334-40 [15776020] Am J Physiol Heart Circ Physiol. 2005 May;288(5):H2280-8 [15604130] J Cell Biol. 2005 Aug 15;170(4):619-26 [16103229] Mol Pharmacol. 2005 Nov;68(5):1484-95 [16113085] J Med Chem. 2007 Jun 14;50(12):2903-15 [17506540] Biochem Biophys Res Commun. 2007 Nov 3;362(4):928-34 [17765871] Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16657-62 [17925438] Br J Pharmacol. 2007 Dec;152(7):1092-101 [17876302] J Cell Sci. 2008 May 15;121(Pt 10):1704-17 [18445684] Nat Methods. 2008 Aug;5(8):727-33 [18587404] Proc Natl Acad Sci U S A. 2008 Sep 23;105(38):14555-60 [18787115] Curr Top Med Chem. 2010;10(8):799-813 [20370712] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bcp.2013.11.020 ER - TY - JOUR T1 - Case-case comparison of smoking and alcohol risk associations with Epstein-Barr virus-positive gastric cancer. AN - 1466374975; 23904115 AB - Helicobacter pylori is the primary cause of gastric cancer. However, monoclonal Epstein-Barr virus (EBV) nucleic acid is also present in up to 10% of these tumors worldwide. EBV prevalence is increased with male sex, nonantral localization and surgically disrupted anatomy. To further examine associations between EBV and gastric cancer, we organized an international consortium of 11 studies with tumor EBV status assessed by in situ hybridization. We pooled individual-level data on 2,648 gastric cancer patients, including 184 (7%) with EBV-positive cancers; all studies had information on cigarette use (64% smokers) and nine had data on alcohol (57% drinkers). We compared patients with EBV-positive and EBV-negative tumors to evaluate smoking and alcohol interactions with EBV status. To account for within-population clustering, multilevel logistic regression models were used to estimate interaction odds ratios (OR) adjusted for distributions of sex (72% male), age (mean 59 years), tumor histology (56% Lauren intestinal-type), anatomic subsite (61% noncardia) and year of diagnosis (1983-2012). In unadjusted analyses, the OR of EBV positivity with smoking was 2.2 [95% confidence interval (CI) 1.6-3.2]. The OR was attenuated to 1.5 (95% CI 1.01-2.3) by adjustment for the possible confounders. There was no significant interaction of EBV status with alcohol drinking (crude OR 1.4; adjusted OR 1.0). Our data indicate the smoking association with gastric cancer is stronger for EBV-positive than EBV-negative tumors. Conversely, the null association with alcohol does not vary by EBV status. Distinct epidemiologic characteristics of EBV-positive cancer further implicate the virus as a cofactor in gastric carcinogenesis. © 2013 UICC. JF - International journal of cancer AU - Camargo, M Constanza AU - Koriyama, Chihaya AU - Matsuo, Keitaro AU - Kim, Woo-Ho AU - Herrera-Goepfert, Roberto AU - Liao, Linda M AU - Eurgast-EPIC Group AU - Yu, Jun AU - Carrasquilla, Gabriel AU - Sung, Joseph J Y AU - Alvarado-Cabrero, Isabel AU - Lissowska, Jolanta AU - Meneses-Gonzalez, Fernando AU - Yatabe, Yashushi AU - Ding, Ti AU - Hu, Nan AU - Taylor, Philip R AU - Morgan, Douglas R AU - Gulley, Margaret L AU - Torres, Javier AU - Akiba, Suminori AU - Rabkin, Charles S AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA. ; Eurgast-EPIC Group Y1 - 2014/02/15/ PY - 2014 DA - 2014 Feb 15 SP - 948 EP - 953 VL - 134 IS - 4 KW - Index Medicus KW - gastric cancer KW - smoking KW - alcohol KW - EBV KW - pooled-analysis KW - Odds Ratio KW - Neoplasm Staging KW - Humans KW - Prognosis KW - Aged KW - Aged, 80 and over KW - Risk Factors KW - Adult KW - Case-Control Studies KW - Follow-Up Studies KW - Middle Aged KW - Female KW - Male KW - Herpesvirus 4, Human -- pathogenicity KW - Adenocarcinoma -- etiology KW - Alcohol Drinking -- adverse effects KW - Smoking -- adverse effects KW - Epstein-Barr Virus Infections -- virology KW - Stomach Neoplasms -- etiology KW - Epstein-Barr Virus Infections -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1466374975?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Case-case+comparison+of+smoking+and+alcohol+risk+associations+with+Epstein-Barr+virus-positive+gastric+cancer.&rft.au=Camargo%2C+M+Constanza%3BKoriyama%2C+Chihaya%3BMatsuo%2C+Keitaro%3BKim%2C+Woo-Ho%3BHerrera-Goepfert%2C+Roberto%3BLiao%2C+Linda+M%3BEurgast-EPIC+Group%3BYu%2C+Jun%3BCarrasquilla%2C+Gabriel%3BSung%2C+Joseph+J+Y%3BAlvarado-Cabrero%2C+Isabel%3BLissowska%2C+Jolanta%3BMeneses-Gonzalez%2C+Fernando%3BYatabe%2C+Yashushi%3BDing%2C+Ti%3BHu%2C+Nan%3BTaylor%2C+Philip+R%3BMorgan%2C+Douglas+R%3BGulley%2C+Margaret+L%3BTorres%2C+Javier%3BAkiba%2C+Suminori%3BRabkin%2C+Charles+S&rft.aulast=Camargo&rft.aufirst=M&rft.date=2014-02-15&rft.volume=134&rft.issue=4&rft.spage=948&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.28402 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-02-20 N1 - Date created - 2013-12-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Cancer. 2011 Jun 28;105(1):38-43 [21654677] Int J Cancer. 2010 Dec 15;127(12):2893-917 [21351269] Cancer Epidemiol. 2011 Dec;35(6):e91-9 [21846596] Ann Oncol. 2012 Jan;23(1):28-36 [21536659] Cancer. 2012 Feb 15;118(4):924-36 [21717425] J Natl Cancer Inst. 2012 Sep 19;104(18):1396-410 [22972969] Cancer Causes Control. 2013 Feb;24(2):217-31 [23224270] Ann Oncol. 2013 Sep;24(9):2245-55 [23788758] Gut. 2014 Feb;63(2):236-43 [23580779] J Med Virol. 2000 Apr;60(4):411-6 [10686024] Gut. 2000 Aug;47(2):170-7 [10896906] Int J Cancer. 2003 Nov 20;107(4):629-34 [14520702] Cancer Epidemiol Biomarkers Prev. 1994 Mar;3(2):173-5 [8049640] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):9131-5 [8090780] Histopathology. 1994 Oct;25(4):323-9 [7835837] Int J Cancer. 1995 Mar 3;60(5):642-4 [7860138] IARC Monogr Eval Carcinog Risks Hum. 1997;70:1-492 [9705682] Int J Cancer. 1999 Jun 11;81(6):871-6 [10362132] Epidemiology. 2005 Jul;16(4):586-90 [15951682] World J Gastroenterol. 2005 Oct 21;11(39):6096-103 [16273633] Am J Med. 2006 Mar;119(3):217-24 [16490464] Asian Pac J Cancer Prev. 2006 Oct-Dec;7(4):633-7 [17250442] Int J Epidemiol. 2007 Feb;36(1):66-76 [17227779] Cancer Sci. 2008 Feb;99(2):350-4 [18201267] J Mol Diagn. 2008 Jul;10(4):279-92 [18556771] Cancer Causes Control. 2008 Sep;19(7):689-701 [18293090] Lab Invest. 2009 Jan;89(1):80-90 [19002111] J Gastroenterol Hepatol. 2009 Mar;24(3):354-65 [19335785] Tumori. 2009 Jan-Feb;95(1):13-22 [19366050] Gastroenterology. 2009 Sep;137(3):824-33 [19445939] Anticancer Res. 2010 Jun;30(6):2469-75 [20651410] Cancer Epidemiol Biomarkers Prev. 2011 Aug;20(8):1665-72 [21680535] J Exp Clin Cancer Res. 2005 Dec;24(4):547-53 [16471317] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.28402 ER - TY - JOUR T1 - ROS and RNS induced apoptosis through p53 and iNOS mediated pathway by a dibasic hydroxamic acid molecule in leukemia cells. AN - 1490773199; 24269727 AB - Anticancer drugs induce apoptosis to cancer cells and also exhibit undesired toxicity to normal cells. Therefore development of novel agents triggering apoptosis and have low toxicity towards normal cells is most important. Hydroxamic acids suppress tumour cell growth through apoptosis but the underlying mechanism is poorly understood. Herein, we describe the apoptotic potential of a dibasic hydroxamic acid derivative, viz., oxayl bis (N-phenyl) hydroxamic acid (OBPHA), which induces apoptosis through generation of both ROS and NO in doxorubicin resistant T-lymphoblastic leukemia, CEM/ADR5000 cells. Present study discloses that OBPHA selectively kills cancerous cells irrespective of their drug resistant phenotype. We also determined the crystal structure of OBPHA to understand the structural requirements for apoptosis; the study reveals that the presence of substituted hydroxamic acid groups (-CO-NH-OH) favours the generation of NO possibly through auto degeneration. Along with the induction of caspase 3 mediated intrinsic apoptosis; OBPHA also activates p53 dependent signalling cascade and downregulates HDAC3 expression in a time dependent manner possibly due to increased ROS and NO production and simultaneous decrease in cellular GSH level. Thus ROS and NO mediated downstream signalling are essential for the anticancer effect of OBPHA. Therefore OBPHA, having a structurally relevant pharmacophore provides important insight into the development of new ROS and RNS generating chemicals inducing p53 dependent apoptosis. Copyright © 2013 Elsevier B.V. All rights reserved. JF - European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences AU - Banerjee, Kaushik AU - Ganguly, Avishek AU - Chakraborty, Paramita AU - Sarkar, Avijit AU - Singh, Suryabhan AU - Chatterjee, Mitali AU - Bhattacharya, Subrato AU - Choudhuri, Soumitra Kumar AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India. ; Department of Pharmacology, Institute of Post Graduate Medical Education and Research, Kolkata, India. ; Department of Chemistry, Banaras Hindu University, Varanasi, India. ; Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India. Electronic address: soumitra01@yahoo.com. Y1 - 2014/02/14/ PY - 2014 DA - 2014 Feb 14 SP - 146 EP - 164 VL - 52 KW - Antineoplastic Agents KW - 0 KW - Benzeneacetamides KW - Hydroxamic Acids KW - Oxalates KW - Reactive Nitrogen Species KW - Reactive Oxygen Species KW - Tumor Suppressor Protein p53 KW - oxalyl bis(N-phenyl)hydroxamic acid KW - Nitric Oxide KW - 31C4KY9ESH KW - NOS2 protein, human KW - EC 1.14.13.39 KW - Nitric Oxide Synthase Type II KW - Caspase 3 KW - EC 3.4.22.- KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Reactive nitrogen species KW - HDAC3 KW - p53 KW - Apoptosis KW - Reactive oxygen species KW - iNOS KW - Glutathione -- metabolism KW - Humans KW - Nitric Oxide -- metabolism KW - Cell Line, Tumor KW - Leukemia -- drug therapy KW - Leukocytes, Mononuclear -- physiology KW - Membrane Potential, Mitochondrial -- drug effects KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Leukemia -- metabolism KW - Apoptosis -- drug effects KW - Nitric Oxide Synthase Type II -- metabolism KW - Leukocytes, Mononuclear -- drug effects KW - Caspase 3 -- metabolism KW - Reactive Oxygen Species -- metabolism KW - Benzeneacetamides -- pharmacology KW - Oxalates -- pharmacology KW - Reactive Nitrogen Species -- metabolism KW - Tumor Suppressor Protein p53 -- metabolism KW - Hydroxamic Acids -- pharmacology KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490773199?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmaceutical+sciences+%3A+official+journal+of+the+European+Federation+for+Pharmaceutical+Sciences&rft.atitle=ROS+and+RNS+induced+apoptosis+through+p53+and+iNOS+mediated+pathway+by+a+dibasic+hydroxamic+acid+molecule+in+leukemia+cells.&rft.au=Banerjee%2C+Kaushik%3BGanguly%2C+Avishek%3BChakraborty%2C+Paramita%3BSarkar%2C+Avijit%3BSingh%2C+Suryabhan%3BChatterjee%2C+Mitali%3BBhattacharya%2C+Subrato%3BChoudhuri%2C+Soumitra+Kumar&rft.aulast=Banerjee&rft.aufirst=Kaushik&rft.date=2014-02-14&rft.volume=52&rft.issue=&rft.spage=146&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmaceutical+sciences+%3A+official+journal+of+the+European+Federation+for+Pharmaceutical+Sciences&rft.issn=1879-0720&rft_id=info:doi/10.1016%2Fj.ejps.2013.11.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-08 N1 - Date created - 2014-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ejps.2013.11.009 ER - TY - CPAPER T1 - Susceptibility to Lung Disease: Integrated Genetic and Genomic Approaches T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AN - 1510100048; 6280205 JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AU - Kleeberger, Steven Y1 - 2014/02/13/ PY - 2014 DA - 2014 Feb 13 KW - Lung diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510100048?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.atitle=Susceptibility+to+Lung+Disease%3A+Integrated+Genetic+and+Genomic+Approaches&rft.au=Kleeberger%2C+Steven&rft.aulast=Kleeberger&rft.aufirst=Steven&rft.date=2014-02-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-24 N1 - Last updated - 2014-03-26 ER - TY - CPAPER T1 - Convergence Technologies on the Horizon T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AN - 1510100046; 6279971 JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AU - Seto, Belinda Y1 - 2014/02/13/ PY - 2014 DA - 2014 Feb 13 KW - Technology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510100046?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.atitle=Convergence+Technologies+on+the+Horizon&rft.au=Seto%2C+Belinda&rft.aulast=Seto&rft.aufirst=Belinda&rft.date=2014-02-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-24 N1 - Last updated - 2014-03-26 ER - TY - CPAPER T1 - Autoimmune Diseases: From Basic Mechanism to Clinical Therapeutics T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AN - 1510095593; 6280212 JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AU - Kaplan, Mariana Y1 - 2014/02/13/ PY - 2014 DA - 2014 Feb 13 KW - Autoimmune diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510095593?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.atitle=Autoimmune+Diseases%3A+From+Basic+Mechanism+to+Clinical+Therapeutics&rft.au=Kaplan%2C+Mariana&rft.aulast=Kaplan&rft.aufirst=Mariana&rft.date=2014-02-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-24 N1 - Last updated - 2014-03-26 ER - TY - CPAPER T1 - Medical, Occupational, Engineering, and Safety Aspects in Biodefense Research T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AN - 1510095448; 6280153 JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AU - Takafuji, Ernest Y1 - 2014/02/13/ PY - 2014 DA - 2014 Feb 13 KW - Safety engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510095448?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.atitle=Medical%2C+Occupational%2C+Engineering%2C+and+Safety+Aspects+in+Biodefense+Research&rft.au=Takafuji%2C+Ernest&rft.aulast=Takafuji&rft.aufirst=Ernest&rft.date=2014-02-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-24 N1 - Last updated - 2014-03-26 ER - TY - CPAPER T1 - Emergence of Protozoal Diseases Impacting Arctic Communities T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AN - 1510094989; 6279802 JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AU - Grigg, Mike Y1 - 2014/02/13/ PY - 2014 DA - 2014 Feb 13 KW - Arctic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510094989?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.atitle=Emergence+of+Protozoal+Diseases+Impacting+Arctic+Communities&rft.au=Grigg%2C+Mike&rft.aulast=Grigg&rft.aufirst=Mike&rft.date=2014-02-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-24 N1 - Last updated - 2014-03-26 ER - TY - CPAPER T1 - Understanding Gene-Environmental Interactions in the Etiology of Addictions T2 - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AN - 1510091795; 6279757 JF - 2014 Annual Meeting of the American Association for the Advancement of Science (AAAS 2014) AU - Compton, Wilson Y1 - 2014/02/13/ PY - 2014 DA - 2014 Feb 13 KW - Etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1510091795?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.atitle=Understanding+Gene-Environmental+Interactions+in+the+Etiology+of+Addictions&rft.au=Compton%2C+Wilson&rft.aulast=Compton&rft.aufirst=Wilson&rft.date=2014-02-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2014/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-24 N1 - Last updated - 2014-03-26 ER - TY - JOUR T1 - Molecular control of δ-opioid receptor signalling. AN - 1499147634; 24413399 AB - Opioids represent widely prescribed and abused medications, although their signal transduction mechanisms are not well understood. Here we present the 1.8 Å high-resolution crystal structure of the human δ-opioid receptor (δ-OR), revealing the presence and fundamental role of a sodium ion in mediating allosteric control of receptor functional selectivity and constitutive activity. The distinctive δ-OR sodium ion site architecture is centrally located in a polar interaction network in the seven-transmembrane bundle core, with the sodium ion stabilizing a reduced agonist affinity state, and thereby modulating signal transduction. Site-directed mutagenesis and functional studies reveal that changing the allosteric sodium site residue Asn 131 to an alanine or a valine augments constitutive β-arrestin-mediated signalling. Asp95Ala, Asn310Ala and Asn314Ala mutations transform classical δ-opioid antagonists such as naltrindole into potent β-arrestin-biased agonists. The data establish the molecular basis for allosteric sodium ion control in opioid signalling, revealing that sodium-coordinating residues act as 'efficacy switches' at a prototypic G-protein-coupled receptor. JF - Nature AU - Fenalti, Gustavo AU - Giguere, Patrick M AU - Katritch, Vsevolod AU - Huang, Xi-Ping AU - Thompson, Aaron A AU - Cherezov, Vadim AU - Roth, Bryan L AU - Stevens, Raymond C AD - 1] Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA [2]. ; 1] National Institute of Mental Health Psychoactive Drug Screening Program and Department of Pharmacology and Division of Chemical Biology and Medicinal Chemistry, University of North Carolina Chapel Hill Medical School, Chapel Hill, North Carolina 27599, USA [2]. ; Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA. ; National Institute of Mental Health Psychoactive Drug Screening Program and Department of Pharmacology and Division of Chemical Biology and Medicinal Chemistry, University of North Carolina Chapel Hill Medical School, Chapel Hill, North Carolina 27599, USA. Y1 - 2014/02/13/ PY - 2014 DA - 2014 Feb 13 SP - 191 EP - 196 VL - 506 IS - 7487 KW - Arrestins KW - 0 KW - Ligands KW - Narcotic Antagonists KW - Receptors, Opioid, delta KW - beta-Arrestins KW - Naltrexone KW - 5S6W795CQM KW - Asparagine KW - 7006-34-0 KW - Sodium KW - 9NEZ333N27 KW - naltrindole KW - G167Z38QA4 KW - Index Medicus KW - Allosteric Site -- genetics KW - Allosteric Regulation -- drug effects KW - Allosteric Site -- drug effects KW - Models, Molecular KW - Humans KW - Naltrexone -- analogs & derivatives KW - Asparagine -- metabolism KW - Naltrexone -- chemistry KW - Structure-Activity Relationship KW - Sodium -- pharmacology KW - Mutagenesis, Site-Directed KW - Allosteric Regulation -- genetics KW - Narcotic Antagonists -- chemistry KW - Asparagine -- genetics KW - Naltrexone -- pharmacology KW - Naltrexone -- metabolism KW - Narcotic Antagonists -- metabolism KW - Crystallography, X-Ray KW - Narcotic Antagonists -- pharmacology KW - Arrestins -- metabolism KW - Sodium -- metabolism KW - Receptors, Opioid, delta -- chemistry KW - Receptors, Opioid, delta -- antagonists & inhibitors KW - Signal Transduction -- drug effects KW - Receptors, Opioid, delta -- metabolism KW - Receptors, Opioid, delta -- agonists KW - Receptors, Opioid, delta -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499147634?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Molecular+control+of+%CE%B4-opioid+receptor+signalling.&rft.au=Fenalti%2C+Gustavo%3BGiguere%2C+Patrick+M%3BKatritch%2C+Vsevolod%3BHuang%2C+Xi-Ping%3BThompson%2C+Aaron+A%3BCherezov%2C+Vadim%3BRoth%2C+Bryan+L%3BStevens%2C+Raymond+C&rft.aulast=Fenalti&rft.aufirst=Gustavo&rft.date=2014-02-13&rft.volume=506&rft.issue=7487&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=1476-4687&rft_id=info:doi/10.1038%2Fnature12944 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-02-19 N1 - Date created - 2014-02-13 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4N6H; PDB N1 - SuppNotes - Cited By: Br J Pharmacol. 2000 Jul;130(5):987-96 [10882382] Neuropharmacology. 2014 Jan;76 Pt B:198-203 [23624289] Eur J Pharmacol. 2000 Sep 1;403(1-2):37-44 [10969141] Pharmacol Rev. 2002 Jun;54(2):323-74 [12037145] J Pharmacol Exp Ther. 2002 Sep;302(3):1070-9 [12183665] J Mol Biol. 2002 Oct 18;323(2):253-62 [12381319] Acta Crystallogr D Biol Crystallogr. 2004 Oct;60(Pt 10):1795-807 [15388926] Science. 1973 Dec 28;182(4119):1359-61 [4128222] J Neurochem. 1982 Apr;38(4):1164-7 [6278084] J Med Chem. 1988 Feb;31(2):281-2 [2828619] Mol Pharmacol. 1990 Mar;37(3):383-94 [2156152] J Biol Chem. 1990 Dec 15;265(35):21590-5 [2174879] Mol Pharmacol. 1991 Apr;39(4):570-8 [2017157] Mol Pharmacol. 1993 Oct;44(4):827-34 [8232233] J Neurochem. 1997 Mar;68(3):1053-61 [9048750] J Pharmacol Exp Ther. 1997 Dec;283(3):1276-84 [9400003] Nat Protoc. 2007;2(4):924-32 [17446874] J Biol Chem. 2007 May 25;282(21):15799-811 [17371869] Proc Natl Acad Sci U S A. 2008 Jan 8;105(1):64-9 [18165312] Nature. 2008 Jul 10;454(7201):183-7 [18563085] Nat Protoc. 2009;4(5):706-31 [19390528] Nature. 2009 May 21;459(7245):356-63 [19458711] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702] Acta Crystallogr D Biol Crystallogr. 2010 Apr;66(Pt 4):486-501 [20383002] J Am Chem Soc. 2010 Aug 25;132(33):11443-5 [20669948] Science. 2010 Nov 19;330(6007):1066-71 [20929726] Science. 2011 Apr 15;332(6027):322-7 [21393508] Structure. 2011 Sep 7;19(9):1283-93 [21885291] Nat Chem Biol. 2011 Nov;7(11):769-78 [21926995] Proc Natl Acad Sci U S A. 2011 Nov 8;108(45):18488-93 [22025698] Nature. 2012 May 17;485(7398):395-9 [22596163] Nature. 2012 May 17;485(7398):400-4 [22596164] Science. 2012 Jul 13;337(6091):232-6 [22798613] Cell. 2012 Sep 28;151(1):14-23 [23021212] Nature. 2012 Dec 13;492(7428):215-20 [23235874] Trends Pharmacol Sci. 2013 Jan;34(1):6-12 [23127545] Annu Rev Pharmacol Toxicol. 2013;53:531-56 [23140243] Science. 2013 May 3;340(6132):615-9 [23519215] J Biol Chem. 2013 May 3;288(18):12511-21 [23493400] Proc Natl Acad Sci U S A. 2013 Jun 25;110(26):10830-5 [23754417] Nat Rev Drug Discov. 2013 Aug;12(8):630-44 [23903222] Biochem Pharmacol. 2000 Sep 1;60(5):669-76 [10927025] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nature12944 ER - TY - JOUR T1 - DLC1 induces expression of E-cadherin in prostate cancer cells through Rho pathway and suppresses invasion. AN - 1499131728; 23376848 AB - E-cadherin is a cell-cell adhesion molecule that acts as a suppressor of cancer cell invasion and its expression is downregulated in many advanced, poorly differentiated, human cancers. In this study, we found that the expression of DLC1 (deleted in liver cancer 1) tumor-suppressor gene in metastatic prostate carcinoma (PCA) cells increased the expression of E-cadherin and resulted in an elevated rate of cell-cell aggregation as measured by aggregation assay. DLC1-mediated increase in E-cadherin expression was not dependent on α-catenin, a DLC1-binding protein associated with E-cadherin, and/or cellular density. The increase of E-cadherin expression occurred at mRNA level and relied on DLC1 RhoGAP function, leading to suppression of high level of RhoA-GTP and RhoC-GTP activity in metastatic PCA cells. Application of Rho/ROCK inhibitors produced the same effect as introduction of DLC1. Knocking down of RhoA produced a moderate increase in E-cadherin whereas knocking down of RhoC resulted in a significant increase of E-cadherin. Downregulation of E-cadherin caused by constitutively active RhoA(V14) and RhoC(V14) could not be reversed by expression of DLC1 in DLC1-negative cell line. DLC1-mediated suppression of metastatic PCA cells invasion was comparable with the one associated with ectopic E-cadherin expression, or caused by suppression of Rho pathway either by Rho/ROCK inhibitors, or by shRNA repression. This study demonstrates that DLC1 expression positively regulates E-cadherin and suppresses highly metastatic PCA cell invasion by modulating Rho pathway, which appears as a feasible therapeutic target in cancers with high activity of RhoGTPases. JF - Oncogene AU - Tripathi, V AU - Popescu, N C AU - Zimonjic, D B AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2014/02/06/ PY - 2014 DA - 2014 Feb 06 SP - 724 EP - 733 VL - 33 IS - 6 KW - Cadherins KW - 0 KW - DLC1 protein, human KW - GTPase-Activating Proteins KW - Tumor Suppressor Proteins KW - rho GTPase-activating protein KW - rho-Associated Kinases KW - EC 2.7.11.1 KW - Index Medicus KW - Neoplasm Invasiveness KW - Gene Knockdown Techniques KW - Cell Differentiation -- physiology KW - Transfection KW - Humans KW - Cell Line, Tumor KW - Cell Aggregation -- physiology KW - Male KW - Prostatic Neoplasms -- metabolism KW - Prostatic Neoplasms -- pathology KW - GTPase-Activating Proteins -- genetics KW - rho-Associated Kinases -- metabolism KW - GTPase-Activating Proteins -- metabolism KW - Tumor Suppressor Proteins -- metabolism KW - GTPase-Activating Proteins -- physiology KW - Tumor Suppressor Proteins -- genetics KW - Prostatic Neoplasms -- genetics KW - rho-Associated Kinases -- genetics KW - Cadherins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499131728?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DLC1+induces+expression+of+E-cadherin+in+prostate+cancer+cells+through+Rho+pathway+and+suppresses+invasion.&rft.au=Tripathi%2C+V%3BPopescu%2C+N+C%3BZimonjic%2C+D+B&rft.aulast=Tripathi&rft.aufirst=V&rft.date=2014-02-06&rft.volume=33&rft.issue=6&rft.spage=724&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2013.7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-26 N1 - Date created - 2014-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1038/onc.2013.7 ER - TY - JOUR T1 - Aprataxin resolves adenylated RNA-DNA junctions to maintain genome integrity. AN - 1499121868; 24362567 AB - Faithful maintenance and propagation of eukaryotic genomes is ensured by three-step DNA ligation reactions used by ATP-dependent DNA ligases. Paradoxically, when DNA ligases encounter nicked DNA structures with abnormal DNA termini, DNA ligase catalytic activity can generate and/or exacerbate DNA damage through abortive ligation that produces chemically adducted, toxic 5'-adenylated (5'-AMP) DNA lesions. Aprataxin (APTX) reverses DNA adenylation but the context for deadenylation repair is unclear. Here we examine the importance of APTX to RNase-H2-dependent excision repair (RER) of a lesion that is very frequently introduced into DNA, a ribonucleotide. We show that ligases generate adenylated 5' ends containing a ribose characteristic of RNase H2 incision. APTX efficiently repairs adenylated RNA-DNA, and acting in an RNA-DNA damage response (RDDR), promotes cellular survival and prevents S-phase checkpoint activation in budding yeast undergoing RER. Structure-function studies of human APTX-RNA-DNA-AMP-Zn complexes define a mechanism for detecting and reversing adenylation at RNA-DNA junctions. This involves A-form RNA binding, proper protein folding and conformational changes, all of which are affected by heritable APTX mutations in ataxia with oculomotor apraxia 1. Together, these results indicate that accumulation of adenylated RNA-DNA may contribute to neurological disease. JF - Nature AU - Tumbale, Percy AU - Williams, Jessica S AU - Schellenberg, Matthew J AU - Kunkel, Thomas A AU - Williams, R Scott AD - 1] Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA [2]. ; 1] Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA [2] Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA [3]. ; 1] Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA [2] Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA. ; Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, North Carolina 27709, USA. Y1 - 2014/02/06/ PY - 2014 DA - 2014 Feb 06 SP - 111 EP - 115 VL - 506 IS - 7486 KW - APTX protein, human KW - 0 KW - DNA-Binding Proteins KW - Nuclear Proteins KW - Schizosaccharomyces pombe Proteins KW - Adenosine Monophosphate KW - 415SHH325A KW - RNA KW - 63231-63-0 KW - DNA KW - 9007-49-2 KW - Exodeoxyribonucleases KW - EC 3.1.- KW - Hnt3 protein, S pombe KW - ribonuclease HII KW - EC 3.1.26.- KW - Ribonuclease H KW - EC 3.1.26.4 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Humans KW - Exodeoxyribonucleases -- metabolism KW - Apraxias -- genetics KW - Nucleic Acid Conformation KW - Ribonuclease H -- metabolism KW - Cell Survival KW - S Phase Cell Cycle Checkpoints KW - Saccharomyces cerevisiae -- genetics KW - Saccharomyces cerevisiae -- metabolism KW - Protein Conformation KW - DNA Repair KW - Models, Molecular KW - Schizosaccharomyces -- metabolism KW - Zinc -- metabolism KW - Structure-Activity Relationship KW - Ataxia Telangiectasia -- genetics KW - Adenosine Monophosphate -- metabolism KW - Schizosaccharomyces pombe Proteins -- metabolism KW - Hypoalbuminemia -- genetics KW - Protein Folding KW - Mutation -- genetics KW - Cerebellar Ataxia -- congenital KW - Schizosaccharomyces pombe Proteins -- chemistry KW - Exodeoxyribonucleases -- chemistry KW - Saccharomyces cerevisiae -- cytology KW - Nuclear Proteins -- genetics KW - DNA-Binding Proteins -- chemistry KW - RNA -- metabolism KW - DNA -- metabolism KW - Genome, Human -- genetics KW - DNA-Binding Proteins -- genetics KW - DNA -- chemistry KW - RNA -- chemistry KW - Nuclear Proteins -- chemistry KW - Nuclear Proteins -- metabolism KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499121868?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Aprataxin+resolves+adenylated+RNA-DNA+junctions+to+maintain+genome+integrity.&rft.au=Tumbale%2C+Percy%3BWilliams%2C+Jessica+S%3BSchellenberg%2C+Matthew+J%3BKunkel%2C+Thomas+A%3BWilliams%2C+R+Scott&rft.aulast=Tumbale&rft.aufirst=Percy&rft.date=2014-02-06&rft.volume=506&rft.issue=7486&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=1476-4687&rft_id=info:doi/10.1038%2Fnature12824 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-02-18 N1 - Date created - 2014-02-06 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4NDI; PDB; 4NDH; 4NDG; 4NDF N1 - SuppNotes - Cited By: DNA Repair (Amst). 2009 Jun 4;8(6):760-6 [19303373] J Biol Chem. 2008 Dec 5;283(49):33994-4001 [18836178] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702] Proc Natl Acad Sci U S A. 2010 Mar 16;107(11):4949-54 [20194773] Nucleic Acids Res. 2010 Apr;38(6):e85 [20008099] Acta Crystallogr D Biol Crystallogr. 2010 Apr;66(Pt 4):486-501 [20383002] DNA Repair (Amst). 2010 Jun 4;9(6):690-9 [20399152] Biochemistry. 2010 Jul 27;49(29):6165-76 [20518483] Nat Chem Biol. 2010 Oct;6(10):774-81 [20729855] Proc Natl Acad Sci U S A. 2011 May 3;108(18):7437-42 [21502511] J Biol Chem. 2011 Sep 9;286(36):31490-500 [21778232] Nat Struct Mol Biol. 2011 Nov;18(11):1189-95 [21984210] EMBO J. 2012 Feb 15;31(4):895-907 [22234187] Cell. 2012 May 25;149(5):1008-22 [22579044] Nature. 2012 Jul 12;487(7406):196-201 [22785315] Mol Cell. 2012 Sep 28;47(6):980-6 [22864116] PLoS Genet. 2012;8(10):e1003016 [23071460] PLoS Genet. 2012;8(11):e1003030 [23144626] Mol Cell. 2013 Mar 7;49(5):1010-5 [23375499] Acta Crystallogr D Biol Crystallogr. 2000 Aug;56(Pt 8):965-72 [10944333] Genetics. 2001 Sep;159(1):47-64 [11560886] Nat Genet. 2001 Oct;29(2):184-8 [11586299] Nat Genet. 2001 Oct;29(2):189-93 [11586300] Cell. 2002 Nov 15;111(4):495-505 [12437923] Cell. 2003 Feb 7;112(3):391-401 [12581528] Neurology. 2003 Mar 11;60(5):868-70 [12629250] Mol Cell Biol. 2003 Apr;23(7):2309-15 [12640116] J Biol Chem. 1997 Sep 5;272(36):22591-9 [9278414] Science. 1997 Oct 10;278(5336):286-90 [9323207] Nature. 2004 Nov 25;432(7016):473-8 [15565146] J Biol Chem. 2006 May 19;281(20):13939-48 [16547001] Nature. 2006 Oct 12;443(7112):713-6 [16964241] J Biol Chem. 2007 Mar 30;282(13):9469-74 [17276982] Annu Rev Biochem. 2008;77:313-38 [18518823] Hum Mol Genet. 2009 Nov 1;18(21):4102-17 [19643912] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nature12824 ER - TY - CPAPER T1 - Sustainable and Climate Resilient Healthcare Facilities: an update on federal efforts T2 - 94th American Meteorological Society Annual Meeting (AMS 2014) AN - 1518611807; 6282169 JF - 94th American Meteorological Society Annual Meeting (AMS 2014) AU - Balbus, John Y1 - 2014/02/02/ PY - 2014 DA - 2014 Feb 02 KW - Health care KW - Climate KW - Sustainable development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518611807?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=94th+American+Meteorological+Society+Annual+Meeting+%28AMS+2014%29&rft.atitle=Sustainable+and+Climate+Resilient+Healthcare+Facilities%3A+an+update+on+federal+efforts&rft.au=Balbus%2C+John&rft.aulast=Balbus&rft.aufirst=John&rft.date=2014-02-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=94th+American+Meteorological+Society+Annual+Meeting+%28AMS+2014%29&rft.issn=&rft_id=info:doi/ L2 - https://ams.confex.com/ams/94Annual/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - JOUR T1 - Building the Strategic National Stockpile Through the NIAID Radiation Nuclear Countermeasures Program AN - 1842512251; 19002850 AB - The possibility of a public health radiological or nuclear emergency in the United States remains a concern. Media attention focused on lost radioactive sources and international nuclear threats, as well as the potential for accidents in nuclear power facilities (e.g., Windscale, Three Mile Island, Chernobyl, and Fukushima) highlight the need to address this critical national security issue. To date, no drugs have been licensed to mitigate/treat the acute and longaterm radiation injuries that would result in the event of largeascale, radiation, or nuclear public health emergency. However, recent evaluation of several candidate radiation medical countermeasures (MCMs) has provided initial proofaofaconcept of efficacy. The goal of the Radiation Nuclear Countermeasures Program (RNCP) of the National Institute of Allergy and Infectious Diseases (National Institutes of Health) is to help ensure the government stockpiling of safe and efficacious MCMs to treat radiation injuries, including, but not limited to, hematopoietic, gastrointestinal, pulmonary, cutaneous, renal, cardiovascular, and central nervous systems. In addition to supporting research in these areas, the RNCP continues to fund research and development of decorporation agents targeting internal radionuclide contamination, and biodosimetry platforms (e.g., biomarkers and devices) to assess the levels of an individual's radiation exposure, capabilities that would be critical in a mass casualty scenario. New areas of research within the program include a focus on special populations, especially pediatric and geriatric civilians, as well as combination studies, in which drugs are tested within the context of expected medical care management (e.g., antibiotics and growth factors). Moving forward, challenges facing the RNCP, as well as the entire radiation research field, include further advancement and qualification of animal models, dose conversion from animal models to humans, biomarker identification, and formulation development. This paper provides a review of recent work and collaborations supported by the RNCP. JF - Drug Development Research AU - Rios, Carmen I AU - Cassatt, David R AU - DiCarlo, Andrea L AU - Macchiarini, Francesca AU - Ramakrishnan, Narayani AU - Norman, MaiaKim AU - Maidment, Bert W AD - Radiation Nuclear Countermeasures Program, Division of Allergy, Immunology and Transplantation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, 20892, USA. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 23 EP - 28 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 75 IS - 1 SN - 0272-4391, 0272-4391 KW - Toxicology Abstracts KW - radiation KW - nuclear KW - medical countermeasures KW - dosimetry KW - animal models KW - mitigators KW - treatment KW - Central nervous system KW - Injuries KW - Contamination KW - Pediatrics KW - Animal models KW - Antibiotics KW - Drug development KW - biomarkers KW - Public health KW - Hypersensitivity KW - Accidents KW - Islands KW - Infectious diseases KW - Radiation KW - Reviews KW - Radioisotopes KW - Kidney KW - Geriatrics KW - Drugs KW - X 24390:Radioactive Materials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842512251?accountid=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=Drug+Development+Research&rft.atitle=Building+the+Strategic+National+Stockpile+Through+the+NIAID+Radiation+Nuclear+Countermeasures+Program&rft.au=Rios%2C+Carmen+I%3BCassatt%2C+David+R%3BDiCarlo%2C+Andrea+L%3BMacchiarini%2C+Francesca%3BRamakrishnan%2C+Narayani%3BNorman%2C+MaiaKim%3BMaidment%2C+Bert+W&rft.aulast=Rios&rft.aufirst=Carmen&rft.date=2014-02-01&rft.volume=75&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Drug+Development+Research&rft.issn=02724391&rft_id=info:doi/10.1002%2Fddr.21163 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-11-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Central nervous system; Contamination; Injuries; Pediatrics; Animal models; Drug development; Antibiotics; biomarkers; Public health; Accidents; Hypersensitivity; Islands; Radiation; Infectious diseases; Reviews; Geriatrics; Kidney; Radioisotopes; Drugs DO - http://dx.doi.org/10.1002/ddr.21163 ER - TY - JOUR T1 - Punishment insensitivity and impaired reinforcement learning in preschoolers AN - 1748688877 AB - Background Youth and adults with psychopathic traits display disrupted reinforcement learning. Advances in measurement now enable examination of this association in preschoolers. The current study examines relations between reinforcement learning in preschoolers and parent ratings of reduced responsiveness to socialization, conceptualized as a developmental vulnerability to psychopathic traits. Methods One hundred and fifty-seven preschoolers (mean age 4.7 ± 0.8 years) participated in a substudy that was embedded within a larger project. Children completed the ‘Stars-in-Jars’ task, which involved learning to select rewarded jars and avoid punished jars. Maternal report of responsiveness to socialization was assessed with the Punishment Insensitivity and Low Concern for Others scales of the Multidimensional Assessment of Preschool Disruptive Behavior (MAP-DB). Results Punishment Insensitivity, but not Low Concern for Others, was significantly associated with reinforcement learning in multivariate models that accounted for age and sex. Specifically, higher Punishment Insensitivity was associated with significantly lower overall performance and more errors on punished trials (‘passive avoidance’). Conclusions Impairments in reinforcement learning manifest in preschoolers who are high in maternal ratings of Punishment Insensitivity. If replicated, these findings may help to pinpoint the neurodevelopmental antecedents of psychopathic tendencies and suggest novel intervention targets beginning in early childhood. JF - Journal of Child Psychology and Psychiatry and Allied Disciplines AU - Briggs-Gowan, Margaret J AU - Nichols, Sara R AU - Voss, Joel AU - Zobel, Elvira AU - Carter, Alice S AU - McCarthy, Kimberly J AU - Pine, Daniel S AU - Blair, James AU - Wakschlag, Lauren S AD - Department of Psychiatry, University of Connecticut Health Center, Farmington, CT, USA. ; Department of Medical Social Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. ; Department of Psychology, University of Massachusetts-Boston, Boston, MA, USA. ; The National Institute of Mental Health, Division of Intramural Research Programs, Rockville, MD, USA. ; Department of Psychiatry, University of Connecticut Health Center, Farmington, CT, USA. Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 154 EP - 161 CY - Cambridge PB - Blackwell Publishing Ltd. VL - 55 IS - 2 SN - 0021-9630 KW - Psychology KW - Assessment KW - Vulnerability KW - Young people KW - Avoidance KW - Childhood KW - Children KW - Disruptive behaviour KW - Early intervention programmes KW - Learning KW - Measurement KW - Passive avoidance KW - Preschool children KW - Psychopathy KW - Punishment KW - Reinforcement KW - Responsiveness KW - Socialization UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1748688877?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Child+Psychology+and+Psychiatry+and+Allied+Disciplines&rft.atitle=Punishment+insensitivity+and+impaired+reinforcement+learning+in+preschoolers&rft.au=Briggs-Gowan%2C+Margaret+J%3BNichols%2C+Sara+R%3BVoss%2C+Joel%3BZobel%2C+Elvira%3BCarter%2C+Alice+S%3BMcCarthy%2C+Kimberly+J%3BPine%2C+Daniel+S%3BBlair%2C+James%3BWakschlag%2C+Lauren+S&rft.aulast=Briggs-Gowan&rft.aufirst=Margaret&rft.date=2014-02-01&rft.volume=55&rft.issue=2&rft.spage=154&rft.isbn=&rft.btitle=&rft.title=Journal+of+Child+Psychology+and+Psychiatry+and+Allied+Disciplines&rft.issn=00219630&rft_id=info:doi/10.1111%2Fjcpp.12132 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-10-14 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1111/jcpp.12132 ER - TY - JOUR T1 - Genome-wide Transcriptional Sequencing Identifies Novel Mutations in Metabolic Genes in Human Hepatocellular Carcinoma AN - 1717493134; PQ0002002377 AB - We report on next-generation transcriptome sequencing results of three human hepatocellular carcinoma tumor/tumor-adjacent pairs. This analysis robustly examined ~12,000 genes for both expression differences and molecular alterations. We observed 4,513 and 1,182 genes demonstrating 2-fold or greater increase or decrease in expression relative to their normal, respectively. Network analysis of expression data identified the Aurora B signaling, FOXM1 transcription factor network and Wnt signaling pathways pairs being altered in HCC. We validated as differential gene expression findings in a large data set containing of 434 liver normal/tumor sample pairs. In addition to known driver mutations in TP53 and CTNNB1, our mutation analysis identified non-synonymous mutations in genes implicated in metabolic diseases, i.e. diabetes and obesity: IRS1, HMGCS1, ATP8B1, PRMT6 and CLU, suggesting a common molecular etiology for HCC of alternative pathogenic origin. JF - Cancer Genomics & Proteomics AU - Meerzaman, Daoud M AU - Yan, Chunhua AU - Chen, Qing-Rong AU - Edmonson, Michael N AU - Schaefer, Carl F AU - Clifford, Robert J AU - Dunn, Barbara K AU - Dong, Li AU - Finney, Richard P AU - Cultraro, Constance M AD - Center for Bioinformatics and Information Technology, National Cancer Institute, Rockville, MD, U.S.A., meerzamd@mail.nih.gov Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 1 EP - 12 PB - International Institute of Anticancer Research, 1st km Kapandritiou-Kalamou Road Kapandriti Attiki 19014 Greece VL - 11 IS - 1 SN - 1109-6535, 1109-6535 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts; Genetics Abstracts; Oncogenes & Growth Factors Abstracts KW - Hepatocellular carcinoma (HCC) KW - RNA-seq KW - gene expression KW - mutation RNA-seq KW - mutation KW - Obesity KW - aurora B protein KW - Etiology KW - Wnt protein KW - Data processing KW - Metabolic disorders KW - Tumors KW - p53 protein KW - Diabetes mellitus KW - Gene expression KW - Transcription factors KW - proteomics KW - Mutation KW - Hepatocellular carcinoma KW - Signal transduction KW - B 26660:Miscellaneous Oncogenes & Growth Factors KW - G 07880:Human Genetics KW - N 14835:Protein-Nucleic Acids Association KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717493134?accountid=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=Genome-wide+Transcriptional+Sequencing+Identifies+Novel+Mutations+in+Metabolic+Genes+in+Human+Hepatocellular+Carcinoma&rft.au=Meerzaman%2C+Daoud+M%3BYan%2C+Chunhua%3BChen%2C+Qing-Rong%3BEdmonson%2C+Michael+N%3BSchaefer%2C+Carl+F%3BClifford%2C+Robert+J%3BDunn%2C+Barbara+K%3BDong%2C+Li%3BFinney%2C+Richard+P%3BCultraro%2C+Constance+M&rft.aulast=Meerzaman&rft.aufirst=Daoud&rft.date=2014-02-01&rft.volume=11&rft.issue=1&rft.spage=1&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 - 2015-09-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Obesity; Etiology; aurora B protein; Data processing; Wnt protein; Metabolic disorders; Tumors; p53 protein; Gene expression; Diabetes mellitus; Transcription factors; proteomics; Mutation; Signal transduction; Hepatocellular carcinoma ER - TY - JOUR T1 - Lung Segmentation in Chest Radiographs Using Anatomical Atlases With Nonrigid Registration AN - 1676352613; PQ0001418089 AB - The National Library of Medicine (NLM) is developing a digital chest X-ray (CXR) screening system for deployment in resource constrained communities and developing countries worldwide with a focus on early detection of tuberculosis. A critical component in the computer-aided diagnosis of digital CXRs is the automatic detection of the lung regions. In this paper, we present a nonrigid registration-driven robust lung segmentation method using image retrieval-based patient specific adaptive lung models that detects lung boundaries, surpassing state-of-the-art performance. The method consists of three main stages: 1) a content-based image retrieval approach for identifying training images (with masks) most similar to the patient CXR using a partial Radon transform and Bhattacharyya shape similarity measure, 2) creating the initial patient-specific anatomical model of lung shape using SIFT-flow for deformable registration of training masks to the patient CXR, and 3) extracting refined lung boundaries using a graph cuts optimization approach with a customized energy function. Our average accuracy of 95.4% on the public JSRT database is the highest among published results. A similar degree of accuracy of 94.1% and 91.7% on two new CXR datasets from Montgomery County, MD, USA, and India, respectively, demonstrates the robustness of our lung segmentation approach. JF - IEEE Transactions on Medical Imaging AU - Candemir, Sema AU - Jaeger, Stefan AU - Palaniappan, Kannappan AU - Musco, Jonathan P AU - Singh, Rahul K AU - Xue, Zhiyun AU - Karargyris, Alexandros AU - Antani, Sameer AU - Thoma, George AU - McDonald, Clement J AD - Lister Hill National Center for Biomedical Communications U. S. National Library of Medicine, National Institutes of Health, Bethesda, MD, USA Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 577 EP - 590 PB - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States VL - 33 IS - 2 SN - 0278-0062, 0278-0062 KW - Biotechnology and Bioengineering Abstracts KW - Mycobacterium KW - Image processing KW - Chest KW - Radon KW - Models KW - Databases KW - Atlases KW - Lung KW - Energy KW - Ionizing radiation KW - Boundaries KW - Segmentation KW - Tuberculosis KW - Radiography KW - Developing countries KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676352613?accountid=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=Lung+Segmentation+in+Chest+Radiographs+Using+Anatomical+Atlases+With+Nonrigid+Registration&rft.au=Candemir%2C+Sema%3BJaeger%2C+Stefan%3BPalaniappan%2C+Kannappan%3BMusco%2C+Jonathan+P%3BSingh%2C+Rahul+K%3BXue%2C+Zhiyun%3BKarargyris%2C+Alexandros%3BAntani%2C+Sameer%3BThoma%2C+George%3BMcDonald%2C+Clement+J&rft.aulast=Candemir&rft.aufirst=Sema&rft.date=2014-02-01&rft.volume=33&rft.issue=2&rft.spage=577&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Medical+Imaging&rft.issn=02780062&rft_id=info:doi/10.1109%2FTMI.2013.2290491 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Image processing; Chest; Radon; Models; Databases; Atlases; Lung; Ionizing radiation; Energy; Segmentation; Boundaries; Tuberculosis; Radiography; Developing countries; Mycobacterium DO - http://dx.doi.org/10.1109/TMI.2013.2290491 ER - TY - JOUR T1 - TRIM5[alpha] Variations Influence Transduction Efficiency With Lentiviral Vectors in Both Human and Rhesus CD34+ Cells In Vitro and In Vivo AN - 1673387559; PQ0001387667 AB - Human immunodeficiency virus type 1 (HIV-1) vectors can transduce human hematopoietic stem cells (HSC), but transduction efficiency varies among individuals. The innate immune factor tripartite motif-containing protein 5[alpha] (TRIM5[alpha]) plays an important role for restriction of retroviral infection. In this study, we examined whether TRIM5[alpha] could account for variations in transduction efficiency using both an established rhesus gene therapy model and human CD34+ cell culture. Evaluation of TRIM5[alpha] genotypes (Mamu-1, -2, -3, -4, -5, and TrimCyp) in 16 rhesus macaques that were transplanted with transduced CD34+ cells showed a significant correlation between TRIM5[alpha] Mamu-4 and high gene marking in both lymphocytes and granulocytes 6 months after transplantation. Since significant human TRIM5[alpha] coding polymorphisms were not known, we evaluated TRIM5[alpha] expression levels in human CD34+ cells from 14 donors. Three days after HIV-1 vector transduction, measured transduction efficiency varied significantly among donors and was negatively correlated with TRIM5[alpha] expression levels. In summary, transduction efficiency in both rhesus and human CD34+ cells was influenced by TRIM5[alpha] variations (genotypes and expression levels). Our findings are important for both understanding and mitigating the variability of transduction efficiency for rhesus and human CD34+ cells. JF - Molecular Therapy AU - Evans, Molly E AU - Kumkhaek, Chutima AU - Hsieh, Matthew M AU - Donahue, Robert E AU - Tisdale, John F AU - Uchida, Naoya AD - Molecular and Clinical Hematology Branch, National Heart Lung and Blood Institutes/National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA, uchidan@nhlbi.nih.gov Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 348 EP - 358 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 22 IS - 2 SN - 1525-0016, 1525-0016 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts KW - Donors KW - Gene therapy KW - Gene polymorphism KW - CD34 antigen KW - Cell culture KW - Lymphocytes KW - Infection KW - Expression vectors KW - Leukocytes (granulocytic) KW - Stem cells KW - Human immunodeficiency virus 1 KW - Macaca mulatta KW - W 30905:Medical Applications KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673387559?accountid=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=TRIM5%5Balpha%5D+Variations+Influence+Transduction+Efficiency+With+Lentiviral+Vectors+in+Both+Human+and+Rhesus+CD34%2B+Cells+In+Vitro+and+In+Vivo&rft.au=Evans%2C+Molly+E%3BKumkhaek%2C+Chutima%3BHsieh%2C+Matthew+M%3BDonahue%2C+Robert+E%3BTisdale%2C+John+F%3BUchida%2C+Naoya&rft.aulast=Evans&rft.aufirst=Molly&rft.date=2014-02-01&rft.volume=22&rft.issue=2&rft.spage=348&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2013.256 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Expression vectors; Leukocytes (granulocytic); Donors; Stem cells; Gene therapy; Gene polymorphism; Cell culture; CD34 antigen; Lymphocytes; Infection; Human immunodeficiency virus 1; Macaca mulatta DO - http://dx.doi.org/10.1038/mt.2013.256 ER - TY - JOUR T1 - Chromosome Segregation in Vibrio cholerae AN - 1664193779; PQ0001238389 AB - The study of chromosome segregation is currently one of the most exciting research frontiers in cell biology. In this review, we discuss our current knowledge of the chromosome segregation process in Vibrio cholerae, based primarily on findings from fluorescence microscopy experiments. This bacterium is of special interest because of its eukaryotic feature of having a divided genome, a feature shared with 10% of known bacteria. We also discuss how the segregation mechanisms of V. cholerae compare with those in other bacteria, and highlight some of the remaining questions regarding the process of bacterial chromosome segregation. copyright 2015 S. Karger AG, Basel JF - Journal of Molecular Microbiology and Biotechnology AU - Ramachandran, Revathy AU - Jha, Jyoti AU - Chattoraj, Dhruba K AD - Laboratory of Biochemistry and Molecular Biology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Md., USA Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 360 EP - 370 PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland VL - 24 IS - 5-6 SN - 1464-1801, 1464-1801 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Bacterial mitosis KW - Divided genomes KW - Coordination of replication and segregation KW - Par-independent polar segregation KW - Genomes KW - Vibrio cholerae KW - Chromosomes KW - Microbiology KW - Cytology KW - Biotechnology KW - Fluorescence microscopy KW - J 02310:Genetics & Taxonomy KW - Q1 08205:Genetics and evolution KW - Q5 08524:Public health, medicines, dangerous organisms KW - G 07770:Bacteria KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664193779?accountid=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+Molecular+Microbiology+and+Biotechnology&rft.atitle=Chromosome+Segregation+in+Vibrio+cholerae&rft.au=Ramachandran%2C+Revathy%3BJha%2C+Jyoti%3BChattoraj%2C+Dhruba+K&rft.aulast=Ramachandran&rft.aufirst=Revathy&rft.date=2014-02-01&rft.volume=24&rft.issue=5-6&rft.spage=360&rft.isbn=&rft.btitle=&rft.title=Journal+of+Molecular+Microbiology+and+Biotechnology&rft.issn=14641801&rft_id=info:doi/10.1159%2F000368853 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Genomes; Chromosomes; Microbiology; Cytology; Biotechnology; Fluorescence microscopy; Vibrio cholerae DO - http://dx.doi.org/10.1159/000368853 ER - TY - JOUR T1 - Race and health profiles in the United States: an examination of the social gradient through the 2009 CHIS adult survey AN - 1660388274; PQ0001118513 AB - The objective of this study is to examine the role of the social gradient on multiple health outcomes and behaviors. It was predicted that higher levels of SES, measured by educational attainment and family income, would be associated with positive health behaviors and health status. The study also examined the differential effects of the social gradient in health among different racial/ethnic groups. The study contributes to the literature by illustrating unique patterns and trends of the social gradient across various racial/ethnic populations in a nationally representative sample. Future studies should further explore temporal trends to track the impact of the social gradient for different racial and ethnic populations in tandem with indices of national income inequalities. JF - Public Health AU - Nguyen, A B AU - Moser, R AU - Chou, W-Y AD - The National Cancer Institute (NCI), Division of Cancer Control and Population Sciences (DCCPS), 9609 Medical Center Dr., Rm 3E638, Rockville, MD 20850-9761, USA, Anh.Nguyen3@nih.gov PY - 2014 SP - 1076 EP - 1086 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 128 IS - 12 SN - 0033-3506, 0033-3506 KW - Health & Safety Science Abstracts KW - Health disparities KW - SES KW - Race KW - Ethnicity KW - Social gradient KW - USA KW - Socioeconomics KW - Ethnic groups KW - Income KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660388274?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+Health&rft.atitle=Race+and+health+profiles+in+the+United+States%3A+an+examination+of+the+social+gradient+through+the+2009+CHIS+adult+survey&rft.au=Nguyen%2C+A+B%3BMoser%2C+R%3BChou%2C+W-Y&rft.aulast=Nguyen&rft.aufirst=A&rft.date=2014-02-01&rft.volume=128&rft.issue=12&rft.spage=1076&rft.isbn=&rft.btitle=&rft.title=Public+Health&rft.issn=00333506&rft_id=info:doi/10.1016%2Fj.puhe.2014.10.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-12-23 N1 - SubjectsTermNotLitGenreText - Socioeconomics; Ethnic groups; Income; USA DO - http://dx.doi.org/10.1016/j.puhe.2014.10.003 ER - TY - JOUR T1 - Coinfection with Plasmodium falciparum and Schistosoma haematobium: Additional Evidence of the Protective Effect of Schistosomiasis on Malaria in Senegalese Children AN - 1647023865; 21172740 AB - Parasitic infections are associated with high morbidity and mortality in developing countries. Several studies focused on the influence of helminth infections on malaria but the nature of the biological interaction is under debate. Our objective was to undertake a study to explore the influence of the measure of excreted egg load caused by Schistosoma haematobium on Plasmodium falciparum parasite densities. Ten measures of malaria parasite density and two measures of schistosomiasis egg urinary excretion over a 2-year follow-up period on 178 Senegalese children were considered. A linear mixed-effect model was developed to take data dependence into account. This work showed that children with a light S. haematobium infection (1-9 eggs/mL of urine) presented lower P. falciparum parasite densities than children not infected by S. haematobium (P < 0.04). Possible changes caused by parasite coinfections should be considered in the anti-helminth treatment of children and in malaria vaccination development. JF - American Journal of Tropical Medicine and Hygiene AU - Lemaitre, Magali AU - Watier, Laurence AU - Briand, Valerie AU - Garcia, Andre AU - LeHesran, Jean Yves AU - Cot, Michel AD - Institut de Recherche pour le Developpement (UMR216), Universite Paris Descartes, Sorbonne Paris Cite, Faculte de Pharmacie, Paris, France; Faculte de pharmacie, Universite Paris Descartes, Paris, France; Inserm, U657, Paris, F-7501 5, France; Institut Pasteur, PhEMI, Paris, F-75015, France; Univ. Versailles Saint Quentin, Faculte de Medecine Paris Ile de France Ouest, EA 4499, F-78035, France; Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, maglemaitre@gmail.com Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 329 EP - 334 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 90 IS - 2 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality KW - Parasites KW - Human diseases KW - Schistosoma haematobium KW - Malaria KW - Infection KW - Eggs KW - Morbidity KW - Models KW - Public health KW - Mortality KW - Data processing KW - Schistosomiasis KW - Plasmodium falciparum KW - Children KW - Vaccination KW - Light effects KW - Urine KW - Excretion KW - Hygiene KW - Developing countries KW - Mortality causes KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08502:Methods and instruments KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647023865?accountid=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=Coinfection+with+Plasmodium+falciparum+and+Schistosoma+haematobium%3A+Additional+Evidence+of+the+Protective+Effect+of+Schistosomiasis+on+Malaria+in+Senegalese+Children&rft.au=Lemaitre%2C+Magali%3BWatier%2C+Laurence%3BBriand%2C+Valerie%3BGarcia%2C+Andre%3BLeHesran%2C+Jean+Yves%3BCot%2C+Michel&rft.aulast=Lemaitre&rft.aufirst=Magali&rft.date=2014-02-01&rft.volume=90&rft.issue=2&rft.spage=329&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.12-0431 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Urine; Schistosomiasis; Excretion; Malaria; Hygiene; Mortality causes; Public health; Mortality; Data processing; Children; Infection; Vaccination; Morbidity; Eggs; Models; Light effects; Developing countries; Schistosoma haematobium; Plasmodium falciparum DO - http://dx.doi.org/10.4269/ajtmh.12-0431 ER - TY - JOUR T1 - Calcified Neurocysticercus, Perilesional Edema, and Histologic Inflammation AN - 1647022849; 21172738 AB - Here, we present the second report of the histopathology of a Taenia solium calcification giving rise to perilesional edema. This has important implications, because if perilesional edema lesions are inflammatory in character, immunosuppressive or anti-inflammatory medications, not just antiepileptic drugs alone, may be useful to prevent or treat recurring episodes in such patients. JF - American Journal of Tropical Medicine and Hygiene AU - Nash, Theodore E AU - Bartelt, Luther A AU - Korpe, Poonum S AU - Lopes, Beatriz AU - Houpt, Eric R AD - National Institute of Allergy and Infectious Diseases, Bethesda, Maryland; Division of Infectious Diseases and International Health, University of Virginia; Department of Pathology, University of Virginia, Charlottesville, Virginia, erh6k@virginia.edu Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 318 EP - 321 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 90 IS - 2 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology KW - Calcification KW - Edema KW - Taenia solium KW - Antiepileptic agents KW - Inflammation KW - K 03400:Human Diseases KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647022849?accountid=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=Calcified+Neurocysticercus%2C+Perilesional+Edema%2C+and+Histologic+Inflammation&rft.au=Nash%2C+Theodore+E%3BBartelt%2C+Luther+A%3BKorpe%2C+Poonum+S%3BLopes%2C+Beatriz%3BHoupt%2C+Eric+R&rft.aulast=Nash&rft.aufirst=Theodore&rft.date=2014-02-01&rft.volume=90&rft.issue=2&rft.spage=318&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.13-0589 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Calcification; Edema; Antiepileptic agents; Inflammation; Taenia solium DO - http://dx.doi.org/10.4269/ajtmh.13-0589 ER - TY - JOUR T1 - Platelet hyperactivity, neurobehavioral symptoms and depression among Indian women chronically exposed to low level of arsenic AN - 1647011667; 21321481 AB - The prevalence of neurobehavioral symptoms (NBS) and depression has been investigated in premenopausal rural women of West Bengal, India enrolled from arsenic (As) endemic (groundwater As 11-50 mu g/L; n =342) and control areas (As level less than or equal to 10 mu g/L; n =312). The subjective symptoms questionnaire and Beck's 21-point depression inventory-II were used for the detection of NBS and depression, respectively. Platelet P-selectin expression was measured by flow cytometry, plasma neurotransmitter activity with high performance liquid chromatography and groundwater As level by atomic absorption spectroscopy. The As level in groundwater was 2.72 plus or minus 1.18 mu g/L in control and 28.3 plus or minus 13.51 mu g/L in endemic areas (p 0.05) from that of controls. Moreover, women from endemic areas had 2.3-times more P-selectin-expressing platelets in their circulation (p <0.001). After controlling the potential confounders, chronic low level As (11-50 mu g/L) exposure showed a positive association with the prevalence of neurobehavioral symptoms and depression among Indian women in their child-bearing age. JF - Neurotoxicology AU - Mukherjee, Bidisha AU - Bindhani, Banani AU - Saha, Hirak AU - Sinha, Dona AU - Ray, Manas Ranjan AD - Department of Experimental Hematology Unit, Chittaranjan National Cancer Institute, Kolkata-700 026, India PY - 2014 SP - 159 EP - 167 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 45 SN - 0161-813X, 0161-813X KW - Environment Abstracts; CSA Neurosciences Abstracts; Toxicology Abstracts KW - Arsenic KW - Water KW - Neurobehavioral symptoms KW - Depression KW - Indian women KW - High-performance liquid chromatography KW - Age KW - Anxiety KW - P-selectin KW - India, West Bengal KW - Extremities KW - Flow cytometry KW - Memory KW - Dopamine KW - Ground water KW - Neurotransmitters KW - Epinephrine KW - Inventories KW - Atomic absorption spectroscopy KW - Fatigue KW - ISW, India, West Bengal KW - Taste KW - Serotonin KW - Liquid chromatography KW - Neurotoxicity KW - Platelets KW - Females KW - Burning KW - Groundwater KW - Olfaction KW - Rural areas KW - N3 11028:Neuropharmacology & toxicology KW - X 24360:Metals KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647011667?accountid=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=Platelet+hyperactivity%2C+neurobehavioral+symptoms+and+depression+among+Indian+women+chronically+exposed+to+low+level+of+arsenic&rft.au=Mukherjee%2C+Bidisha%3BBindhani%2C+Banani%3BSaha%2C+Hirak%3BSinha%2C+Dona%3BRay%2C+Manas+Ranjan&rft.aulast=Mukherjee&rft.aufirst=Bidisha&rft.date=2014-02-01&rft.volume=45&rft.issue=&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/10.1016%2Fj.neuro.2014.10.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - High-performance liquid chromatography; Inventories; Atomic absorption spectroscopy; Arsenic; Fatigue; Depression; Anxiety; P-selectin; Taste; Serotonin; Flow cytometry; Memory; Dopamine; Platelets; Ground water; Burning; Neurotransmitters; Epinephrine; Olfaction; Extremities; Age; Liquid chromatography; Neurotoxicity; Females; Groundwater; Rural areas; ISW, India, West Bengal; India, West Bengal DO - http://dx.doi.org/10.1016/j.neuro.2014.10.011 ER - TY - JOUR T1 - N super(6)-methyladenosine modification destabilizes developmental regulators in embryonic stem cells AN - 1566842939; 20108949 AB - N super(6)-methyladenosine (m super(6)A) has been identified as the most abundant internal modification of messenger RNA in eukaryotes. m super(6)A modification is involved in cell fate determination in yeast and embryo development in plants. Its mammalian function remains unknown but thousands of mammalian mRNAs and long non-coding RNAs (lncRNAs) show m super(6)A modification and m super(6)A demethylases are required for mammalian energy homeostasis and fertility. We identify two proteins, the putative m super(6)A MTase, methyltransferase-like 3 (Mettl3; ref. ), and a related but uncharacterized protein Mettl14, that function synergistically to control m super(6)A formation in mammalian cells. Knockdown of Mettl3 and Mettl14 in mouse embryonic stem cells (mESCs) led to similar phenotypes, characterized by lack of m super(6)A RNA methylation and lost self-renewal capability. A large number of transcripts, including many encoding developmental regulators, exhibit m super(6)A methylation inversely correlated with mRNA stability and gene expression. The human antigen R (HuR) and microRNA pathways were linked to these effects. This gene regulatory mechanism operating in mESCs through m super(6)A methylation is required to keep mESCs at their ground state and may be relevant to thousands of mRNAs and lncRNAs in various cell types. JF - Nature Cell Biology AU - Wang, Yang AU - Li, Yue AU - Toth, Julia I AU - Petroski, Matthew D AU - Zhang, Zhaolei AU - Zhao, Jing Crystal AD - Tumor Initiation and Maintenance Program, NCI-designated Cancer Center, Sanford Burnham Medical Research Institute, La Jolla, California 92037, USA Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 191 EP - 198 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 16 IS - 2 SN - 1465-7392, 1465-7392 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - mRNA stability KW - Fertility KW - miRNA KW - non-coding RNA KW - mRNA KW - Gene expression KW - HuR protein KW - Stem cells KW - Mammalian cells KW - Energy balance KW - Embryo cells KW - DNA methylation KW - Cell fate KW - W 30940:Products KW - G 07800:Plants and Algae UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566842939?accountid=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=Nature+Cell+Biology&rft.atitle=N+super%286%29-methyladenosine+modification+destabilizes+developmental+regulators+in+embryonic+stem+cells&rft.au=Wang%2C+Yang%3BLi%2C+Yue%3BToth%2C+Julia+I%3BPetroski%2C+Matthew+D%3BZhang%2C+Zhaolei%3BZhao%2C+Jing+Crystal&rft.aulast=Wang&rft.aufirst=Yang&rft.date=2014-02-01&rft.volume=16&rft.issue=2&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=Nature+Cell+Biology&rft.issn=14657392&rft_id=info:doi/10.1038%2Fncb2902 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Fertility; mRNA stability; miRNA; non-coding RNA; mRNA; Gene expression; Stem cells; HuR protein; Embryo cells; Energy balance; Mammalian cells; DNA methylation; Cell fate DO - http://dx.doi.org/10.1038/ncb2902 ER - TY - JOUR T1 - Re: The sonopartogram: a novel method for recording the progress of labor by ultrasound. W. A. Hassan, T. Eggeboe, M. Ferguson, A. Gillett, J. Studd, D. Pasupathy and C. C. Lees. Ultrasound Obstet Gynecol 2014; 43: 189-194 AN - 1560106699; 19433860 AB - Linked Comment: Ultrasound Obstet Gynecol 2014; 43: 189-194 JF - Ultrasound in Obstetrics and Gynecology AU - Yeo, L AD - Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA. Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 137 EP - 138 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 43 IS - 2 SN - 0960-7692, 0960-7692 KW - Biotechnology and Bioengineering Abstracts KW - Gynecology KW - Ultrasound KW - Obstetrics KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560106699?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ultrasound+in+Obstetrics+and+Gynecology&rft.atitle=Re%3A+The+sonopartogram%3A+a+novel+method+for+recording+the+progress+of+labor+by+ultrasound.+W.+A.+Hassan%2C+T.+Eggeboe%2C+M.+Ferguson%2C+A.+Gillett%2C+J.+Studd%2C+D.+Pasupathy+and+C.+C.+Lees.+Ultrasound+Obstet+Gynecol+2014%3B+43%3A+189-194&rft.au=Yeo%2C+L&rft.aulast=Yeo&rft.aufirst=L&rft.date=2014-02-01&rft.volume=43&rft.issue=2&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=Ultrasound+in+Obstetrics+and+Gynecology&rft.issn=09607692&rft_id=info:doi/10.1002%2Fuog.13300 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-09-05 N1 - SubjectsTermNotLitGenreText - Gynecology; Obstetrics; Ultrasound DO - http://dx.doi.org/10.1002/uog.13300 ER - TY - JOUR T1 - Imaging of lipids in rat heart by MALDI-MS with silver nanoparticles AN - 1551080608; 20113106 AB - Lipids are a major component of heart tissue and perform several important functions such as energy storage, signaling, and as building blocks of biological membranes. The heart lipidome is quite diverse consisting of glycerophospholipids such as phosphatidylcholines (PCs), phosphatidylethanolamines (PEs), phosphatidylinositols (Pis), phosphatidylglycerols (PGs), cardiolipins (CLs), and glycerolipids, mainly triacylglycerols (TAGs). In this study, mass spectrometry imaging (MSI) enabled by matrix implantation of ionized silver nanoparticles (AgNP) was used to map several classes of lipids in heart tissue. The use of AgNP matrix implantation was motivated by our previous work showing that implantation doses of only 10 super(l4)/cm super(2) of 2 nm gold nanoparticulates into the first 10 nm of the near surface of the tissue enabled detection of most brain lipids (including neutral lipid species such as cerebrosides) more efficiently than traditional organic MALDI matrices. Herein, a similar implantation of 500 eV AgNP super(-) across the entire heart tissue section results in a quick, reproducible, solvent-free, uniform matrix concentration of 6 nm AgNP residing near the tissue surface. MALDI-MSI analysis of either positive or negative ions produce high-quality images of several heart lipid species. In negative ion mode, 24 lipid species [16 PEs, 4 PIs, 1 PG, 1 CL, 2 sphingomyelins (SMs)] were imaged. Positive ion images were also obtained from 29 lipid species (10 PCs, 5 PEs, 5 SMs, 9 TAGs) with the TAG species being heavily concentrated in vascular regions of the heart. JF - Analytical and Bioanalytical Chemistry AU - Jackson, Shelley N AU - Baldwin, Kathrine AU - Muller, Ludovic AU - Womack, Virginia M AU - Schultz, J Albert AU - Balaban, Carey AU - Woods, Amina S AD - Structural Biology Unit, NIDA IRP, NIH, 333 Cassell Drive, Room 1120, Baltimore, MD 21224, USA, awoods@intra.nida.nih.gov PY - 2014 SP - 1377 EP - 1386 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 406 IS - 5 SN - 1618-2642, 1618-2642 KW - Aqualine Abstracts; Water Resources Abstracts KW - MALDI KW - Mass spectrometry imaging KW - Lipids KW - Silver nanoparticles KW - Mass Spectrometry KW - Ions KW - Buildings KW - Storage KW - Gold KW - Biological Membranes KW - Silver KW - AQ 00001:Water Resources and Supplies KW - SW 0540:Properties of water UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551080608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+Bioanalytical+Chemistry&rft.atitle=Imaging+of+lipids+in+rat+heart+by+MALDI-MS+with+silver+nanoparticles&rft.au=Jackson%2C+Shelley+N%3BBaldwin%2C+Kathrine%3BMuller%2C+Ludovic%3BWomack%2C+Virginia+M%3BSchultz%2C+J+Albert%3BBalaban%2C+Carey%3BWoods%2C+Amina+S&rft.aulast=Jackson&rft.aufirst=Shelley&rft.date=2014-02-01&rft.volume=406&rft.issue=5&rft.spage=1377&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs0026-013-7525-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 39 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Storage; Ions; Mass Spectrometry; Lipids; Gold; Biological Membranes; Buildings; Silver DO - http://dx.doi.org/10.1007/s0026-013-7525-6 ER - TY - JOUR T1 - Impact of body size and physical activity during adolescence and adult life on overall and cause-specific mortality in a large cohort study from Iran AN - 1534846874; 19441623 AB - We conducted this study to examine life-course body size and physical activity in relation to total and cause-specific mortality, which has not previously been studied in the low and middle-income countries in Asia. The Golestan Cohort Study is a population-based cohort in northeastern Iran in which 50,045 people above the age of 40 have been followed since 2004. Participants were shown a validated pictogram to assess body size at ages 15, 30, and the time of recruitment. Information on occupational physical activity at these ages was also collected. Subjects were followed up annually, and cause of death was determined. Cox regression models were adjusted for age at cohort start, smoking, socioeconomic status, ethnicity, place of residence, education, and opium use. Models for body size were also adjusted for physical activity at the same age, and vice versa. During a total of 252,740 person-years of follow-up (mean follow-up duration 5.1 plus or minus 1.3 years) through December 2011, 2,529 of the cohort participants died. Larger body sizes at ages 15 or 30 in both sexes were associated with increased overall mortality. Cancer mortality was more strongly associated with adolescent obesity, and cardiovascular mortality with early adulthood body size. Weight gain between these ages was associated with cardiovascular mortality. Obese adolescents who lost weight still had increased mortality from all medical causes in both sexes. Physical activity during adolescence and early adulthood had no association with mortality, but at cohort baseline higher levels of activity were associated with reduced mortality. Mortality in this Middle-Eastern population was associated with obesity both during adolescence and early adult life. JF - European Journal of Epidemiology AU - Etemadi, Arash AU - Abnet, Christian C AU - Kamangar, Farin AU - Islami, Farhad AU - Khademi, Hooman AU - Pourshams, Akram AU - Poustchi, Hossein AU - Bagheri, Mohammad AU - Sohrabpour, Amir Ali AU - Aliasgar, Ali AU - Khoshnia, Masoud AU - Wacholder, Sholom AU - Matthews, Charles C AU - Pharoah, Paul D AU - Brennan, Paul AU - Boffetta, Paolo AU - Malekzadeh, Reza AU - Dawsey, Sanford M AD - Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran, arash.etemadi@nih.gov Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 95 EP - 109 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 29 IS - 2 SN - 0393-2990, 0393-2990 KW - Physical Education Index KW - Anthropometry KW - Obesity KW - Death KW - Weight KW - Adolescence KW - Cardiorespiratory KW - Exercise KW - Adults KW - Sex KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534846874?accountid=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=European+Journal+of+Epidemiology&rft.atitle=Impact+of+body+size+and+physical+activity+during+adolescence+and+adult+life+on+overall+and+cause-specific+mortality+in+a+large+cohort+study+from+Iran&rft.au=Etemadi%2C+Arash%3BAbnet%2C+Christian+C%3BKamangar%2C+Farin%3BIslami%2C+Farhad%3BKhademi%2C+Hooman%3BPourshams%2C+Akram%3BPoustchi%2C+Hossein%3BBagheri%2C+Mohammad%3BSohrabpour%2C+Amir+Ali%3BAliasgar%2C+Ali%3BKhoshnia%2C+Masoud%3BWacholder%2C+Sholom%3BMatthews%2C+Charles+C%3BPharoah%2C+Paul+D%3BBrennan%2C+Paul%3BBoffetta%2C+Paolo%3BMalekzadeh%2C+Reza%3BDawsey%2C+Sanford+M&rft.aulast=Etemadi&rft.aufirst=Arash&rft.date=2014-02-01&rft.volume=29&rft.issue=2&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Epidemiology&rft.issn=03932990&rft_id=info:doi/10.1007%2Fs10654-014-9883-6 LA - English DB - Physical Education Index N1 - Date revised - 2014-06-01 N1 - Number of references - 48 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Anthropometry; Obesity; Death; Weight; Adolescence; Cardiorespiratory; Adults; Exercise; Sex DO - http://dx.doi.org/10.1007/s10654-014-9883-6 ER - TY - JOUR T1 - RADIATION-EXPOSED POPULATIONS: WHO, WHY, AND HOW TO STUDY AN - 1524411550; 19642280 AB - Everyone is exposed to natural and man-made ionizing radiation that can originate from sources in the environment and in medical and occupational settings. Our present understanding of radiation- related health risks derives primarily from multidisciplinary health risk (epidemiologic) studies that provide the key information on radiation-associated health outcomes, quantify radiation-related disease risks, and enhance understanding of mechanisms of radiation-related disease pathogenesis. Such information is central to quantifying risks in relation to benefits; addressing public concerns, including societal and clinical needs in relation to radiation exposure; and providing the database needed for establishing recommendations for radiation protection. This paper describes a wide range of populations exposed to radiation and the motivation and key methodological criteria that drive the rationale and priority of studying such populations. Also, discussed are alternative methods for evaluating radiation-related health risks in these populations, with a major focus on epidemiologic approaches. This paper concludes with a short summary of major high-lights from radiation epidemiologic research and important unanswered questions. JF - Health Physics AU - Simon, Steven L AU - Linet, Martha S AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 9609 Medical Center Dr., Bethesda, MD 20892-9778, ssimon@mail.nih.gov Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 182 EP - 195 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 106 IS - 2 SN - 0017-9078, 0017-9078 KW - Risk Abstracts; Health & Safety Science Abstracts KW - epidemiology KW - exposure, occupational KW - medical radiation KW - National Council on Radiation Protection and Measurements KW - Health risks KW - Radiation KW - Ionizing radiation KW - Priorities KW - Public concern 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/1524411550?accountid=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=RADIATION-EXPOSED+POPULATIONS%3A+WHO%2C+WHY%2C+AND+HOW+TO+STUDY&rft.au=Simon%2C+Steven+L%3BLinet%2C+Martha+S&rft.aulast=Simon&rft.aufirst=Steven&rft.date=2014-02-01&rft.volume=106&rft.issue=2&rft.spage=182&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000006 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2015-05-27 N1 - SubjectsTermNotLitGenreText - Health risks; Radiation; Ionizing radiation; Priorities; Public concern DO - http://dx.doi.org/10.1097/HP.0000000000000006 ER - TY - JOUR T1 - INCREASED OCCUPATIONAL RADIATION DOSES: NUCLEAR FUEL CYCLE AN - 1520378502; 19642289 AB - The increased occupational doses resulting from the Chernobyl nuclear reactor accident that occurred in Ukraine in April 1986, the reactor accident of Fukushima that took place in Japan in March 2011, and the early operations of the Mayak Production Association in Russia in the 1940s and 1950s are presented and discussed. For comparison purposes, the occupational doses due to the other two major reactor accidents (Windscale in the United Kingdom in 1957 and Three Mile Island in the United States in 1979) and to the main plutonium-producing facility in the United States (Hanford Works) are also covered but in less detail. Both for the Chernobyl nuclear reactor accident and the routine operations at Mayak, the considerable efforts made to reconstruct individual doses from external irradiation to a large number of workers revealed that the recorded doses had been overestimated by a factor of about two. JF - Health Physics AU - Bouville, Andre AU - Kryuchkovt, Victor AD - Federal Medical Biological Agency, Burnasyan Federal Medical Biophysical Center, 46 Zhivopisnaya Street, 123182, Moscow, Russia, andre.bouville@nih.gov Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 259 EP - 271 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 106 IS - 2 SN - 0017-9078, 0017-9078 KW - Pollution Abstracts; Health & Safety Science Abstracts KW - National Council on Radiation Protection and Measurements KW - accidents, nuclear KW - Chernobyl KW - occupational safety KW - USA KW - Ukraine, Chernobyl KW - Accidents KW - Nuclear reactors KW - Radiation KW - Irradiation KW - USA, Washington, Hanford KW - Ukraine KW - Nuclear fuels KW - Russia KW - H 1000:Occupational Safety and Health KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520378502?accountid=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=INCREASED+OCCUPATIONAL+RADIATION+DOSES%3A+NUCLEAR+FUEL+CYCLE&rft.au=Bouville%2C+Andre%3BKryuchkovt%2C+Victor&rft.aulast=Bouville&rft.aufirst=Andre&rft.date=2014-02-01&rft.volume=106&rft.issue=2&rft.spage=259&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000066 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2015-05-27 N1 - SubjectsTermNotLitGenreText - Accidents; Nuclear reactors; Radiation; Irradiation; Nuclear fuels; Ukraine, Chernobyl; USA; Ukraine; USA, Washington, Hanford; Russia DO - http://dx.doi.org/10.1097/HP.0000000000000066 ER - TY - JOUR T1 - NUCLEAR REACTOR ACCIDENTS: EXPOSURES AND HEALTH EFFECTS AMONG MEMBERS OF THE PUBLIC AN - 1520364341; 19642295 AB - THE FIRST notable nuclear reactor accident occurred in 1957 at the Windscale Plant in Britain. Radioactive super(131)I was released from the reactor building into the surrounding area, but a 50 y follow-up of the highest-exposed group-workers involved in cleanup-found no exposure-related effects on cancer or mortality rates (McGeoghegan et al. 2010). JF - Health Physics AU - Hatch, Maureen AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, hatchm@mail.nih.gov Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 307 EP - 308 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 106 IS - 2 SN - 0017-9078, 0017-9078 KW - Health & Safety Science Abstracts; Pollution Abstracts KW - British Isles KW - Mortality KW - Accidents KW - Nuclear reactors KW - H 8000:Radiation Safety/Electrical Safety KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520364341?accountid=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=NUCLEAR+REACTOR+ACCIDENTS%3A+EXPOSURES+AND+HEALTH+EFFECTS+AMONG+MEMBERS+OF+THE+PUBLIC&rft.au=Hatch%2C+Maureen&rft.aulast=Hatch&rft.aufirst=Maureen&rft.date=2014-02-01&rft.volume=106&rft.issue=2&rft.spage=307&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000014 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2015-05-27 N1 - SubjectsTermNotLitGenreText - Mortality; Accidents; Nuclear reactors; British Isles DO - http://dx.doi.org/10.1097/HP.0000000000000014 ER - TY - JOUR T1 - Funding Strategies for Population Researchers: Perspectives from the National Institutes of Health AN - 1520340973; 201419305 AB - The purpose of this article is to briefly describe the application and funding process at the National Institutes of Health (NIH). We target our discussion to demographic and population science at the Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD), but the general strategies are applicable to social and behavioral scientists for all NIH funding opportunities. Adapted from the source document. JF - Population Research and Policy Review AU - Bures, Regina AU - Clark, Rebecca AU - King, Rosalind AU - Newcomer, Susan AD - Population Dynamics Branch (PDB), NICHD, 6100 Executive Boulevard, Bethesda, MD, 20892-7510, USA regina.bures@nih.gov Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 1 EP - 11 PB - Springer, Dordrecht The Netherlands VL - 33 IS - 1 SN - 0167-5923, 0167-5923 KW - Social Scientists KW - Health KW - Children KW - article KW - 1837: demography and human biology; demography (population studies) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520340973?accountid=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=Population+Research+and+Policy+Review&rft.atitle=Funding+Strategies+for+Population+Researchers%3A+Perspectives+from+the+National+Institutes+of+Health&rft.au=Bures%2C+Regina%3BClark%2C+Rebecca%3BKing%2C+Rosalind%3BNewcomer%2C+Susan&rft.aulast=Bures&rft.aufirst=Regina&rft.date=2014-02-01&rft.volume=33&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Population+Research+and+Policy+Review&rft.issn=01675923&rft_id=info:doi/10.1007%2Fs11113-013-9306-5 LA - English DB - Sociological Abstracts N1 - Date revised - 2014-05-01 N1 - Last updated - 2016-09-28 N1 - CODEN - PRPRE8 N1 - SubjectsTermNotLitGenreText - Health; Social Scientists; Children DO - http://dx.doi.org/10.1007/s11113-013-9306-5 ER - TY - JOUR T1 - Profile of male forensic psychiatric inpatients in South India AN - 1520312790; 201410503 AB - Aim: The study explored the socio-demographic, clinical and legal profile of forensic psychiatric inpatients in an attempt to improve the existing mental health services for prisoners within the prison and in psychiatric hospitals. Methodology: A chart review of 135 forensic psychiatric inpatients admitted between January 2005 and December 2009 was done. A structured data-extraction tool was used for data collection and a descriptive approach for analyses. Results: Subjects were referred either directly from prison (62.2%) or from court (37.8%) for diagnosis, treatment or certification. References to the Mental Health Act 1987, charges and inclusion of first investigation report and behavioural observation report was lacking in most. The majority of prisoners (85.7%) were under trial, murder being the most common charge. Psychiatric diagnosis was made in 90.3%, the most common being psychosis. Substance use (nicotine, alcohol, cannabis) and high-risk behaviours were also common. Conclusion: There is a need to streamline the procedure of referral and to sensitize the referral authorities about the Mental Health Act and mental illnesses, and the need to enclose first investigation reports and behavioural observation reports. De-addiction services and facilities need to be established within prison premises so that the inmates get the benefit of treatment at the earliest opportunity. [Reprinted by permission of Sage Publications Ltd., copyright holder.] JF - International Journal of Social Psychiatry AU - Kumar, Dayachandra AU - Viswanath, Biju AU - Sebestian, Ami AU - Holla, Bharath AU - Konduru, Reddema AU - Chandrashekar, Chanapatna Rajannachar AU - Math, Suresh Bada AD - Department of Psychiatric Nursing, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 55 EP - 62 PB - Sage Publications, London UK VL - 60 IS - 1 SN - 0020-7640, 0020-7640 KW - Forensic psychiatry prison legal KW - Prisons KW - Diagnosis KW - Psychiatric hospitals KW - Referrals KW - Mental health KW - Prisoners KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520312790?accountid=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=Profile+of+male+forensic+psychiatric+inpatients+in+South+India&rft.au=Kumar%2C+Dayachandra%3BViswanath%2C+Biju%3BSebestian%2C+Ami%3BHolla%2C+Bharath%3BKonduru%2C+Reddema%3BChandrashekar%2C+Chanapatna+Rajannachar%3BMath%2C+Suresh+Bada&rft.aulast=Kumar&rft.aufirst=Dayachandra&rft.date=2014-02-01&rft.volume=60&rft.issue=1&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Social+Psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764012461334 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-05-01 N1 - Number of references - 16 N1 - Last updated - 2016-09-27 N1 - CODEN - IJSPAG N1 - SubjectsTermNotLitGenreText - Psychiatric hospitals; Prisoners; Prisons; Diagnosis; Mental health; Referrals DO - http://dx.doi.org/10.1177/0020764012461334 ER - TY - JOUR T1 - Global DNA methylation and one-carbon metabolism gene polymorphisms and the risk of breast cancer in the Sister Study AN - 1512323016; 19325022 AB - Summary Our finding that LINE-1 undermethylation was present in blood collected from women before clinical detection of their tumor provides evidence from a prospective study that lower global methylation is associated with increased risk of breast cancer. Summary Our finding that LINE-1 undermethylation was present in blood collected from women before clinical detection of their tumor provides evidence from a prospective study that lower global methylation is associated with increased risk of breast cancer. JF - Carcinogenesis AU - DeRoo, Lisa A AU - Bolick, Sophia CE AU - Xu, Zongli AU - Umbach, David M AU - Shore, David AU - Weinberg, Clarice R AU - Sandler, Dale P AU - Taylor, Jack A AD - super(1)Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA,, taylor@niehs.nih.gov Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 333 EP - 338 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 35 IS - 2 SN - 0143-3334, 0143-3334 KW - Toxicology Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Blood KW - Gene polymorphism KW - Carcinogenesis KW - DNA methylation KW - Breast cancer KW - Tumors KW - Metabolism KW - G 07880:Human Genetics KW - N 14820:DNA Metabolism & Structure KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512323016?accountid=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=Global+DNA+methylation+and+one-carbon+metabolism+gene+polymorphisms+and+the+risk+of+breast+cancer+in+the+Sister+Study&rft.au=DeRoo%2C+Lisa+A%3BBolick%2C+Sophia+CE%3BXu%2C+Zongli%3BUmbach%2C+David+M%3BShore%2C+David%3BWeinberg%2C+Clarice+R%3BSandler%2C+Dale+P%3BTaylor%2C+Jack+A&rft.aulast=DeRoo&rft.aufirst=Lisa&rft.date=2014-02-01&rft.volume=35&rft.issue=2&rft.spage=333&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/10.1093%2Fcarcin%2Fbgt342 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Blood; Gene polymorphism; Carcinogenesis; DNA methylation; Breast cancer; Tumors; Metabolism DO - http://dx.doi.org/10.1093/carcin/bgt342 ER - TY - JOUR T1 - The Role of Hemocytes in Anopheles gambiae Antiplasmodial Immunity AN - 1512322459; 19422958 AB - Hemocytes synthesize key components of the mosquito complement-like system, but their role in the activation of antiplasmodial responses has not been established. The effect of activating Toll signaling in hemocytes on Plasmodium survival was investigated by transferring hemocytes or cell-free hemolymph from donor mosquitoes in which the suppressor cactus was silenced. These transfers greatly enhanced antiplasmodial immunity, indicating that hemocytes are active players in the activation of the complement-like system, through an effector/effectors regulated by the Toll pathway. A comparative analysis of hemocyte populations between susceptible G3 and the refractory L3-5 Anopheles gambiae mosquito strains did not reveal significant differences under basal conditions or in response to Plasmodium berghei infection. The response of susceptible mosquitoes to different Plasmodium species revealed similar kinetics following infection with P. berghei,P. yoelii or P. falciparum, but the strength of the priming response was stronger in less compatible mosquito-parasite pairs. The Toll, Imd,STAT or JNK signaling cascades were not essential for the production of the hemocyte differentiation factor (HDF) in response to P. berghei infection, but disruption of Toll, STAT or JNK abolished hemocyte differentiation in response to HDF. We conclude that hemocytes are key mediators of A. gambiae antiplasmodial responses. copyright 2013 S. Karger AG, Basel JF - Journal of Innate Immunity AU - Ramirez, Jose Luis AU - Garver, Lindsey S AU - Brayner, Fbio Andr AU - Alves, Luiz Carlos AU - Rodrigues, Janneth AU - Molina-Cruz, Alvaro AU - Barillas-Mury, Carolina AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Md., USA Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 119 EP - 128 PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland VL - 6 IS - 2 SN - 1662-811X, 1662-811X KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts KW - Hemocyte differentiation KW - Plasmodium KW - Malaria KW - Immune priming KW - Cell survival KW - Hemolymph KW - c-Jun amino-terminal kinase KW - Pest control KW - Immunity KW - Infection KW - Strains KW - Anopheles gambiae KW - Plasmodium berghei KW - Differentiation KW - Suppressors KW - Kinetics KW - Hemocytes KW - Antiprotozoal agents KW - Aquatic insects KW - Signal transduction KW - K 03340:Effects of Physical & Chemical Factors KW - F 06945:Insect Immunity 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/1512322459?accountid=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+Innate+Immunity&rft.atitle=The+Role+of+Hemocytes+in+Anopheles+gambiae+Antiplasmodial+Immunity&rft.au=Ramirez%2C+Jose+Luis%3BGarver%2C+Lindsey+S%3BBrayner%2C+Fbio+Andr%3BAlves%2C+Luiz+Carlos%3BRodrigues%2C+Janneth%3BMolina-Cruz%2C+Alvaro%3BBarillas-Mury%2C+Carolina&rft.aulast=Ramirez&rft.aufirst=Jose&rft.date=2014-02-01&rft.volume=6&rft.issue=2&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Journal+of+Innate+Immunity&rft.issn=1662811X&rft_id=info:doi/10.1159%2F000353765 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2016-09-14 N1 - SubjectsTermNotLitGenreText - Suppressors; Pest control; Immunity; Strains; Aquatic insects; Cell survival; Hemolymph; Differentiation; c-Jun amino-terminal kinase; Kinetics; Hemocytes; Antiprotozoal agents; Infection; Signal transduction; Anopheles gambiae; Plasmodium berghei DO - http://dx.doi.org/10.1159/000353765 ER - TY - JOUR T1 - Print News Coverage of School-Based Human Papillomavirus Vaccine Mandates AN - 1512193567; 201404606 AB - In 2007, legislation was proposed in 24 states and the District of Columbia for school-based human papillomavirus (HPV) vaccine mandates, and mandates were enacted in Texas, Virginia, and the District of Columbia. Media coverage of these events was extensive, and media messages both reflected and contributed to controversy surrounding these legislative activities. Messages communicated through the media are an important influence on adolescent and parent understanding of school-based vaccine mandates. We conducted structured text analysis of newspaper coverage, including quantitative analysis of 169 articles published in mandate jurisdictions from 2005 to 2009, and qualitative analysis of 63 articles from 2007. Our structured analysis identified topics, key stakeholders and sources, tone, and the presence of conflict. Qualitative thematic analysis identified key messages and issues. Media coverage was often incomplete, providing little context about cervical cancer or screening. Skepticism and autonomy concerns were common. Messages reflected conflict and distrust of government activities, which could negatively impact this and other youth-focused public health initiatives. If school health professionals are aware of the potential issues raised in media coverage of school-based health mandates, they will be more able to convey appropriate health education messages and promote informed decision-making by parents and students. Adapted from the source document. JF - Journal of School Health AU - Casciotti, Dana M AU - Smith, Katherine C AU - Andon, Lindsay AU - Vernick, Jon AU - Tsui, Amy AU - Klassen, Ann C AD - Program Analyst, National Library of Medicine, National Institutes of Health, 8600 Rockville Pike, Bethesda, MD 20894 danacasciotti@yahoo.com Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 71 EP - 81 PB - Wiley-Blackwell, UK VL - 84 IS - 2 SN - 0022-4391, 0022-4391 KW - Coverage KW - Quantitative analysis KW - School based KW - Vaccines KW - Parents KW - Human papillomaviruses KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512193567?accountid=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+Health&rft.atitle=Print+News+Coverage+of+School-Based+Human+Papillomavirus+Vaccine+Mandates&rft.au=Casciotti%2C+Dana+M%3BSmith%2C+Katherine+C%3BAndon%2C+Lindsay%3BVernick%2C+Jon%3BTsui%2C+Amy%3BKlassen%2C+Ann+C&rft.aulast=Casciotti&rft.aufirst=Dana&rft.date=2014-02-01&rft.volume=84&rft.issue=2&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Journal+of+School+Health&rft.issn=00224391&rft_id=info:doi/10.1111%2Fjosh.12126 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-04-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Coverage; School based; Vaccines; Human papillomaviruses; Parents; Quantitative analysis DO - http://dx.doi.org/10.1111/josh.12126 ER - TY - JOUR T1 - Biomechanics of Atherosclerotic Coronary Plaque: Site, Stability and In Vivo Elasticity Modeling AN - 1505340384; 19348019 AB - Coronary atheroma develop in local sites that are widely variable among patients and are considerably variable in their vulnerability for rupture. This article summarizes studies conducted by our collaborative laboratories on predictive biomechanical modeling of coronary plaques. It aims to give insights into the role of biomechanics in the development and localization of atherosclerosis, the morphologic features that determine vulnerable plaque stability, and emerging in vivo imaging techniques that may detect and characterize vulnerable plaque. Composite biomechanical and hemodynamic factors that influence the actual site of development of plaques have been studied. Plaque vulnerability, in vivo, is more challenging to assess. Important steps have been made in defining the biomechanical factors that are predictive of plaque rupture and the likelihood of this occurring if characteristic features are known. A critical key in defining plaque vulnerability is the accurate quantification of both the morphology and the mechanical properties of the diseased arteries. Recently, an early IVUS based palpography technique developed to assess local strain, elasticity and mechanical instabilities has been successfully revisited and improved to account for complex plaque geometries. This is based on an initial best estimation of the plaque components' contours, allowing subsequent iteration for elastic modulus assessment as a basis for plaque stability determination. The improved method has also been preliminarily evaluated in patients with successful histologic correlation. Further clinical evaluation and refinement are on the horizon. JF - Annals of Biomedical Engineering AU - Ohayon, Jacques AU - Finet, Gerard AU - Floc'h, Simon AU - Cloutier, Guy AU - Gharib, Ahmed M AU - Heroux, Julie AU - Pettigrew, Roderic I AD - Laboratory TIMC-IMAG/DyCTiM, UJF, CNRS UMR 5525, In3S, Grenoble, France, rpettigrew@nih.gov Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 269 EP - 279 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 42 IS - 2 SN - 0090-6964, 0090-6964 KW - Biotechnology and Bioengineering Abstracts KW - Arteries KW - Rupture KW - Hemodynamics KW - Plaques KW - Arteriosclerosis KW - imaging KW - Biomechanics KW - Mechanical properties KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1505340384?accountid=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=Annals+of+Biomedical+Engineering&rft.atitle=Biomechanics+of+Atherosclerotic+Coronary+Plaque%3A+Site%2C+Stability+and+In+Vivo+Elasticity+Modeling&rft.au=Ohayon%2C+Jacques%3BFinet%2C+Gerard%3BFloc%27h%2C+Simon%3BCloutier%2C+Guy%3BGharib%2C+Ahmed+M%3BHeroux%2C+Julie%3BPettigrew%2C+Roderic+I&rft.aulast=Ohayon&rft.aufirst=Jacques&rft.date=2014-02-01&rft.volume=42&rft.issue=2&rft.spage=269&rft.isbn=&rft.btitle=&rft.title=Annals+of+Biomedical+Engineering&rft.issn=00906964&rft_id=info:doi/10.1007%2Fs10439-013-0888-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Number of references - 83 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Arteries; Hemodynamics; Rupture; Plaques; Arteriosclerosis; imaging; Biomechanics; Mechanical properties DO - http://dx.doi.org/10.1007/s10439-013-0888-1 ER - TY - JOUR T1 - Fighting Noise Pollution: A Public Health Strategy AN - 1505339462; 19339770 AB - In this issue of EHP, investigators from the University of Michigan at Ann Arbor describe the most serious health effects of noise and propose a blueprint for an effective U.S. public health response. super(1) The team, led by Richard L. Neitzel, an assistant professor of environmental health sciences, estimated that nearly one-third of Americans are exposed to noise levels deemed injurious to hearing by the U.S. Environmental Protection Agency (EPA) - a 24-hour average noise level exceeding 70 dBA. super(1) The authors based this figure on 1981 estimates from the EPA. super(2) JF - Environmental Health Perspectives AU - Holzman, David C AD - David C. Holzman writes on science, medicine, energy, economics, and cars from Lexington and Wellfleet, MA. His work has appeared in Smithsonian, The Atlantic Monthly, and the Journal of the National Cancer Institute. Y1 - 2014/02/01/ PY - 2014 DA - 2014 Feb 01 SP - A58 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 122 IS - 2 SN - 0091-6765, 0091-6765 KW - Pollution Abstracts; Environment Abstracts; Health & Safety Science Abstracts; Sustainability Science Abstracts KW - EPA KW - Noise levels KW - Environmental health KW - Noise pollution KW - Public health KW - P 7000:NOISE KW - M3 1010:Issues in Sustainable Development 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/1505339462?accountid=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=Environmental+Health+Perspectives&rft.atitle=Fighting+Noise+Pollution%3A+A+Public+Health+Strategy&rft.au=Holzman%2C+David+C&rft.aulast=Holzman&rft.aufirst=David&rft.date=2014-02-01&rft.volume=122&rft.issue=2&rft.spage=A58&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.122-A58 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - EPA; Noise levels; Environmental health; Noise pollution; Public health DO - http://dx.doi.org/10.1289/ehp.122-A58 ER - TY - JOUR T1 - Reduction of DNA mismatch repair protein expression in airway epithelial cells of premenopausal women chronically exposed to biomass smoke AN - 1505330512; 19299307 AB - Biomass burning is a major source of indoor air pollution in rural India. This study examined whether chronic inhalation of biomass smoke causes change in the DNA mismatch repair (MMR) pathway in the airway cells. For this, airway cells exfoliated in sputum were collected from 72 premenopausal nonsmoking rural women (median age 34 years) who cooked with biomass (wood, dung, crop residues) and 68 control women who cooked with cleaner fuel liquefied petroleum gas (LPG) for the past 5 years or more. The levels of particulate matters with diameters less than 10 and 2.5 mu m (PM sub(10) and PM sub(2.5)) in indoor air were measured by real-time aerosol monitor. Benzene exposure was monitored by measuring trans,trans-muconic acid (t,t-MA) in urine by high-performance liquid chromatography with ultraviolet detector. Generation of reactive oxygen species (ROS) and level of superoxide dismutase (SOD) in airway cells were measured by flow cytometry and spectrophotometry, respectively. Immunocytochemical assay revealed lower percentage of airway epithelial cells expressing MMR proteins mutL homolog 1 (MLH1) and mutS homolog 2 (MSH2) in biomass-using women compared to LPG-using controls. Women who cooked with biomass had 6.7 times higher level of urinary t,t-MA, twofold increase in ROS generation, and 31 % depletion of SOD. Indoor air of biomass-using households had three times more particulate matters than that of controls. ROS, urinary t,t-MA, and particulate pollution in biomass-using kitchen had negative correlation, while SOD showed positive correlation with MSH2 and MLH1 expression. It appears that chronic exposure to biomass smoke reduces MMR response in airway epithelial cells, and oxidative stress plays an important role in the process. JF - Environmental Science and Pollution Research International AU - Mukherjee, Bidisha AU - Dutta, Anindita AU - Chowdhury, Saswati AU - Roychoudhury, Sanghita AU - Ray, Manas Ranjan AD - Department of Experimental Hematology, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata, 700 026, India, manasrray@rediffmail.com PY - 2014 SP - 2826 EP - 2836 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 21 IS - 4 SN - 0944-1344, 0944-1344 KW - Biochemistry Abstracts 2: Nucleic Acids; Environment Abstracts; Pollution Abstracts KW - High-performance liquid chromatography KW - Inhalation KW - Epithelial cells KW - MLH1 protein KW - Fuels KW - Particulate matter KW - Particulate pollution KW - Particulates KW - Benzene KW - India KW - Flow cytometry KW - U.V. radiation KW - Reactive oxygen species KW - Oxidative stress KW - Chronic exposure KW - Superoxide dismutase KW - Petroleum KW - Spectrophotometry KW - Respiratory tract KW - MMR protein KW - Aerosols KW - MSH2 protein KW - mismatch repair KW - Wood KW - Crop residues KW - Biomass KW - DNA repair KW - Air pollution KW - Smoke KW - Liquid chromatography KW - Urine KW - Households KW - DNA KW - Dung KW - Proteins KW - Burning KW - Sputum KW - Indoor environments KW - Rural areas KW - P 0000:AIR POLLUTION KW - N 14845:Miscellaneous KW - ENA 01:Air Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1505330512?accountid=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+Science+and+Pollution+Research+International&rft.atitle=Reduction+of+DNA+mismatch+repair+protein+expression+in+airway+epithelial+cells+of+premenopausal+women+chronically+exposed+to+biomass+smoke&rft.au=Mukherjee%2C+Bidisha%3BDutta%2C+Anindita%3BChowdhury%2C+Saswati%3BRoychoudhury%2C+Sanghita%3BRay%2C+Manas+Ranjan&rft.aulast=Mukherjee&rft.aufirst=Bidisha&rft.date=2014-02-01&rft.volume=21&rft.issue=4&rft.spage=2826&rft.isbn=&rft.btitle=&rft.title=Environmental+Science+and+Pollution+Research+International&rft.issn=09441344&rft_id=info:doi/10.1007%2Fs11356-013-2218-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-03-01 N1 - Number of references - 58 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Inhalation; High-performance liquid chromatography; MLH1 protein; Epithelial cells; Fuels; Particulate matter; Particulate pollution; Benzene; Flow cytometry; U.V. radiation; Reactive oxygen species; Superoxide dismutase; Chronic exposure; Oxidative stress; Petroleum; Spectrophotometry; Respiratory tract; MMR protein; MSH2 protein; Aerosols; mismatch repair; Crop residues; DNA repair; Biomass; Smoke; Air pollution; Urine; Dung; Sputum; Burning; Wood; Particulates; Liquid chromatography; Households; DNA; Proteins; Indoor environments; Rural areas; India DO - http://dx.doi.org/10.1007/s11356-013-2218-4 ER - TY - JOUR T1 - Quantitative genetics of response to novelty and other stimuli by infant rhesus macaques (Macaca Mulatta) across three behavioral assessments AN - 1504157079; 4535133 AB - Primate behavior is influenced by both heritable factors and environmental experience during development. Previous studies of rhesus macaques ( Macaca mulatta ) examined the effects of genetic variation on expressed behavior and related neurobiological traits (heritability and/or genetic association) using a variety of study designs. Most of these prior studies examined genetic effects on the behavior of adults or adolescent rhesus macaques, not in young macaques early in development. To assess environmental and additive genetic variation in behavioral reactivity and response to novelty among infants, we investigated a range of behavioral traits in a large number ( N = 428) of pedigreed infants born and housed in large outdoor corrals at the Oregon National Primate Research Center (ONPRC). We recorded the behavior of each subject during a series of brief tests, involving exposure of each infant to a novel environment, to a social threat without the mother present, and to a novel environment with its mother present but sedated. We found significant heritability ( h 2 ) for willingness to move away from the mother and explore a novel environment ( Italic h 2 = 0.25 ± 0.13; P = 0.003). The infants also exhibited a range of heritable behavioral reactions to separation stress or to threat when the mother was not present ( h Italic 2 = 0.23 ± 0.13-0.24 ± 0.15, P < 0.01). We observed no evidence of maternal environmental effects on these traits. Our results extend knowledge of genetic influences on temperament and reactivity in nonhuman primates by demonstrating that several measures of behavioral reactivity among infant rhesus macaques are heritable. Reprinted by permission of Springer JF - International journal of primatology AU - Fawcett, G L AU - Dettmer, A M AU - Kay, D AU - Raveendran, M AU - Higley, J D AU - Ryan, N D AU - Cameron, J L AU - Rogers, J AD - Baylor College of Medicine ; National Institutes of Health ; University of Florida ; Brigham Young University ; University of Pittsburgh Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 325 EP - 339 VL - 35 IS - 1 SN - 0164-0291, 0164-0291 KW - Anthropology KW - Genetics KW - Primatology KW - Anxiety KW - Old World monkeys KW - Primates KW - Infants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504157079?accountid=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=International+journal+of+primatology&rft.atitle=Quantitative+genetics+of+response+to+novelty+and+other+stimuli+by+infant+rhesus+macaques+%28Macaca+Mulatta%29+across+three+behavioral+assessments&rft.au=Fawcett%2C+G+L%3BDettmer%2C+A+M%3BKay%2C+D%3BRaveendran%2C+M%3BHigley%2C+J+D%3BRyan%2C+N+D%3BCameron%2C+J+L%3BRogers%2C+J&rft.aulast=Fawcett&rft.aufirst=G&rft.date=2014-02-01&rft.volume=35&rft.issue=1&rft.spage=325&rft.isbn=&rft.btitle=&rft.title=International+journal+of+primatology&rft.issn=01640291&rft_id=info:doi/10.1007%2Fs10764-014-9750-z LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-03-04 N1 - Last updated - 2014-03-05 N1 - SubjectsTermNotLitGenreText - 1147 4196; 5460 1615 8573 11325; 10149; 10148; 6495 2212; 8910 10148 DO - http://dx.doi.org/10.1007/s10764-014-9750-z ER - TY - JOUR T1 - Consent under pressure: the puzzle of third party coercion AN - 1504156823; 4535360 AB - Coercion by the recipient of consent renders that consent invalid. But what about when the coercive force comes from a third party, not from the person to whom consent would be proffered? In this paper I analyze how threats from a third party affect consent. I argue that, as with other cases of coercion, we should distinguish threats that render consent invalid from threats whose force is too weak to invalidate consent and threats that are legitimate. Illegitimate controlling third party threats render consent invalid just as they do in two party cases. However, knowing that the consent is invalid is not sufficient to tell the recipient of consent what she may or should do. I argue that when presented with a token of consent from someone whom she thinks is experiencing an illegitimate controlling threat, the recipient may act on that token if and only if doing so represents a reasonable joint decision for her and the victim of coercion. The appropriate action for someone faced with third party coercion therefore depends on the other options open to her and those open to the victim of coercion. Reprinted by permission of Springer JF - Ethical theory and moral practice AU - Millum, Joseph AD - National Institutes of Health Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 113 EP - 127 VL - 17 IS - 1 SN - 1386-2820, 1386-2820 KW - Sociology KW - Two-party systems KW - Legitimacy KW - Medical research KW - Third-party intervention KW - Illegitimacy KW - Victims of crime UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1504156823?accountid=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=Ethical+theory+and+moral+practice&rft.atitle=Consent+under+pressure%3A+the+puzzle+of+third+party+coercion&rft.au=Millum%2C+Joseph&rft.aulast=Millum&rft.aufirst=Joseph&rft.date=2014-02-01&rft.volume=17&rft.issue=1&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=Ethical+theory+and+moral+practice&rft.issn=13862820&rft_id=info:doi/10.1007%2Fs10677-013-9419-2 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-03-04 N1 - Last updated - 2014-03-05 N1 - SubjectsTermNotLitGenreText - 7886 10902; 12749 2703 2698 6828 7869 5200 5574 10472; 6216 13133 7253; 13035 9253; 13307 3015 11881; 7333 7315 9705 DO - http://dx.doi.org/10.1007/s10677-013-9419-2 ER - TY - JOUR T1 - Differential expression of p53 family proteins in colorectal adenomas and carcinomas: Prognostic and predictive values. AN - 1503554675; 23996743 AB - We studied the contribution of p53 family proteins and their isoforms to the development and progression of colorectal carcinoma in relation to VEGF. p53, p63, p73 and VEGF proteins were assessed in 45 colorectal adenomas (CRAs), 80 carcinomas (CRCs) and 36 normal colonic tissue samples (NCT) by immunohistochemistry. Different p63 and p73 isoforms were assessed by RT-PCR. Aberrant protein and RNA expressions were correlated to patients' characteristics, disease free and overall survival (DFS and OS). p53, p63, p73 and VEGF proteins were detected in 22.2%, 73.3%, 33.3%, 46.7% CRAs; in 68.8%, 38.8%, 62.5%, 62.5% CRCs and 16.7%, 83.3%; 13.9%, 41.7% NCT (p<0.05 except for VEGF). Commonest isoforms were TAp63α, ΔNp63, TAp73α in CRA and ΔNp63, TAp63α, ΔNp73, TAp73β in CRC. Significant correlations were found between aggressive tumor phenotypes and aberrations in p73, p53, p63, VEGF. DFS correlated with advanced stage, p73 and VEGF aberrations. While advanced stage, positive lymph nodes, p73 and p53 correlated with OS. Prognosis was worse in patients with aberrant p63 and p73 than in those with normal p63 and p73 expression regardless of p53 gene status (p⟨0.05). p53 family proteins and VEGF play a pivotal role in colorectal carcinogenesis. p53 prognostic potential is augmented by p73 and p63 aberrations indicating a synergistic effect between the three family members. Nodal status, stage, p73, VEGF and p53 could be used as predictors of DFS and OS. JF - Histology and histopathology AU - Bahnassy, Abeer A AU - Zekri, Abdel-Rahman N AU - Salem, Salem E AU - Abou-Bakr, Amany A AU - Sakr, Mona A AU - Abdel-Samiaa, Ayman G AU - Al-Bradei, Manal AD - Pathology Department, National Cancer Institute, Cairo University, Cairo, Egypt. chaya2000@hotmail.com. ; Cancer Biology Department, National Cancer Institute, Cairo University, Cairo, Egypt. ; Medical Oncology Department, National Cancer Institute, Cairo University, Cairo, Egypt. ; Pathology Department, National Cancer Institute, Cairo University, Cairo, Egypt. ; Radiotherapy Department, National Cancer Institute, Cairo University, Cairo, Egypt. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 207 EP - 216 VL - 29 IS - 2 KW - CKAP4 protein, human KW - 0 KW - DNA-Binding Proteins KW - Membrane Proteins KW - Nuclear Proteins KW - Tumor Protein p73 KW - Tumor Suppressor Protein p53 KW - Tumor Suppressor Proteins KW - Vascular Endothelial Growth Factor A KW - delta Np73 protein, human KW - p73 protein, human KW - Index Medicus KW - Young Adult KW - Colon -- pathology KW - Humans KW - Prognosis KW - Intestinal Mucosa -- metabolism KW - Predictive Value of Tests KW - Prospective Studies KW - Colon -- metabolism KW - Adult KW - Intestinal Mucosa -- pathology KW - Middle Aged KW - Female KW - Male KW - Nuclear Proteins -- genetics KW - Colorectal Neoplasms -- metabolism KW - Membrane Proteins -- metabolism KW - Tumor Suppressor Proteins -- genetics KW - DNA-Binding Proteins -- genetics KW - Colorectal Neoplasms -- genetics KW - Membrane Proteins -- genetics KW - Tumor Suppressor Protein p53 -- metabolism KW - Adenoma -- metabolism KW - Carcinoma -- pathology KW - Colorectal Neoplasms -- pathology KW - Tumor Suppressor Proteins -- metabolism KW - Tumor Suppressor Protein p53 -- genetics KW - Nuclear Proteins -- metabolism KW - Adenoma -- genetics KW - Adenoma -- pathology KW - Carcinoma -- metabolism KW - Vascular Endothelial Growth Factor A -- genetics KW - Vascular Endothelial Growth Factor A -- metabolism KW - Carcinoma -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1503554675?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Histology+and+histopathology&rft.atitle=Differential+expression+of+p53+family+proteins+in+colorectal+adenomas+and+carcinomas%3A+Prognostic+and+predictive+values.&rft.au=Bahnassy%2C+Abeer+A%3BZekri%2C+Abdel-Rahman+N%3BSalem%2C+Salem+E%3BAbou-Bakr%2C+Amany+A%3BSakr%2C+Mona+A%3BAbdel-Samiaa%2C+Ayman+G%3BAl-Bradei%2C+Manal&rft.aulast=Bahnassy&rft.aufirst=Abeer&rft.date=2014-02-01&rft.volume=29&rft.issue=2&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Histology+and+histopathology&rft.issn=1699-5848&rft_id=info:doi/10.14670%2FHH-29.207 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-19 N1 - Date created - 2014-02-04 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.14670/HH-29.207 ER - TY - JOUR T1 - Metabolism of synthetic cannabinoids PB-22 and its 5-fluoro analog, 5F-PB-22, by human hepatocyte incubation and high-resolution mass spectrometry. AN - 1503550510; 24518903 AB - PB-22 (1-pentyl-8-quinolinyl ester-1H-indole-3-carboxylic acid) and 5F-PB-22 (1-(5-fluoropentyl)-8-quinolinyl ester-1H-indole-3-carboxylic acid) are new synthetic cannabinoids with a quinoline substructure and the first marketed substances with an ester bond linkage. No human metabolism data are currently available, making it difficult to document PB-22 and 5F-PB-22 intake from urine analysis, and complicating assessment of the drugs' pharmacodynamic and toxicological properties. We incubated 10 μmol/l PB-22 and 5F-PB-22 with pooled cryopreserved human hepatocytes up to 3 h and analyzed samples on a TripleTOF 5600+ high-resolution mass spectrometer. Data were acquired via TOF scan, followed by information-dependent acquisition triggered product ion scans with mass defect filtering (MDF). The accurate mass full scan MS and MS/MS metabolite datasets were analyzed with multiple data processing techniques, including MDF, neutral loss and product ion filtering. The predominant metabolic pathway for PB-22 and 5F-PB-22 was ester hydrolysis yielding a wide variety of (5-fluoro)pentylindole-3-carboxylic acid metabolites. Twenty metabolites for PB-22 and 22 metabolites for 5F-PB-22 were identified, with the majority generated by oxidation with or without glucuronidation. For 5F-PB-22, oxidative defluorination occurred forming PB-22 metabolites. Both compounds underwent epoxide formation followed by internal hydrolysis and also produced a cysteine conjugate. Human hepatic metabolic profiles were generated for PB-22 and 5F-PB-22. Pentylindole-3-carboxylic acid, hydroxypentyl-PB-22 and PB-22 pentanoic acid for PB-22, and 5'-fluoropentylindole-3-carboxylic acid, PB-22 pentanoic acid and the hydroxy-5F-PB-22 metabolite with oxidation at the quinoline system for 5F-PB-22 are likely the best targets to incorporate into analytical methods for urine to document PB-22 and 5F-PB-22 intake. JF - Analytical and bioanalytical chemistry AU - Wohlfarth, Ariane AU - Gandhi, Adarsh S AU - Pang, Shaokun AU - Zhu, Mingshe AU - Scheidweiler, Karl B AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Boulevard, Baltimore, MD, 21224, USA. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 1763 EP - 1780 VL - 406 IS - 6 KW - Cannabinoids KW - 0 KW - Indoles KW - indole-3-carboxylic acid KW - 771-50-6 KW - Index Medicus KW - Oxidation-Reduction KW - Spectrometry, Mass, Electrospray Ionization KW - Cells, Cultured KW - Humans KW - Indoles -- metabolism KW - Tandem Mass Spectrometry KW - Indoles -- chemistry KW - Hydrolysis KW - Cannabinoids -- metabolism KW - Cannabinoids -- chemistry KW - Hepatocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1503550510?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+bioanalytical+chemistry&rft.atitle=Metabolism+of+synthetic+cannabinoids+PB-22+and+its+5-fluoro+analog%2C+5F-PB-22%2C+by+human+hepatocyte+incubation+and+high-resolution+mass+spectrometry.&rft.au=Wohlfarth%2C+Ariane%3BGandhi%2C+Adarsh+S%3BPang%2C+Shaokun%3BZhu%2C+Mingshe%3BScheidweiler%2C+Karl+B%3BHuestis%2C+Marilyn+A&rft.aulast=Wohlfarth&rft.aufirst=Ariane&rft.date=2014-02-01&rft.volume=406&rft.issue=6&rft.spage=1763&rft.isbn=&rft.btitle=&rft.title=Analytical+and+bioanalytical+chemistry&rft.issn=1618-2650&rft_id=info:doi/10.1007%2Fs00216-014-7668-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-21 N1 - Date created - 2014-02-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00216-014-7668-0 ER - TY - JOUR T1 - Assessment of CASP10 contact-assisted predictions AN - 1500796382; 19044590 AB - In CASP10, for the first time, contact-assisted structure predictions have been assessed. Sets of pairs of contacting residues from target structures were provided to predictors for a second round of prediction after the initial round in which they were given only sequences. The objective of the experiment was to measure model quality improvement resulting from the added contact information and thereby assess and help develop so-called hybrid prediction methods-methods where some experimentally determined distance constraints are used to augment de novo computational prediction methods. The results of the experiment were, overall, quite promising. Proteins 2014; 82(Suppl 2):84-97. copyright 2013 Wiley Periodicals, Inc. JF - Proteins: Structure, Function and Bioinformatics AU - Taylor, Todd J AU - Bai, Hongjun AU - Tai, Chin-Hsien AU - Lee, Byungkook AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 84 EP - 97 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States VL - 82 SN - 0887-3585, 0887-3585 KW - Biotechnology and Bioengineering Abstracts KW - Bioinformatics KW - Hybrids KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500796382?accountid=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=Assessment+of+CASP10+contact-assisted+predictions&rft.au=Taylor%2C+Todd+J%3BBai%2C+Hongjun%3BTai%2C+Chin-Hsien%3BLee%2C+Byungkook&rft.aulast=Taylor&rft.aufirst=Todd&rft.date=2014-02-01&rft.volume=82&rft.issue=&rft.spage=84&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24367 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Last updated - 2014-03-20 N1 - SubjectsTermNotLitGenreText - Hybrids DO - http://dx.doi.org/10.1002/prot.24367 ER - TY - JOUR T1 - Assessment of template-free modeling in CASP10 and ROLL AN - 1500784250; 19044580 AB - We present the assessment of predictions for Template-Free Modeling in CASP10 and a report on the first ROLL experiment wherein predictions are collected year round for review at the regular CASP season. Models were first clustered so that duplicated or very similar ones were grouped together and represented by one model in the cluster. The representatives were then compared with targets using GDT_TS, QCS, and three additional superposition-independent score functions newly developed for CASP10. For each target, the top 15 representatives by each score were pooled to form the Top15Union set. All models in this set were visually inspected by four of us independently using the new plugin, EvalScore, which we developed with the UCSF Chimera group. The best models were selected for each target after extensive debate among the four examiners. Groups were ranked by the number of targets (hits) for which a group's model was selected as one of the best models. The Keasar group had most hits in both categories, with four of 19 FM and eight of 36 ROLL targets. The most successful prediction servers were QUARK from Zhang's group for FM category with three hits and Zhang-server for the ROLL category with seven hits. As observed in CASP9, many successful groups were not true "template-free" modelers but used remote templates and/or server models to obtain their winning models. The results of the first ROLL experiment were broadly similar to those of the CASP10 FM exercise. Proteins 2014; 82(Suppl 2):57-83. copyright 2013 Wiley Periodicals, Inc. JF - Proteins: Structure, Function and Bioinformatics AU - Tai, Chin-Hsien AU - Bai, Hongjun AU - Taylor, Todd J AU - Lee, Byungkook AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, 20892. Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 57 EP - 83 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States VL - 82 SN - 0887-3585, 0887-3585 KW - Biotechnology and Bioengineering Abstracts KW - Bioinformatics KW - Models KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500784250?accountid=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=Assessment+of+template-free+modeling+in+CASP10+and+ROLL&rft.au=Tai%2C+Chin-Hsien%3BBai%2C+Hongjun%3BTaylor%2C+Todd+J%3BLee%2C+Byungkook&rft.aulast=Tai&rft.aufirst=Chin-Hsien&rft.date=2014-02-01&rft.volume=82&rft.issue=&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24470 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Last updated - 2014-03-20 N1 - SubjectsTermNotLitGenreText - Models DO - http://dx.doi.org/10.1002/prot.24470 ER - TY - JOUR T1 - Evaluation of engraftment and immunological tolerance after reduced intensity conditioning in a rhesus hematopoietic stem cell gene therapy model AN - 1500780058; 19282638 AB - Reduced intensity conditioning (RIC) is desirable for hematopoietic stem cell (HSC) targeted gene therapy; however, RIC may be insufficient for efficient engraftment and inducing immunological tolerance to transgenes. We previously established long-term gene marking in our rhesus macaque autologous HSC transplantation model following 10 Gy total body irradiation (TBI). In this study, we evaluated RIC transplantation with 4 Gy TBI in two rhesus macaques that received equal parts of CD34 super(+) cells transduced with green fluorescent protein (GFP)-expressing lentiviral vector and empty vector not expressing transgenes. In both animals, equivalently low gene marking between GFP and empty vectors was observed 6 months post-transplantation, even with efficient transduction of CD34 super(+) cells in vitro. Autologous lymphocyte infusion with GFP marking resulted in an increase of gene marking in lymphocytes in a control animal with GFP tolerance, but not in the two RIC-transplanted animals. In vitro assays revealed strong cellular and humoral immune responses to GFP protein in the two RIC-transplanted animals, but this was not observed in controls. In summary, 4 Gy TBI is insufficient to permit engraftment of genetically modified HSCs and induce immunological tolerance to transgenes. Our findings should help in the design of conditioning regimens in gene therapy trials. JF - Gene Therapy AU - Uchida, N AU - Weitzel, R P AU - Evans, M E AU - Green, R AU - Bonifacino, A C AU - Krouse, A E AU - Metzger, M E AU - Hsieh, M M AU - Donahue, R E AU - Tisdale, J 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, MD, USA Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 148 EP - 157 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 21 IS - 2 SN - 0969-7128, 0969-7128 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Autografts KW - Macaca mulatta KW - Immunological tolerance KW - W 30905:Medical Applications KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500780058?accountid=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=Evaluation+of+engraftment+and+immunological+tolerance+after+reduced+intensity+conditioning+in+a+rhesus+hematopoietic+stem+cell+gene+therapy+model&rft.au=Uchida%2C+N%3BWeitzel%2C+R+P%3BEvans%2C+M+E%3BGreen%2C+R%3BBonifacino%2C+A+C%3BKrouse%2C+A+E%3BMetzger%2C+M+E%3BHsieh%2C+M+M%3BDonahue%2C+R+E%3BTisdale%2C+J+F&rft.aulast=Uchida&rft.aufirst=N&rft.date=2014-02-01&rft.volume=21&rft.issue=2&rft.spage=148&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2013.67 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Last updated - 2014-03-20 N1 - SubjectsTermNotLitGenreText - Immunological tolerance; Macaca mulatta DO - http://dx.doi.org/10.1038/gt.2013.67 ER - TY - JOUR T1 - Definition and classification of evaluation units for CASP10 AN - 1500759241; 19044582 AB - For the 10th experiment on Critical Assessment of the techniques of protein Structure Prediction (CASP), the prediction target proteins were broken into independent evaluation units (EUs), which were then classified into template-based modeling (TBM) or free modeling (FM) categories. We describe here how the EUs were defined and classified, what issues arose in the process, and how we resolved them. EUs are frequently not the whole target proteins but the constituting structural domains. However, the assessors from CASP7 on combined more than one domain into 1 EU for some targets, which implied that the assessment also included evaluation of the prediction of the relative position and orientation of these domains. In CASP10, we followed and expanded this notion by defining multidomain EUs for a number of targets. These included 3 EUs, each made of two domains of familiar fold but arranged in a novel manner and for which the focus of evaluation was the interdomain arrangement. An EU was classified to the TBM category if a template could be found by sequence similarity searches and to FM if a structural template could not be found by structural similarity searches. The EUs that did not fall cleanly in either of these cases were classified case-by-case, often including consideration of the overall quality and characteristics of the predictions. Proteins 2014; 82(Suppl 2):14-25. copyright 2013 Wiley Periodicals, Inc. JF - Proteins: Structure, Function and Bioinformatics AU - Taylor, Todd J AU - Tai, Chin-Hsien AU - Huang, Yuanpeng J AU - Block, Jeremy AU - Bai, Hongjun AU - Kryshtafovych, Andriy AU - Montelione, Gaetano T AU - Lee, Byungkook AD - Laboratory of Molecular Biology, Center for Cancer Research National Cancer Institute National Institutes of Health, Bethesda, Maryland, 20892-4264. Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 14 EP - 25 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States VL - 82 SN - 0887-3585, 0887-3585 KW - Biotechnology and Bioengineering Abstracts KW - Bioinformatics KW - Protein structure KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1500759241?accountid=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=Definition+and+classification+of+evaluation+units+for+CASP10&rft.au=Taylor%2C+Todd+J%3BTai%2C+Chin-Hsien%3BHuang%2C+Yuanpeng+J%3BBlock%2C+Jeremy%3BBai%2C+Hongjun%3BKryshtafovych%2C+Andriy%3BMontelione%2C+Gaetano+T%3BLee%2C+Byungkook&rft.aulast=Taylor&rft.aufirst=Todd&rft.date=2014-02-01&rft.volume=82&rft.issue=&rft.spage=14&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24434 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Last updated - 2014-03-20 N1 - SubjectsTermNotLitGenreText - Protein structure DO - http://dx.doi.org/10.1002/prot.24434 ER - TY - JOUR T1 - Stereospecific PARP trapping by BMN 673 and comparison with olaparib and rucaparib. AN - 1499149824; 24356813 AB - Anti-PARP drugs were initially developed as catalytic inhibitors to block the repair of DNA single-strand breaks. We recently reported that several PARP inhibitors have an additional cytotoxic mechanism by trapping PARP-DNA complexes, and that both olaparib and niraparib act as PARP poisons at pharmacologic concentrations. Therefore, we have proposed that PARP inhibitors should be evaluated based both on catalytic PARP inhibition and PARP-DNA trapping. Here, we evaluated the novel PARP inhibitor, BMN 673, and compared its effects on PARP1 and PARP2 with two other clinical PARP inhibitors, olaparib and rucaparib, using biochemical and cellular assays in genetically modified chicken DT40 and human cancer cell lines. Although BMN 673, olaparib, and rucaparib are comparable at inhibiting PARP catalytic activity, BMN 673 is ∼100-fold more potent at trapping PARP-DNA complexes and more cytotoxic as single agent than olaparib, whereas olaparib and rucaparib show similar potencies in trapping PARP-DNA complexes. The high level of resistance of PARP1/2 knockout cells to BMN 673 demonstrates the selectivity of BMN 673 for PARP1/2. Moreover, we show that BMN 673 acts by stereospecific binding to PARP1 as its enantiomer, LT674, is several orders of magnitude less efficient. BMN 673 is also approximately 100-fold more cytotoxic than olaparib and rucaparib in combination with the DNA alkylating agents methyl methane sulfonate (MMS) and temozolomide. Our study demonstrates that BMN 673 is the most potent clinical PARP inhibitor tested to date with the highest efficiency at trapping PARP-DNA complexes. JF - Molecular cancer therapeutics AU - Murai, Junko AU - Huang, Shar-Yin N AU - Renaud, Amèlie AU - Zhang, Yiping AU - Ji, Jiuping AU - Takeda, Shunichi AU - Morris, Joel AU - Teicher, Beverly AU - Doroshow, James H AU - Pommier, Yves AD - Corresponding Author: Yves Pommier, Developmental Therapeutics Branch, Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, 37 Convent Drive, Building 37, Room 5068, NIH, Bethesda, MD 20892-4255. pommier@nih.gov. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 433 EP - 443 VL - 13 IS - 2 KW - Enzyme Inhibitors KW - 0 KW - Indoles KW - Phthalazines KW - Piperazines KW - Poly(ADP-ribose) Polymerase Inhibitors KW - talazoparib KW - Dacarbazine KW - 7GR28W0FJI KW - rucaparib KW - 8237F3U7EH KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - DNA KW - 9007-49-2 KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - olaparib KW - WOH1JD9AR8 KW - temozolomide KW - YF1K15M17Y KW - Index Medicus KW - Molecular Structure KW - Immunoblotting KW - Animals KW - Stereoisomerism KW - Poly(ADP-ribose) Polymerases -- chemistry KW - Dose-Response Relationship, Drug KW - Humans KW - DNA -- metabolism KW - Cell Line, Tumor KW - Poly(ADP-ribose) Polymerases -- metabolism KW - Methyl Methanesulfonate -- pharmacology KW - Fluorescence Polarization KW - Cell Survival -- drug effects KW - Dacarbazine -- analogs & derivatives KW - Dacarbazine -- pharmacology KW - Adenosine Triphosphate -- metabolism KW - DNA -- chemistry KW - Enzyme Inhibitors -- pharmacology KW - Inhibitory Concentration 50 KW - Drug Synergism KW - Cell Cycle -- drug effects KW - Phthalazines -- chemistry KW - Indoles -- pharmacology KW - Piperazines -- pharmacology KW - Phthalazines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499149824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+cancer+therapeutics&rft.atitle=Stereospecific+PARP+trapping+by+BMN+673+and+comparison+with+olaparib+and+rucaparib.&rft.au=Murai%2C+Junko%3BHuang%2C+Shar-Yin+N%3BRenaud%2C+Am%C3%A8lie%3BZhang%2C+Yiping%3BJi%2C+Jiuping%3BTakeda%2C+Shunichi%3BMorris%2C+Joel%3BTeicher%2C+Beverly%3BDoroshow%2C+James+H%3BPommier%2C+Yves&rft.aulast=Murai&rft.aufirst=Junko&rft.date=2014-02-01&rft.volume=13&rft.issue=2&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=Molecular+cancer+therapeutics&rft.issn=1538-8514&rft_id=info:doi/10.1158%2F1535-7163.MCT-13-0803 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-19 N1 - Date created - 2014-02-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2012 Jan 19;481(7381):287-94 [22258607] J Biol Chem. 2012 Feb 3;287(6):4198-210 [22158865] Nat Biotechnol. 2012 Mar;30(3):283-8 [22343925] BMC Med. 2012;10:25 [22401667] Nature. 2012 Mar 29;483(7391):570-5 [22460902] Nat Struct Mol Biol. 2012 Apr;19(4):417-23 [22388737] EMBO J. 2006 Mar 22;25(6):1305-14 [16498404] Nat Rev Mol Cell Biol. 2006 Jul;7(7):517-28 [16829982] Cancer Res. 2006 Aug 15;66(16):8109-15 [16912188] Front Biosci. 2008;13:3046-82 [17981777] Nat Rev Cancer. 2008 Mar;8(3):193-204 [18256616] J Clin Oncol. 2008 Aug 1;26(22):3785-90 [18591545] Clin Cancer Res. 2008 Dec 1;14(23):7917-23 [19047122] J Clin Oncol. 2009 Jun 1;27(16):2705-11 [19364967] N Engl J Med. 2009 Jul 9;361(2):123-34 [19553641] N Engl J Med. 2009 Oct 8;361(15):1475-85 [19812404] EMBO Mol Med. 2009 Sep;1(6-7):315-22 [20049735] Nat Rev Cancer. 2010 Apr;10(4):293-301 [20200537] Cell. 2010 Apr 16;141(2):243-54 [20362325] Mol Cancer Ther. 2010 May;9(5):1451-60 [20442306] Mol Endocrinol. 2010 Jun;24(6):1287-96 [20375240] Mol Cell. 2010 Jul 9;39(1):8-24 [20603072] Nat Rev Clin Oncol. 2010 Sep;7(9):508-19 [20700108] Nat Rev Drug Discov. 2010 Nov;9(11):843-56 [21031001] Neoplasia. 2011 Feb;13(2):145-53 [21403840] Nucleic Acids Res. 2011 May;39(9):3607-20 [21227924] Mol Oncol. 2011 Aug;5(4):387-93 [21821475] PLoS One. 2011;6(10):e26152 [22028822] Science. 2012 May 11;336(6082):728-32 [22582261] Cancer Res. 2012 Jul 15;72(14):3499-511 [22802077] Breast Cancer Res Treat. 2012 Jul;134(2):649-59 [22678161] Cancer Res. 2012 Nov 1;72(21):5588-99 [23118055] Cancer Discov. 2013 Jan;3(1):68-81 [23103855] Nat Struct Mol Biol. 2013 Mar;20(3):347-54 [23396353] PLoS One. 2013;8(4):e61520 [23634208] Clin Cancer Res. 2013 Sep 15;19(18):5003-15 [23881923] Mol Aspects Med. 2013 Dec;34(6):1217-56 [23370117] Oncogene. 2013 Nov 21;32(47):5377-87 [23934192] Science. 1999 Dec 3;286(5446):1897-905 [10583946] Mol Cell Biol. 2000 Jun;20(11):3977-87 [10805740] Clin Cancer Res. 2000 Jul;6(7):2860-7 [10914735] Nature. 1992 Mar 26;356(6367):356-8 [1549180] Br J Cancer. 1995 Oct;72(4):849-56 [7547230] Mol Cell Biol. 2005 Feb;25(3):1124-34 [15657438] Nature. 2005 Apr 14;434(7035):913-7 [15829966] Nature. 2005 Apr 14;434(7035):917-21 [15829967] Mol Cell Biol. 2005 Aug;25(16):7158-69 [16055725] Nat Cell Biol. 2005 Nov;7(11):1133-9 [16244666] Mol Cancer Ther. 2006 Mar;5(3):564-74 [16546970] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1535-7163.MCT-13-0803 ER - TY - JOUR T1 - The interactive roles of zinc and calcium in mitochondrial dysfunction and neurodegeneration. AN - 1499140028; 24127746 AB - Zinc has been implicated in neurodegeneration following ischemia. In analogy with calcium, zinc has been proposed to induce toxicity via mitochondrial dysfunction, but the relative role of each cation in mitochondrial damage remains unclear. Here, we report that under conditions mimicking ischemia in hippocampal neurons - normal (2 mM) calcium plus elevated (> 100 μM) exogenous zinc - mitochondrial dysfunction evoked by glutamate, kainate or direct depolarization is, despite significant zinc uptake, primarily governed by calcium. Thus, robust mitochondrial ion accumulation, swelling, depolarization, and reactive oxygen species generation were only observed after toxic stimulation in calcium-containing media. This contrasts with the lack of any mitochondrial response in zinc-containing but calcium-free medium, even though zinc uptake and toxicity were strong under these conditions. Indeed, abnormally high, ionophore-induced zinc uptake was necessary to elicit any mitochondrial depolarization. In calcium- and zinc-containing media, depolarization-induced zinc uptake facilitated cell death and enhanced accumulation of mitochondrial calcium, which localized to characteristic matrix precipitates. Some of these contained detectable amounts of zinc. Together these data indicate that zinc uptake is generally insufficient to trigger mitochondrial dysfunction, so that mechanism(s) of zinc toxicity must be different from that of calcium. Published 2013. This article is a U.S. Government work and is in the public domain in the USA. JF - Journal of neurochemistry AU - Pivovarova, Natalia B AU - Stanika, Ruslan I AU - Kazanina, Galina AU - Villanueva, Idalis AU - Andrews, S Brian AD - Laboratory of Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 592 EP - 602 VL - 128 IS - 4 KW - Calcium Channels KW - 0 KW - Indicators and Reagents KW - Reactive Oxygen Species KW - Receptors, AMPA KW - Zinc KW - J41CSQ7QDS KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - cell death KW - hippocampal neurons KW - excitotoxicity KW - ischemia KW - electron microscopy KW - Mitochondrial Swelling -- physiology KW - Electron Probe Microanalysis KW - Animals KW - Cytosol -- metabolism KW - Calcium Channels -- physiology KW - Receptors, AMPA -- physiology KW - Pregnancy KW - Hippocampus -- drug effects KW - Rats KW - Microscopy, Fluorescence KW - Electrophysiological Phenomena -- drug effects KW - Rats, Sprague-Dawley KW - Brain Ischemia -- pathology KW - Cells, Cultured KW - Hippocampus -- cytology KW - Microscopy, Electron KW - Female KW - Neurodegenerative Diseases -- physiopathology KW - Zinc -- pharmacology KW - Calcium -- toxicity KW - Mitochondrial Diseases -- physiopathology KW - Mitochondrial Diseases -- metabolism KW - Zinc -- physiology KW - Zinc -- toxicity KW - Neurodegenerative Diseases -- metabolism KW - Calcium -- physiology KW - Calcium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499140028?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=The+interactive+roles+of+zinc+and+calcium+in+mitochondrial+dysfunction+and+neurodegeneration.&rft.au=Pivovarova%2C+Natalia+B%3BStanika%2C+Ruslan+I%3BKazanina%2C+Galina%3BVillanueva%2C+Idalis%3BAndrews%2C+S+Brian&rft.aulast=Pivovarova&rft.aufirst=Natalia&rft.date=2014-02-01&rft.volume=128&rft.issue=4&rft.spage=592&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=1471-4159&rft_id=info:doi/10.1111%2Fjnc.12489 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-08 N1 - Date created - 2014-02-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Neurochem. 2008 Sep;106(5):2184-93 [18624907] Ann Neurol. 2008 Jun;63(6):720-8 [18496842] J Neurosci. 2009 Jan 28;29(4):1105-14 [19176819] J Neurochem. 2009 Mar;108(5):1300-8 [19183267] Cell Calcium. 2009 May;45(5):447-55 [19349076] Nat Rev Neurosci. 2009 Nov;10(11):780-91 [19826435] J Cereb Blood Flow Metab. 2011 Apr;31(4):1073-84 [20978516] J Neurochem. 2011 Apr;117(2):231-43 [21255017] Trends Pharmacol Sci. 2011 Aug;32(8):480-6 [21621864] Neuron. 2011 Sep 22;71(6):1116-26 [21943607] J Neurosci. 2011 Nov 9;31(45):16076-85 [22072659] J Neurosci. 2012 May 9;32(19):6642-50 [22573686] Science. 2012 Aug 31;337(6098):1062-5 [22936770] J Physiol. 2000 Oct 1;528 Pt 1:39-52 [11018104] J Neurosci. 2001 Mar 15;21(6):1893-901 [11245674] Neurobiol Dis. 2002 Jun;10(1):41-53 [12079403] Neuron. 2004 Feb 5;41(3):351-65 [14766175] J Neurosci. 2004 Jun 16;24(24):5611-22 [15201334] J Biol Chem. 2004 Jul 30;279(31):32989-3000 [15166243] Neuron. 1993 Jan;10(1):43-9 [7678965] J Neurosci. 1995 May;15(5 Pt 1):3318-27 [7751912] J Neurosci. 1998 Oct 1;18(19):7727-38 [9742143] Proc Natl Acad Sci U S A. 1999 Mar 2;96(5):2414-9 [10051656] J Neurosci. 1999 Aug 1;19(15):6372-84 [10414966] J Neurosci. 2005 Jan 12;25(2):308-17 [15647474] J Neurosci. 2005 Oct 12;25(41):9507-14 [16221861] J Neurosci. 2006 Jun 21;26(25):6851-62 [16793892] J Neurosci. 2007 Jan 31;27(5):1129-38 [17267568] J Physiol. 2007 Dec 15;585(Pt 3):741-58 [17947304] J Neurosci. 2008 Mar 19;28(12):3114-22 [18354014] Neuroscience. 2009 Jan 12;158(1):126-36 [18353558] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/jnc.12489 ER - TY - JOUR T1 - Lundep, a sand fly salivary endonuclease increases Leishmania parasite survival in neutrophils and inhibits XIIa contact activation in human plasma. AN - 1499136132; 24516388 AB - Neutrophils are the host's first line of defense against infections, and their extracellular traps (NET) were recently shown to kill Leishmania parasites. Here we report a NET-destroying molecule (Lundep) from the salivary glands of Lutzomyia longipalpis. Previous analysis of the sialotranscriptome of Lu. longipalpis showed the potential presence of an endonuclease. Indeed, not only was the cloned cDNA (Lundep) shown to encode a highly active ss- and dsDNAse, but also the same activity was demonstrated to be secreted by salivary glands of female Lu. longipalpis. Lundep hydrolyzes both ss- and dsDNA with little sequence specificity with a calculated DNase activity of 300000 Kunitz units per mg of protein. Disruption of PMA (phorbol 12 myristate 13 acetate)- or parasite-induced NETs by treatment with recombinant Lundep or salivary gland homogenates increases parasite survival in neutrophils. Furthermore, co-injection of recombinant Lundep with metacyclic promastigotes significantly exacerbates Leishmania infection in mice when compared with PBS alone or inactive (mutagenized) Lundep. We hypothesize that Lundep helps the parasite to establish an infection by allowing it to escape from the leishmanicidal activity of NETs early after inoculation. Lundep may also assist blood meal intake by lowering the local viscosity caused by the release of host DNA and as an anticoagulant by inhibiting the intrinsic pathway of coagulation. JF - PLoS pathogens AU - Chagas, Andrezza C AU - Oliveira, Fabiano AU - Debrabant, Alain AU - Valenzuela, Jesus G AU - Ribeiro, José M C AU - Calvo, Eric AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America. ; Laboratory of Emerging Pathogens, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland, United States of America. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 1 VL - 10 IS - 2 KW - Endonucleases KW - EC 3.1.- KW - Factor XIIa KW - EC 3.4.21.38 KW - Index Medicus KW - Animals KW - Disease Vectors KW - Salivary Glands -- immunology KW - Blood Coagulation -- physiology KW - Neutrophils -- immunology KW - Humans KW - Amino Acid Sequence KW - Mice KW - Salivary Glands -- enzymology KW - Polymerase Chain Reaction KW - Leishmania KW - Blotting, Western KW - Neutrophils -- parasitology KW - Factor XIIa -- metabolism KW - Molecular Sequence Data KW - Endonucleases -- metabolism KW - Endonucleases -- immunology KW - Leishmaniasis -- enzymology KW - Host-Parasite Interactions -- physiology KW - Psychodidae -- parasitology KW - Psychodidae -- immunology KW - Leishmaniasis -- immunology KW - Psychodidae -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499136132?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+pathogens&rft.atitle=Lundep%2C+a+sand+fly+salivary+endonuclease+increases+Leishmania+parasite+survival+in+neutrophils+and+inhibits+XIIa+contact+activation+in+human+plasma.&rft.au=Chagas%2C+Andrezza+C%3BOliveira%2C+Fabiano%3BDebrabant%2C+Alain%3BValenzuela%2C+Jesus+G%3BRibeiro%2C+Jos%C3%A9+M+C%3BCalvo%2C+Eric&rft.aulast=Chagas&rft.aufirst=Andrezza&rft.date=2014-02-01&rft.volume=10&rft.issue=2&rft.spage=e1003923&rft.isbn=&rft.btitle=&rft.title=PLoS+pathogens&rft.issn=1553-7374&rft_id=info:doi/10.1371%2Fjournal.ppat.1003923 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-03 N1 - Date created - 2014-02-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Infect Immun. 2011 Mar;79(3):1124-33 [21189319] J Immunol. 2010 Oct 1;185(7):4319-27 [20826753] J Leukoc Biol. 2011 Sep;90(3):575-82 [21685247] PLoS Negl Trop Dis. 2011 Aug;5(8):e1288 [21886852] PLoS One. 2012;7(5):e35671 [22693548] Front Cell Infect Microbiol. 2012;2:59 [22919650] Thromb Res. 2012 Oct;130 Suppl 1:S78-83 [23026673] J Invest Dermatol. 2012 Dec;132(12):2735-43 [22739793] Hamostaseologie. 2013;33(1):37-42 [23328880] Acta Crystallogr D Biol Crystallogr. 2000 May;56(Pt 5):567-72 [10771425] J Biol Chem. 2000 May 26;275(21):16366-72 [10748102] Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6704-9 [10841567] Science. 2000 Nov 17;290(5495):1351-4 [11082061] J Immunol. 2001 Nov 1;167(9):5226-30 [11673536] Infect Immun. 2002 Feb;70(2):826-35 [11796617] J Exp Biol. 2004 Oct;207(Pt 21):3717-29 [15371479] Science. 1988 Mar 11;239(4845):1306-8 [3344436] Comput Appl Biosci. 1994 Apr;10(2):189-91 [8019868] Trends Biochem Sci. 1998 Oct;23(10):403-5 [9810230] J Mol Biol. 1999 May 21;288(5):975-87 [10329193] Curr Biol. 2006 Feb 21;16(4):396-400 [16488874] Curr Biol. 2006 Feb 21;16(4):401-7 [16488875] J Exp Biol. 2006 Jul;209(Pt 14):2651-9 [16809456] Proc Natl Acad Sci U S A. 2008 Jul 22;105(29):10125-30 [18626016] Science. 2008 Aug 15;321(5891):970-4 [18703742] PLoS Negl Trop Dis. 2008;2(9):e294 [18820742] Parasitol Int. 2009 Mar;58(1):1-5 [18768167] Proc Natl Acad Sci U S A. 2009 Mar 10;106(10):3728-33 [19234127] Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6748-53 [19346483] J Biomed Biotechnol. 2010;2010:719361 [19884987] J Innate Immun. 2009;1(3):225-30 [20375580] J Innate Immun. 2009;1(6):527-42 [20375609] Proc Natl Acad Sci U S A. 2010 Sep 7;107(36):15880-5 [20798043] Cell Mol Life Sci. 2011 Jun;68(11):1863-70 [21369708] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.ppat.1003923 ER - TY - JOUR T1 - Evaluation in mice of a conjugate vaccine for cholera made from Vibrio cholerae O1 (Ogawa) O-specific polysaccharide. AN - 1499136113; 24516685 AB - Protective immunity against cholera is serogroup specific. Serogroup specificity in Vibrio cholerae is determined by the O-specific polysaccharide (OSP) of lipopolysaccharide (LPS). Generally, polysaccharides are poorly immunogenic, especially in young children. Here we report the evaluation in mice of a conjugate vaccine for cholera (OSP:TThc) made from V. cholerae O1 Ogawa O-Specific Polysaccharide-core (OSP) and recombinant tetanus toxoid heavy chain fragment (TThc). We immunized mice intramuscularly on days 0, 21, and 42 with OSP:TThc or OSP only, with or without dmLT, a non-toxigenic immunoadjuvant derived from heat labile toxin of Escherichia coli. We detected significant serum IgG antibody responses targeting OSP following a single immunization in mice receiving OSP:TThc with or without adjuvant. Anti-LPS IgG responses were detected following a second immunization in these cohorts. No anti-OSP or anti-LPS IgG responses were detected at any time in animals receiving un-conjugated OSP with or without immunoadjuvant, and in animals receiving immunoadjuvant alone. Responses were highest following immunization with adjuvant. Serum anti-OSP IgM responses were detected in mice receiving OSP:TThc with or without immunoadjuvant, and in mice receiving unconjugated OSP. Serum anti-LPS IgM and vibriocidal responses were detected in all vaccine cohorts except in mice receiving immunoadjuvant alone. No significant IgA anti-OSP or anti-LPS responses developed in any group. Administration of OSP:TThc and adjuvant also induced memory B cell responses targeting OSP and resulted in 95% protective efficacy in a mouse lethality cholera challenge model. We describe a protectively immunogenic cholera conjugate in mice. Development of a cholera conjugate vaccine could assist in inducing long-term protective immunity, especially in young children who respond poorly to polysaccharide antigens. JF - PLoS neglected tropical diseases AU - Alam, Mohammad Murshid AU - Bufano, Megan Kelly AU - Xu, Peng AU - Kalsy, Anuj AU - Yu, Y AU - Freeman, Y Wu AU - Sultana, Tania AU - Rashu, Md Rasheduzzaman AU - Desai, Ishaan AU - Eckhoff, Grace AU - Leung, Daniel T AU - Charles, Richelle C AU - LaRocque, Regina C AU - Harris, Jason B AU - Clements, John D AU - Calderwood, Stephen B AU - Qadri, Firdausi AU - Vann, W F AU - Kováč, Pavol AU - Ryan, Edward T AD - Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; International Centre for Diarrheal Disease Research, Bangladesh (ICDDR,B), Dhaka, Bangladesh. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America. ; NIDDK, LBC, National Institutes of Health, Bethesda, Maryland, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; International Centre for Diarrheal Disease Research, Bangladesh (ICDDR,B), Dhaka, Bangladesh ; Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, United States of America. ; Tulane University School of Medicine, New Orleans, Louisiana, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America ; Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, United States of America. ; International Centre for Diarrheal Disease Research, Bangladesh (ICDDR,B), Dhaka, Bangladesh. ; CBER, FDA, Laboratory of Bacterial Toxins, Bethesda, Maryland, United States of America. ; Division of Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, United States of America ; Department of Medicine, Harvard Medical School, Boston, Massachusetts, United States of America ; Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 1 VL - 8 IS - 2 KW - Antibodies, Bacterial KW - 0 KW - Cholera Vaccines KW - O Antigens KW - Recombinant Proteins KW - Vaccines, Conjugate KW - Index Medicus KW - Animals KW - Recombinant Proteins -- metabolism KW - Recombinant Proteins -- immunology KW - Antibodies, Bacterial -- blood KW - Disease Models, Animal KW - Mice KW - Recombinant Proteins -- chemistry KW - Female KW - Cholera Vaccines -- chemistry KW - Cholera -- mortality KW - Vaccines, Conjugate -- immunology KW - Cholera -- immunology KW - Cholera Vaccines -- immunology KW - O Antigens -- metabolism KW - O Antigens -- immunology KW - Cholera -- prevention & control KW - Vaccines, Conjugate -- chemistry KW - O Antigens -- chemistry KW - Cholera Vaccines -- metabolism KW - Vaccines, Conjugate -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499136113?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+neglected+tropical+diseases&rft.atitle=Evaluation+in+mice+of+a+conjugate+vaccine+for+cholera+made+from+Vibrio+cholerae+O1+%28Ogawa%29+O-specific+polysaccharide.&rft.au=Alam%2C+Mohammad+Murshid%3BBufano%2C+Megan+Kelly%3BXu%2C+Peng%3BKalsy%2C+Anuj%3BYu%2C+Y%3BFreeman%2C+Y+Wu%3BSultana%2C+Tania%3BRashu%2C+Md+Rasheduzzaman%3BDesai%2C+Ishaan%3BEckhoff%2C+Grace%3BLeung%2C+Daniel+T%3BCharles%2C+Richelle+C%3BLaRocque%2C+Regina+C%3BHarris%2C+Jason+B%3BClements%2C+John+D%3BCalderwood%2C+Stephen+B%3BQadri%2C+Firdausi%3BVann%2C+W+F%3BKov%C3%A1%C4%8D%2C+Pavol%3BRyan%2C+Edward+T&rft.aulast=Alam&rft.aufirst=Mohammad&rft.date=2014-02-01&rft.volume=8&rft.issue=2&rft.spage=e2683&rft.isbn=&rft.btitle=&rft.title=PLoS+neglected+tropical+diseases&rft.issn=1935-2735&rft_id=info:doi/10.1371%2Fjournal.pntd.0002683 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-03 N1 - Date created - 2014-02-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Infect Immun. 2000 Feb;68(2):977-81 [10639476] Vaccine. 2009 Aug 6;27(36):4917-22 [19563890] Lancet. 2009 Nov 14;374(9702):1694-702 [19819004] Glycoconj J. 2010 Jan;27(1):69-77 [19757026] Vaccine. 2010 Feb 3;28(5):1404-11 [19897067] Cochrane Database Syst Rev. 2010;(8):CD000974 [20687062] Cochrane Database Syst Rev. 2011;(3):CD008603 [21412922] Clin Vaccine Immunol. 2011 Apr;18(4):546-51 [21288994] Clin Vaccine Immunol. 2011 May;18(5):844-50 [21346055] Clin Vaccine Immunol. 2011 Aug;18(8):1317-25 [21697337] J Infect Dis. 2011 Sep 15;204(6):912-8 [21849288] Wkly Epidemiol Rec. 2012 Aug 3;87(31/32):289–304 [22905370] Clin Vaccine Immunol. 2012 Nov;19(11):1712-21 [22993410] PLoS One. 2012;7(12):e51718 [23284753] Pathog Dis. 2013 Mar;67(2):136-58 [23620159] Clin Vaccine Immunol. 2013 Jun;20(6):780-8 [23515016] J Mass Spectrom. 2013 Oct;48(10):1083-90 [24130011] Glycoconj J. 2013 Dec;30(9):857-70 [23949787] Glycoconj J. 2013 Dec;30(9):871-80 [23955520] Pathog Dis. 2014 Mar;70(2):153-7 [23966359] Bioconjug Chem. 2011 Oct 19;22(10):2179-85 [21899371] PLoS Negl Trop Dis. 2011 Oct;5(10):e1289 [22028938] Bull World Health Organ. 2012 Mar 1;90(3):209-218A [22461716] Clin Vaccine Immunol. 2012 Apr;19(4):594-602 [22357651] Expert Rev Anti Infect Ther. 2012 Apr;10(4):435-44 [22512753] Clin Vaccine Immunol. 2012 May;19(5):690-8 [22441386] Clin Vaccine Immunol. 2012 Jun;19(6):842-8 [22518009] Lancet. 2012 Jun 30;379(9835):2466-76 [22748592] Clin Vaccine Immunol. 2012 Aug;19(8):1304-11 [22739692] Carbohydr Res. 2001 Feb 28;330(4):479-86 [11269399] Infect Immun. 2001 May;69(5):3488-93 [11292781] Infect Immun. 2001 Jun;69(6):3581-90 [11349017] Bull World Health Organ. 1968;38(3):327-34 [5302327] J Infect Dis. 1970 May;121:Suppl 121:1-9 [4912069] J Infect Dis. 1981 Jun;143(6):818-20 [7252264] Infect Immun. 1984 Sep;45(3):582-91 [6332076] J Infect Dis. 1985 Feb;151(2):236-42 [3968450] Infect Immun. 1992 Aug;60(8):3201-8 [1639490] Biochem Biophys Res Commun. 1993 Nov 15;196(3):1309-15 [7504475] J Infect Dis. 1994 Mar;169(3):709-10 [8158063] Carbohydr Res. 1994 Mar 18;256(1):113-28 [8194067] Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11388-92 [7972070] Infect Immun. 1995 Jan;63(1):317-23 [7528734] EMBO J. 1995 Jan 16;14(2):209-16 [7835331] Infect Immun. 1996 Jan;64(1):10-5 [8557325] Glycoconj J. 1996 Apr;13(2):315-9 [8737256] Carbohydr Res. 1996 Aug 26;290(1):59-65 [8805782] Infect Immun. 1996 Oct;64(10):4373-7 [8926115] J Immunol Methods. 1996 Nov 29;199(1):37-46 [8960096] Infect Immun. 1997 Jul;65(7):2941-9 [9199470] Infect Immun. 1997 Aug;65(8):3118-25 [9234763] Infect Immun. 1997 Sep;65(9):3571-6 [9284121] J Biol Chem. 1998 Jan 30;273(5):2777-83 [9446585] Infect Immun. 1998 Jul;66(7):3095-9 [9632571] Nature. 2005 Aug 4;436(7051):696-700 [16079845] FEMS Immunol Med Microbiol. 2006 Nov;48(2):237-51 [17010106] Carbohydr Res. 2008 Feb 4;343(2):196-210 [18048016] PLoS Negl Trop Dis. 2008;2(2):e173 [18299707] PLoS Negl Trop Dis. 2008;2(4):e221 [18398491] Am J Trop Med Hyg. 2008 Nov;79(5):708-14 [18981509] Infect Immun. 2000 Sep;68(9):5037-43 [10948122] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pntd.0002683 ER - TY - JOUR T1 - Inhibition of tumorigenesis by the thyroid hormone receptor β in xenograft models. AN - 1499136035; 23731250 AB - Previous studies showed a close association between several types of human cancers and somatic mutations of thyroid hormone receptor β (TRβ) and reduced expression of TRβ due to epigenetic inactivation and/or deletion of the THRB gene. These observations suggest that TRβ could act as a tumor suppressor in carcinogenesis. However, the mechanisms by which TRβ could function to inhibit tumorigenesis are less well understood. We used the human follicular thyroid cancer cell lines (FTC-133 and FTC-236 cells) to elucidate how functional expression of the THRB gene could affect tumorigenesis. We stably expressed the THRB gene in FTC cells and evaluated the effects of the expressed TRβ on cancer cell proliferation, migration, and tumor growth in cell-based studies and xenograft models. Expression of TRβ in FTC-133 cells, as compared with control FTC cells without TRβ, reduced cancer cell proliferation and impeded migration of tumor cells through inhibition of the AKT-mTOR-p70 S6K pathway. TRβ expression in FTC-133 and FTC-236 led to less tumor growth in xenograft models. Importantly, new vessel formation was significantly suppressed in tumors induced by FTC cells expressing TRβ compared with control FTC cells without TRβ. The decrease in vessel formation was mediated by the downregulation of vascular endothelial growth factor in FTC cells expressing TRβ. These findings indicate that TRβ acts as a tumor suppressor through downregulation of the AKT-mTOR-p70 S6K pathway and decreased vascular endothelial growth factor expression in FTC cells. The present results raise the possibility that TRβ could be considered as a potential therapeutic target for thyroid cancer. JF - Thyroid : official journal of the American Thyroid Association AU - Kim, Won Gu AU - Zhao, Li AU - Kim, Dong Wook AU - Willingham, Mark C AU - Cheng, Sheue-yann AD - Laboratory of Molecular Biology, Center for Cancer Research , National Cancer Institute, Bethesda, Maryland. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 260 EP - 269 VL - 24 IS - 2 KW - Angiogenesis Inhibitors KW - 0 KW - Thyroid Hormone Receptors beta KW - Tumor Suppressor Proteins KW - VEGFA protein, human KW - Vascular Endothelial Growth Factor A KW - Triiodothyronine KW - 06LU7C9H1V KW - MTOR protein, human KW - EC 2.7.1.1 KW - TOR Serine-Threonine Kinases KW - Index Medicus KW - Heterografts KW - Angiogenesis Inhibitors -- physiology KW - Animals KW - Vascular Endothelial Growth Factor A -- biosynthesis KW - Triiodothyronine -- pharmacology KW - Humans KW - Cell Line, Tumor KW - Mice KW - Mice, Nude KW - Vascular Endothelial Growth Factor A -- antagonists & inhibitors KW - Neoplasm Transplantation KW - Adenocarcinoma, Follicular -- pathology KW - Thyroid Neoplasms -- pathology KW - Male KW - Tumor Suppressor Proteins -- physiology KW - Thyroid Hormone Receptors beta -- biosynthesis KW - Thyroid Hormone Receptors beta -- physiology KW - Thyroid Hormone Receptors beta -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499136035?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Thyroid+%3A+official+journal+of+the+American+Thyroid+Association&rft.atitle=Inhibition+of+tumorigenesis+by+the+thyroid+hormone+receptor+%CE%B2+in+xenograft+models.&rft.au=Kim%2C+Won+Gu%3BZhao%2C+Li%3BKim%2C+Dong+Wook%3BWillingham%2C+Mark+C%3BCheng%2C+Sheue-yann&rft.aulast=Kim&rft.aufirst=Won&rft.date=2014-02-01&rft.volume=24&rft.issue=2&rft.spage=260&rft.isbn=&rft.btitle=&rft.title=Thyroid+%3A+official+journal+of+the+American+Thyroid+Association&rft.issn=1557-9077&rft_id=info:doi/10.1089%2Fthy.2013.0054 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-10-21 N1 - Date created - 2014-02-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Lett. 2000 Jul 31;155(2):145-52 [10822129] Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13209-14 [11069286] Hum Mol Genet. 2001 Feb 1;10(3):251-8 [11159944] Thyroid. 2001 Mar;11(3):281-91 [11327621] Physiol Rev. 2001 Jul;81(3):1097-142 [11427693] Cancer Res. 2001 Aug 15;61(16):6105-11 [11507060] Mol Cell Biol. 2001 Oct;21(20):6782-95 [11564863] J Clin Endocrinol Metab. 2001 Nov;86(11):5572-6 [11701737] Carcinogenesis. 2002 Jan;23(1):25-33 [11756220] J Clin Endocrinol Metab. 2002 Mar;87(3):1120-8 [11889175] Oncogene. 2002 Jun 20;21(27):4307-16 [12082618] Nat Rev Cancer. 2002 Oct;2(10):795-803 [12360282] Thyroid. 2002 Nov;12(11):963-9 [12490073] Endocr J. 2003 Feb;50(1):77-83 [12733712] Science. 1989 Dec 8;246(4935):1306-9 [2479986] World J Surg. 1992 Jul-Aug;16(4):770-6 [1384245] Melanoma Res. 1993 Dec;3(6):457-61 [7909244] Cancer Res. 1994 Jun 1;54(11):3021-4 [7910519] J Clin Endocrinol Metab. 1994 Aug;79(2):401-8 [8045955] World J Surg. 1994 Jul-Aug;18(4):569-75; discussion 575-6 [7725746] Biochem Biophys Res Commun. 1995 May 16;210(2):464-71 [7538760] Mol Carcinog. 1999 Sep;26(1):53-61 [10487522] Mol Cell Biol. 2005 Jan;25(1):124-35 [15601836] Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1780-5 [16446424] J Clin Invest. 2006 Nov;116(11):2972-84 [17039256] Carcinogenesis. 2007 Dec;28(12):2451-8 [17660507] J Clin Endocrinol Metab. 2007 Dec;92(12):4766-70 [17911173] Oncogene. 2009 Jan 29;28(4):509-17 [18997818] Cancer Genet Cytogenet. 2010 Jan 15;196(2):140-5 [20082849] Vascul Pharmacol. 2010 Mar-Apr;52(3-4):142-5 [19879961] Oncogene. 2010 Apr 1;29(13):1909-19 [20062085] Endocr Rev. 2010 Apr;31(2):139-70 [20051527] Carcinogenesis. 2010 Jul;31(7):1284-91 [20299527] Ann Surg Oncol. 2010 Aug;17(8):2222-8 [20155399] Nat Med. 2011;17(11):1359-70 [22064426] Clin Cancer Res. 2012 Mar 1;18(5):1281-90 [22271876] Cancer Res. 2012 Apr 15;72(8):1909-14 [22508695] Endocrinology. 2013 Jan;154(1):25-35 [23183175] Biochim Biophys Acta. 2013 Jul;1830(7):3928-36 [22507269] Am J Hum Genet. 1989 Feb;44(2):282-7 [2536219] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1089/thy.2013.0054 ER - TY - JOUR T1 - The naturally occurring luteinizing hormone surge is diminished in mice lacking estrogen receptor Beta in the ovary. AN - 1499120417; 24337314 AB - Female ESR2-null mice (betaERKO) display defects in ovarian function and are subfertile. Follicular maturation is impaired and explains smaller litters, but betaERKO also produce fewer litters, which may be partially due to inadequate ovulatory signals. To test this, the amplitude and timing of the naturally occurring luteinizing hormone (LH) surge was measured in individual intact betaERKO and wild-type (WT) mice. Vaginal cytology was evaluated daily, and blood samples were taken from mice in proestrus. The amplitude of the LH surge was severely blunted in betaERKO mice compared to WT, but pituitary LH levels revealed no differences. The betaERKO mice did not produce a preovulatory estradiol surge. To determine if the smaller LH surges and the reduced number of litters in betaERKO were due to the lack of ESR2 in the hypothalamic-pituitary axis or due to the absence of ESR2 in the ovary, ovaries were transplanted from WT into betaERKO mice and vice versa. The size of the LH surge was reduced only in mice lacking ESR2 within the ovary, and these mice had fewer litters. Fertility and size of the LH surge were rescued in betaERKO mice receiving a WT ovary. These data provide the first experimental evidence that the LH surge is impaired in betaERKO females and may contribute to their reduced fertility. ESR2 is not necessary within the pituitary and hypothalamus for the generation of a normal LH surge and for normal fertility, but ESR2 is essential within the ovary to provide proper signals. JF - Biology of reproduction AU - Jayes, Friederike L AU - Burns, Katherine A AU - Rodriguez, Karina F AU - Kissling, Grace E AU - Korach, Kenneth S AD - Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 24 VL - 90 IS - 2 KW - Estrogen Receptor beta KW - 0 KW - Luteinizing Hormone KW - 9002-67-9 KW - Index Medicus KW - positive feedback KW - naturally occurring luteinizing hormone surge KW - ovarian transplants KW - fertility KW - HPO axis KW - estrogen receptor beta KW - ESR2 KW - Animals KW - Infertility, Female -- blood KW - Mice KW - Estrous Cycle -- blood KW - Estrous Cycle -- genetics KW - Mice, Knockout KW - Down-Regulation KW - Hypothalamus -- metabolism KW - Mice, Inbred C57BL KW - Pituitary Gland -- metabolism KW - Infertility, Female -- genetics KW - Female KW - Male KW - Luteinizing Hormone -- secretion KW - Ovary -- metabolism KW - Luteinizing Hormone -- blood KW - Estrogen Receptor beta -- metabolism KW - Ovary -- transplantation KW - Estrogen Receptor beta -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499120417?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+reproduction&rft.atitle=The+naturally+occurring+luteinizing+hormone+surge+is+diminished+in+mice+lacking+estrogen+receptor+Beta+in+the+ovary.&rft.au=Jayes%2C+Friederike+L%3BBurns%2C+Katherine+A%3BRodriguez%2C+Karina+F%3BKissling%2C+Grace+E%3BKorach%2C+Kenneth+S&rft.aulast=Jayes&rft.aufirst=Friederike&rft.date=2014-02-01&rft.volume=90&rft.issue=2&rft.spage=24&rft.isbn=&rft.btitle=&rft.title=Biology+of+reproduction&rft.issn=1529-7268&rft_id=info:doi/10.1095%2Fbiolreprod.113.113316 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-21 N1 - Date created - 2014-02-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Science. 1997 Sep 5;277(5331):1508-10 [9278514] Science. 1979 Nov 30;206(4422):1099-101 [573924] Endocr Rev. 1998 Jun;19(3):302-30 [9626556] Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15677-82 [9861029] Steroids. 1998 Dec;63(12):616-29 [9870258] Endocr Rev. 1999 Jun;20(3):358-417 [10368776] Ann Endocrinol (Paris). 1999 Jul;60(2):143-8 [10456188] J Endocrinol. 2005 Jan;184(1):59-68 [15642783] Biometrics. 2005 Mar;61(1):141-50 [15737087] Q Rev Biol. 1979 Sep;54(3):265-99 [390600] Endocrinology. 1980 Mar;106(3):959-66 [7188749] J Steroid Biochem. 1987;27(4-6):665-75 [2826901] Endocrinology. 1992 Sep;131(3):1458-66 [1505477] Endocrinology. 1993 Apr;132(4):1687-91 [8462469] Endocrinology. 1993 Oct;133(4):1650-6 [8404606] Endocrinology. 2008 Jan;149(1):20-7 [17947360] Endocrinology. 2008 Feb;149(2):597-604 [18006629] Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2433-8 [18268329] J Neuroendocrinol. 2009 Mar;21(4):305-11 [19207812] J Neuroendocrinol. 2009 Mar;21(4):327-33 [19207821] J Neurosci. 2009 Apr 29;29(17):5616-27 [19403828] Mol Cell Endocrinol. 2009 May 6;303(1-2):25-33 [19428988] Endocrinology. 2010 Jun;151(6):2826-34 [20378682] Mol Endocrinol. 2012 May;26(5):887-98 [22446102] Neuroscience. 2005;131(4):945-51 [15749347] Endocrinology. 2005 Jun;146(6):2817-26 [15731357] Endocrinology. 2005 Aug;146(8):3247-62 [15831568] Lab Anim (NY). 2005 Oct;34(9):39-43 [16195737] Neuron. 2006 Oct 19;52(2):271-80 [17046690] Mol Endocrinol. 2007 Jan;21(1):1-13 [16556737] Ernst Schering Found Symp Proc. 2006;(1):25-44 [17824170] Development. 2000 Oct;127(19):4277-91 [10976058] J Biol Rhythms. 2001 Aug;16(4):283-301 [11506375] Biol Reprod. 2001 Sep;65(3):680-8 [11514328] Mol Endocrinol. 2003 Jun;17(6):1039-53 [12624116] J Neurosci. 2003 Jul 2;23(13):5771-7 [12843281] Neuroendocrinology. 2003 Oct;78(4):204-9 [14583652] Endocrinology. 2003 Dec;144(12):5640-9 [14500575] Toxicol Sci. 2004 Jul;80(1):14-25 [15084758] Neuroendocrinology. 2004;79(5):247-58 [15205556] J Endocrinol. 1973 May;57(2):235-45 [4735927] Endocrinology. 1979 May;104(5):1247-55 [571329] Biol Reprod. 1979 Jun;20(5):1005-8 [573145] Biol Reprod. 1979 Aug;21(1):235-9 [486640] Endocrinology. 1997 Nov;138(11):4613-21 [9348186] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1095/biolreprod.113.113316 ER - TY - JOUR T1 - Risk of ovarian cancer and the NF-κB pathway: genetic association with IL1A and TNFSF10. AN - 1499115951; 24272484 AB - A missense single-nucleotide polymorphism (SNP) in the immune modulatory gene IL1A has been associated with ovarian cancer risk (rs17561). Although the exact mechanism through which this SNP alters risk of ovarian cancer is not clearly understood, rs17561 has also been associated with risk of endometriosis, an epidemiologic risk factor for ovarian cancer. Interleukin-1α (IL1A) is both regulated by and able to activate NF-κB, a transcription factor family that induces transcription of many proinflammatory genes and may be an important mediator in carcinogenesis. We therefore tagged SNPs in more than 200 genes in the NF-κB pathway for a total of 2,282 SNPs (including rs17561) for genotype analysis of 15,604 cases of ovarian cancer in patients of European descent, including 6,179 of high-grade serous (HGS), 2,100 endometrioid, 1,591 mucinous, 1,034 clear cell, and 1,016 low-grade serous, including 23,235 control cases spanning 40 studies in the Ovarian Cancer Association Consortium. In this large population, we confirmed the association between rs17561 and clear cell ovarian cancer [OR, 0.84; 95% confidence interval (CI), 0.76-0.93; P = 0.00075], which remained intact even after excluding participants in the prior study (OR, 0.85; 95% CI, 0.75-0.95; P = 0.006). Considering a multiple-testing-corrected significance threshold of P < 2.5 × 10(-5), only one other variant, the TNFSF10 SNP rs6785617, was associated significantly with a risk of ovarian cancer (low malignant potential tumors OR, 0.85; 95% CI, 0.79-0.91; P = 0.00002). Our results extend the evidence that borderline tumors may have a distinct genetic etiology. Further investigation of how these SNPs might modify ovarian cancer associations with other inflammation-related risk factors is warranted. JF - Cancer research AU - Charbonneau, Bridget AU - Block, Matthew S AU - Bamlet, William R AU - Vierkant, Robert A AU - Kalli, Kimberly R AU - Fogarty, Zachary AU - Rider, David N AU - Sellers, Thomas A AU - Tworoger, Shelley S AU - Poole, Elizabeth AU - Risch, Harvey A AU - Salvesen, Helga B AU - Kiemeney, Lambertus A AU - Baglietto, Laura AU - Giles, Graham G AU - Severi, Gianluca AU - Trabert, Britton AU - Wentzensen, Nicolas AU - Chenevix-Trench, Georgia AU - for AOCS/ACS group AU - Whittemore, Alice S AU - Sieh, Weiva AU - Chang-Claude, Jenny AU - Bandera, Elisa V AU - Orlow, Irene AU - Terry, Kathryn AU - Goodman, Marc T AU - Thompson, Pamela J AU - Cook, Linda S AU - Rossing, Mary Anne AU - Ness, Roberta B AU - Narod, Steven A AU - Kupryjanczyk, Jolanta AU - Lu, Karen AU - Butzow, Ralf AU - Dörk, Thilo AU - Pejovic, Tanja AU - Campbell, Ian AU - Le, Nhu D AU - Bunker, Clareann H AU - Bogdanova, Natalia AU - Runnebaum, Ingo B AU - Eccles, Diana AU - Paul, James AU - Wu, Anna H AU - Gayther, Simon A AU - Hogdall, Estrid AU - Heitz, Florian AU - Kaye, Stanley B AU - Karlan, Beth Y AU - Anton-Culver, Hoda AU - Gronwald, Jacek AU - Hogdall, Claus K AU - Lambrechts, Diether AU - Fasching, Peter A AU - Menon, Usha AU - Schildkraut, Joellen AU - Pearce, Celeste Leigh AU - Levine, Douglas A AU - Kjaer, Susanne Kruger AU - Cramer, Daniel AU - Flanagan, James M AU - Phelan, Catherine M AU - Brown, Robert AU - Massuger, Leon F A G AU - Song, Honglin AU - Doherty, Jennifer A AU - Krakstad, Camilla AU - Liang, Dong AU - Odunsi, Kunle AU - Berchuck, Andrew AU - Jensen, Allan AU - Lubinski, Jan AU - Nevanlinna, Heli AU - Bean, Yukie T AU - Lurie, Galina AU - Ziogas, Argyrios AU - Walsh, Christine AU - Despierre, Evelyn AU - Brinton, Louise AU - Hein, Alexander AU - Rudolph, Anja AU - Dansonka-Mieszkowska, Agnieszka AU - Olson, Sara H AU - Harter, Philipp AU - Tyrer, Jonathan AU - Vitonis, Allison F AU - Brooks-Wilson, Angela AU - Aben, Katja K AU - Pike, Malcolm C AU - Ramus, Susan J AU - Wik, Elisabeth AU - Cybulski, Cezary AU - Lin, Jie AU - Sucheston, Lara AU - Edwards, Robert AU - McGuire, Valerie AU - Lester, Jenny AU - du Bois, Andreas AU - Lundvall, Lene AU - Wang-Gohrke, Shan AU - Szafron, Lukasz M AU - Lambrechts, Sandrina AU - Yang, Hannah AU - Beckmann, Matthias W AU - Pelttari, Liisa M AU - Van Altena, Anne M AU - van den Berg, David AU - Halle, Mari K AU - Gentry-Maharaj, Aleksandra AU - Schwaab, Ira AU - Chandran, Urmila AU - Menkiszak, Janusz AU - Ekici, Arif B AU - Wilkens, Lynne R AU - Leminen, Arto AU - Modugno, Francesmary AU - Friel, Grace AU - Rothstein, Joseph H AU - Vergote, Ignace AU - Garcia-Closas, Montserrat AU - Hildebrandt, Michelle A T AU - Sobiczewski, Piotr AU - Kelemen, Linda E AU - Pharoah, Paul D P AU - Moysich, Kirsten AU - Knutson, Keith L AU - Cunningham, Julie M AU - Fridley, Brooke L AU - Goode, Ellen L AD - Authors' Affiliations: Departments of Health Sciences Research, Division of Epidemiology, Medical Oncology, Health Sciences Research, Division of Biomedical Statistics and Informatics, Immunology, and Laboratory Medicine and Pathology, Division of Experimental Pathology, Mayo Clinic, Rochester, Minnesota; Department of Cancer Epidemiology, Division of Population Sciences, Moffitt Cancer Center, Tampa, Florida; Channing Division of Network Medicine, Obstetrics and Gynecology Epidemiology Center, Brigham and Women's Hospital, Harvard Medical School; Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts; Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, Connecticut; Department of Clinical Science, University of Bergen; Departments of Gynecology and Obstetrics, and Pathology, Haukeland University Hospital, Bergen, Norway; Departments for Health Evidence, Urology, and Gynaecology, Radboud University Medical Centre, Nijmegen; Comprehensive Cancer Center The Netherlands, Utrecht, the Netherlands; Cancer Epidemiology Centre, The Cancer Council Victoria; Centre for Molecular, Environmental, Genetic and Analytical Epidemiology, Department of Pathology, and Sir Peter MacCallum Department of Oncology, University of Melbourne; Department of Epidemiology and Preventive Medicine, Monash University; Peter MacCallum Cancer Institute; Research Division, Peter MacCallum Cancer Centre, Melbourne, Victoria; Cancer Division, Queensland Institute of Medical Research, Herston, Queensland, Australia; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland; Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Palo Alto; Samuel Oschin Comprehensive Cancer Institute; Women's Cancer Program, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center; Department of Preventive Medicine, Keck School of Medicine, University of Sout ; for AOCS/ACS group Y1 - 2014/02/01/ PY - 2014 DA - 2014 Feb 01 SP - 852 EP - 861 VL - 74 IS - 3 KW - Interleukin-1alpha KW - 0 KW - NF-kappa B KW - TNF-Related Apoptosis-Inducing Ligand KW - TNFSF10 protein, human KW - Index Medicus KW - Risk KW - Polymorphism, Single Nucleotide KW - Humans KW - Genetic Association Studies KW - Case-Control Studies KW - Female KW - TNF-Related Apoptosis-Inducing Ligand -- genetics KW - Ovarian Neoplasms -- metabolism KW - Ovarian Neoplasms -- genetics KW - Ovarian Neoplasms -- pathology KW - Signal Transduction KW - NF-kappa B -- metabolism KW - Interleukin-1alpha -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499115951?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Risk+of+ovarian+cancer+and+the+NF-%CE%BAB+pathway%3A+genetic+association+with+IL1A+and+TNFSF10.&rft.au=Charbonneau%2C+Bridget%3BBlock%2C+Matthew+S%3BBamlet%2C+William+R%3BVierkant%2C+Robert+A%3BKalli%2C+Kimberly+R%3BFogarty%2C+Zachary%3BRider%2C+David+N%3BSellers%2C+Thomas+A%3BTworoger%2C+Shelley+S%3BPoole%2C+Elizabeth%3BRisch%2C+Harvey+A%3BSalvesen%2C+Helga+B%3BKiemeney%2C+Lambertus+A%3BBaglietto%2C+Laura%3BGiles%2C+Graham+G%3BSeveri%2C+Gianluca%3BTrabert%2C+Britton%3BWentzensen%2C+Nicolas%3BChenevix-Trench%2C+Georgia%3Bfor+AOCS%2FACS+group%3BWhittemore%2C+Alice+S%3BSieh%2C+Weiva%3BChang-Claude%2C+Jenny%3BBandera%2C+Elisa+V%3BOrlow%2C+Irene%3BTerry%2C+Kathryn%3BGoodman%2C+Marc+T%3BThompson%2C+Pamela+J%3BCook%2C+Linda+S%3BRossing%2C+Mary+Anne%3BNess%2C+Roberta+B%3BNarod%2C+Steven+A%3BKupryjanczyk%2C+Jolanta%3BLu%2C+Karen%3BButzow%2C+Ralf%3BD%C3%B6rk%2C+Thilo%3BPejovic%2C+Tanja%3BCampbell%2C+Ian%3BLe%2C+Nhu+D%3BBunker%2C+Clareann+H%3BBogdanova%2C+Natalia%3BRunnebaum%2C+Ingo+B%3BEccles%2C+Diana%3BPaul%2C+James%3BWu%2C+Anna+H%3BGayther%2C+Simon+A%3BHogdall%2C+Estrid%3BHeitz%2C+Florian%3BKaye%2C+Stanley+B%3BKarlan%2C+Beth+Y%3BAnton-Culver%2C+Hoda%3BGronwald%2C+Jacek%3BHogdall%2C+Claus+K%3BLambrechts%2C+Diether%3BFasching%2C+Peter+A%3BMenon%2C+Usha%3BSchildkraut%2C+Joellen%3BPearce%2C+Celeste+Leigh%3BLevine%2C+Douglas+A%3BKjaer%2C+Susanne+Kruger%3BCramer%2C+Daniel%3BFlanagan%2C+James+M%3BPhelan%2C+Catherine+M%3BBrown%2C+Robert%3BMassuger%2C+Leon+F+A+G%3BSong%2C+Honglin%3BDoherty%2C+Jennifer+A%3BKrakstad%2C+Camilla%3BLiang%2C+Dong%3BOdunsi%2C+Kunle%3BBerchuck%2C+Andrew%3BJensen%2C+Allan%3BLubinski%2C+Jan%3BNevanlinna%2C+Heli%3BBean%2C+Yukie+T%3BLurie%2C+Galina%3BZiogas%2C+Argyrios%3BWalsh%2C+Christine%3BDespierre%2C+Evelyn%3BBrinton%2C+Louise%3BHein%2C+Alexander%3BRudolph%2C+Anja%3BDansonka-Mieszkowska%2C+Agnieszka%3BOlson%2C+Sara+H%3BHarter%2C+Philipp%3BTyrer%2C+Jonathan%3BVitonis%2C+Allison+F%3BBrooks-Wilson%2C+Angela%3BAben%2C+Katja+K%3BPike%2C+Malcolm+C%3BRamus%2C+Susan+J%3BWik%2C+Elisabeth%3BCybulski%2C+Cezary%3BLin%2C+Jie%3BSucheston%2C+Lara%3BEdwards%2C+Robert%3BMcGuire%2C+Valerie%3BLester%2C+Jenny%3Bdu+Bois%2C+Andreas%3BLundvall%2C+Lene%3BWang-Gohrke%2C+Shan%3BSzafron%2C+Lukasz+M%3BLambrechts%2C+Sandrina%3BYang%2C+Hannah%3BBeckmann%2C+Matthias+W%3BPelttari%2C+Liisa+M%3BVan+Altena%2C+Anne+M%3Bvan+den+Berg%2C+David%3BHalle%2C+Mari+K%3BGentry-Maharaj%2C+Aleksandra%3BSchwaab%2C+Ira%3BChandran%2C+Urmila%3BMenkiszak%2C+Janusz%3BEkici%2C+Arif+B%3BWilkens%2C+Lynne+R%3BLeminen%2C+Arto%3BModugno%2C+Francesmary%3BFriel%2C+Grace%3BRothstein%2C+Joseph+H%3BVergote%2C+Ignace%3BGarcia-Closas%2C+Montserrat%3BHildebrandt%2C+Michelle+A+T%3BSobiczewski%2C+Piotr%3BKelemen%2C+Linda+E%3BPharoah%2C+Paul+D+P%3BMoysich%2C+Kirsten%3BKnutson%2C+Keith+L%3BCunningham%2C+Julie+M%3BFridley%2C+Brooke+L%3BGoode%2C+Ellen+L&rft.aulast=Charbonneau&rft.aufirst=Bridget&rft.date=2014-02-01&rft.volume=74&rft.issue=3&rft.spage=852&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-13-1051 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-04-15 N1 - Date created - 2014-02-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nat Rev Cancer. 2008 Oct;8(10):782-98 [18813321] Int J Cancer. 2008 Jan 1;122(1):170-6 [17721999] Bioinformatics. 2010 Sep 15;26(18):2336-7 [20634204] Cell Res. 2011 Jan;21(1):55-70 [21187856] Cancer Causes Control. 2011 May;22(5):785-801 [21359843] BMC Bioinformatics. 2011;12:129 [21535878] Lancet Oncol. 2011 Sep;12(9):900-4 [21835693] Endocr Relat Cancer. 2011 Oct;18(5):627-42 [21813729] Br J Cancer. 2011 Oct 25;105(9):1436-42 [21915124] J Leukoc Biol. 2011 Nov;90(5):855-65 [21562052] J Endocrinol. 2011 Dec;211(3):273-83 [21903865] Cancer Res. 2012 Mar 1;72(5):1064-9 [22282663] Lancet Oncol. 2012 Apr;13(4):385-94 [22361336] Arch Gynecol Obstet. 2012 Jul;286(1):99-103 [22546953] Fertil Steril. 2012 Sep;98(3):520-8 [22771029] Am J Epidemiol. 2000 Aug 1;152(3):233-41 [10933270] J Natl Cancer Inst. 2002 Jan 2;94(1):32-8 [11773280] EMBO J. 2002 Oct 1;21(19):5184-94 [12356734] Cell Death Differ. 2003 Jan;10(1):66-75 [12655296] Immunity. 2003 Jun;18(6):763-75 [12818158] Curr Cancer Drug Targets. 2004 Feb;4(1):29-42 [14965265] Am J Hum Genet. 2004 Apr;74(4):765-9 [14997420] Trends Immunol. 2004 Jun;25(6):280-8 [15145317] Curr Opin Pharmacol. 2004 Aug;4(4):333-9 [15251125] Cell. 2004 Aug 6;118(3):285-96 [15294155] Nature. 2004 Sep 23;431(7007):461-6 [15329734] Int J Cancer. 1991 Aug 19;49(1):50-6 [1874569] Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8485-9 [1924307] Food Chem Toxicol. 1994 Dec;32(12):1173-84 [7813991] Cancer Epidemiol Biomarkers Prev. 1995 Jul-Aug;4(5):447-51 [7549798] Blood. 1996 Apr 15;87(8):3410-7 [8605359] Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):6971-6 [9618523] Trends Cell Biol. 1998 Mar;8(3):107-11 [9695819] J Exp Med. 2005 Nov 21;202(10):1423-31 [16301747] Mol Cell Endocrinol. 2006 Mar 9;247(1-2):4-21 [16297528] Nat Genet. 2006 Aug;38(8):904-9 [16862161] Immunogenetics. 2007 Jun;59(6):441-8 [17440718] Bioinformatics. 2007 Oct 15;23(20):2741-6 [17846035] J Hum Genet. 2013 Aug;58(8):517-20 [23635948] Cancer Causes Control. 2008 Mar;19(2):163-73 [18038187] Am J Hum Genet. 2008 Feb;82(2):290-303 [18252211] Lancet. 2008 Jan 26;371(9609):277-8 [18294980] Immunol Rev. 2008 Apr;222:222-41 [18364005] J Immunol. 2008 Jul 15;181(2):918-30 [18606643] Am J Hum Genet. 2007 Sep;81(3):559-75 [17701901] J Exp Med. 2012 Oct 22;209(11):1937-52 [23071253] Cancer Res. 2012 Nov 1;72(21):5494-504 [22942254] Acta Obstet Gynecol Scand. 2013 Mar;92(3):245-55 [23240575] Immunity. 2013 Feb 21;38(2):285-95 [23395675] Nat Genet. 2013 Apr;45(4):362-70, 370e1-2 [23535730] Bioinformatics. 2008 Oct 1;24(19):2209-14 [18653518] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/0008-5472.CAN-13-1051 ER - TY - JOUR T1 - Cognitive and affective perceptions of vulnerability as predictors of exercise intentions among people with type 2 diabetes AN - 1496959934; 4521778 AB - Most conventional measures of risk perception such as perceived likelihood address largely deliberative or cognitive perceptions of vulnerability. Nevertheless, affective perceptions of vulnerability such as worry may have different antecedents and consequences than do these conventional measures, serve as stronger predictors of behavior, and qualify effects of conventional deliberative risk perceptions on behavior. In this study, we assessed how worry - the most common measure of affective perceptions of vulnerability compared with three conventional measures of risk (absolute risk, comparative risk, and conditional risk) in predicting behavioral intentions. Participants were 83 adults with type 2 diabetes who assessed their risk of heart disease and reported their intentions to increase physical activity (which reduces heart disease risk). As predicted, worry was the only significant predictor of exercise intentions such that higher worry was associated with higher intentions. Importantly, this relationship was stronger among individuals who perceived their absolute risk to be relatively higher and those who perceived their comparative risk to be relatively lower, demonstrating that cognitive and affective perceptions interact. These findings highlight the importance of not conflating affective and cognitive perceptions of vulnerability when assessing perceived risk and suggest the need for more research on how to best conceptualize perceived risk in different samples and settings. Reprinted by permission of Carfax Publishing, Taylor & Francis Ltd JF - Journal of risk research AU - Portnoy, David B AU - Kaufman, Annette R AU - Klein, William M.P. AU - Doyle, Todd A AU - Groot, Mary de AD - US National Cancer Institute ; Ohio University ; Indiana University, Indianapolis Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 177 EP - 193 VL - 17 IS - 2 SN - 1366-9877, 1366-9877 KW - Sociology KW - Comparative analysis KW - Perception KW - Physical activity KW - Diseases KW - Cognition KW - Risk theory KW - Diabetes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496959934?accountid=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+risk+research&rft.atitle=Cognitive+and+affective+perceptions+of+vulnerability+as+predictors+of+exercise+intentions+among+people+with+type+2+diabetes&rft.au=Portnoy%2C+David+B%3BKaufman%2C+Annette+R%3BKlein%2C+William+M.P.%3BDoyle%2C+Todd+A%3BGroot%2C+Mary+de&rft.aulast=Portnoy&rft.aufirst=David&rft.date=2014-02-01&rft.volume=17&rft.issue=2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Journal+of+risk+research&rft.issn=13669877&rft_id=info:doi/10.1080%2F13669877.2013.794153 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-01-23 N1 - Last updated - 2014-02-11 N1 - SubjectsTermNotLitGenreText - 9506; 3524 6220; 11040 11035; 9382; 3617 6220; 2630 971; 2449 10404 DO - http://dx.doi.org/10.1080/13669877.2013.794153 ER - TY - JOUR T1 - Role of neuroticism and coping strategies in psychological reactions to a racist incident among African American University students AN - 1496951074; 4522728 AB - A total of 562 African American university students provided data on individual differences in neuroticism; coping with a recent experience being the target of prejudice, racism, and/or discrimination; and psychological reactions to the incident. Higher negative affect, lower positive affect, more intrusive thoughts about the incident, and lack of forgiveness for the perpetrator were used to index distress in response to the racist incident. Using factor analyses, we determined the factor structure of the Brief COPE in our sample. Using structural equation modeling, we then examined neuroticism and each coping factor as unique predictors of reactions to the race-related incident. We documented that there were direct and indirect associations (via the selection of coping strategies) between neuroticism and the outcome measures. Neuroticism also moderated the association between particular coping strategies and reactions to the racist incident. There was also evidence for direct associations between various coping strategies and the outcome measures. The research, though preliminary, suggests the importance of neuroticism and coping strategies in understanding psychological reactions to being the target of racism. Reprinted by permission of Sage Publications, Inc. JF - Journal of black psychology AU - Pearson, Matthew R AU - Derlega, Valerian J AU - Henson, James M AU - Holmes, Karen Y AU - Ferrer, Rebecca A AU - Harrison, Scott B AD - Old Dominion University ; Norfolk State University ; National Cancer Institute, Rockville Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 81 EP - 111 VL - 40 IS - 1 SN - 0095-7984, 0095-7984 KW - Sociology KW - Racism KW - Social psychology KW - Survival strategy KW - Personality KW - Africa KW - Discrimination KW - U.S.A. KW - Students UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496951074?accountid=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+black+psychology&rft.atitle=Role+of+neuroticism+and+coping+strategies+in+psychological+reactions+to+a+racist+incident+among+African+American+University+students&rft.au=Pearson%2C+Matthew+R%3BDerlega%2C+Valerian+J%3BHenson%2C+James+M%3BHolmes%2C+Karen+Y%3BFerrer%2C+Rebecca+A%3BHarrison%2C+Scott+B&rft.aulast=Pearson&rft.aufirst=Matthew&rft.date=2014-02-01&rft.volume=40&rft.issue=1&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Journal+of+black+psychology&rft.issn=00957984&rft_id=info:doi/10.1177%2F0095798412471682 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2014-01-23 N1 - Last updated - 2014-02-11 N1 - SubjectsTermNotLitGenreText - 3612 3549 2688 2449 10404; 9416 2153; 12432; 10575 10566 3612 3549 2688 2449 10404 9680; 11901 10404; 12334 4049; 2; 433 293 14 DO - http://dx.doi.org/10.1177/0095798412471682 ER - TY - JOUR T1 - A High-Throughput Screening Assay for Fungicidal Compounds against Cryptococcus neoformans AN - 1496898167; 19022822 AB - Cryptococcus neoformans is a pathogenic fungus that causes meningitis worldwide, particularly in human immunodeficiency virus (HIV)-infected individuals. Although amphotericin B is the "gold standard" treatment for cryptococcal meningitis, the toxicity and inconvenience of intravenous injection emphasize a need for development of new anticryptocccal drugs. Recent data from humans and animal studies suggested that a nutrient-deprived host environment may exist in cryptococcal meningitis. Thus, a screening assay for identifying fungicidal compounds under nutrient-deprived conditions may provide an alternative strategy to develop new anticryptococcal drugs for this disease. A high-throughput fungicidal assay was developed using a profluorescent dye, alamarBlue, to detect residual metabolic activity of C. neoformans under nutrient-limiting conditions. Screening the Library of Pharmacologically Active Compounds (LOPAC) with this assay identified a potential chemical scaffold, 10058-F4, that exhibited fungicidal activity in the low micromolar range. These results thus demonstrate the feasibility of this alamarBlue-based assay for high-throughput screening of fungicidal compounds under nutrient-limiting conditions for new anticryptococcal drug development. JF - Journal of Biomolecular Screening AU - Rabjohns, Jennifer LA AU - Park, Yoon-Dong AU - Dehdashti, Jean AU - Sun, Wei AU - Henderson, Christina AU - Zelazny, Adrian AU - Metallo, Steven J AU - Zheng, Wei AU - Williamson, Peter R AD - Laboratory of Clinical Infectious Diseases, National Institutes of Health, Bethesda, MD, USA Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 270 EP - 277 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 19 IS - 2 SN - 1087-0571, 1087-0571 KW - Toxicology Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts C: Algology, Mycology & Protozoology; Biotechnology and Bioengineering Abstracts KW - Amphotericin B KW - Intravenous administration KW - Data processing KW - Fungicidal activity KW - Drug development KW - Toxicity KW - scaffolds KW - Meningitis KW - Cryptococcus neoformans KW - Human immunodeficiency virus KW - high-throughput screening KW - Drugs KW - A 01380:Plant Protection, Fungicides & Seed Treatments KW - K 03400:Human Diseases KW - W 30965:Miscellaneous, Reviews KW - X 24330:Agrochemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496898167?accountid=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+High-Throughput+Screening+Assay+for+Fungicidal+Compounds+against+Cryptococcus+neoformans&rft.au=Rabjohns%2C+Jennifer+LA%3BPark%2C+Yoon-Dong%3BDehdashti%2C+Jean%3BSun%2C+Wei%3BHenderson%2C+Christina%3BZelazny%2C+Adrian%3BMetallo%2C+Steven+J%3BZheng%2C+Wei%3BWilliamson%2C+Peter+R&rft.aulast=Rabjohns&rft.aufirst=Jennifer&rft.date=2014-02-01&rft.volume=19&rft.issue=2&rft.spage=270&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Screening&rft.issn=10870571&rft_id=info:doi/10.1177%2F1087057113496847 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Number of references - 30 N1 - Last updated - 2014-06-12 N1 - SubjectsTermNotLitGenreText - Amphotericin B; Intravenous administration; Data processing; Fungicidal activity; high-throughput screening; Drug development; Toxicity; Drugs; scaffolds; Meningitis; Cryptococcus neoformans; Human immunodeficiency virus DO - http://dx.doi.org/10.1177/1087057113496847 ER - TY - JOUR T1 - Characterization of the Noncoding Regions of the 1918 Influenza A H1N1 Virus AN - 1496895963; 19010477 AB - The terminal noncoding region (NCR) sequences of the eight gene segments of the influenza A/Brevig Mission/1/1918 (H1N1) virus were determined by rapid amplification of cDNA ends (RACE). Chimeric viruses encoding the open reading frames of the 1918 virus but flanked by either the wild-type 1918 NCR sequences or the NCR sequences of two other H1N1 virus strains, A/WSN/1933 and A/New York/312/2001, were produced. No growth differences between the NCR variant 1918 influenza viruses were noted. JF - Journal of Virology AU - Wang, Ruixue AU - Taubenberger, Jeffery K Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 1815 EP - 1818 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 88 IS - 3 SN - 0022-538X, 0022-538X KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Influenza KW - Influenza A KW - Viruses KW - Open reading frames KW - USA, New York KW - H 0500:General KW - V 22310:Genetics, Taxonomy & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496895963?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Characterization+of+the+Noncoding+Regions+of+the+1918+Influenza+A+H1N1+Virus&rft.au=Wang%2C+Ruixue%3BTaubenberger%2C+Jeffery+K&rft.aulast=Wang&rft.aufirst=Ruixue&rft.date=2014-02-01&rft.volume=88&rft.issue=3&rft.spage=1815&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.03098-13 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Number of references - 22 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Influenza A; Open reading frames; Influenza; Viruses; USA, New York DO - http://dx.doi.org/10.1128/JVI.03098-13 ER - TY - JOUR T1 - A possible outbreak of swine influenza, 1892 AN - 1496894068; 19028604 AB - Influenza A viruses are globally enzootic in swine populations. Swine influenza has been recognised only since 1918, but an anecdotal report suggests that a swine-influenza epizootic might have occurred in England in 1892, at the same time as an explosive epidemic (or pandemic recurrence) of human influenza. This outbreak suggests that the ecobiological association between human and swine influenza could extend to before 1918. By contrast with the recent documentation of swine influenza, influenza in horses has been well documented for hundreds of years, and was often linked temporally and geographically to epidemics of human influenza. Both decreased contact between people and horses, and the concomitant increase in swine production over the past century, might have altered the character and dynamics of influenza host-switch events between people and domestic mammals. JF - Lancet Infectious Diseases AU - Morens, David M AU - Taubenberger, Jeffery K AD - Office of the Director, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 169 EP - 172 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 14 IS - 2 SN - 1473-3099, 1473-3099 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Epidemics KW - Influenza KW - British Isles, England KW - Swine influenza KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496894068?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+Infectious+Diseases&rft.atitle=A+possible+outbreak+of+swine+influenza%2C+1892&rft.au=Morens%2C+David+M%3BTaubenberger%2C+Jeffery+K&rft.aulast=Morens&rft.aufirst=David&rft.date=2014-02-01&rft.volume=14&rft.issue=2&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=Lancet+Infectious+Diseases&rft.issn=14733099&rft_id=info:doi/10.1016%2FS1473-3099%2813%2970227-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Last updated - 2014-03-20 N1 - SubjectsTermNotLitGenreText - Swine influenza; Influenza; British Isles, England DO - http://dx.doi.org/10.1016/S1473-3099(13)70227-5 ER - TY - JOUR T1 - Social Theory Applied to Body Image and Chronic Illness in Youth AN - 1496883676; 19002616 AB - Changes in appearance and functional limitations of youth with chronic illness place them at greater risk for negative body image and poor psychosocial and medical outcomes compared with their healthy peers. Sociocultural pressures from the media, family, and peers, as well as social comparison processes to some extent explain the development of negative or positive body image in young people. This article discusses social theories applied to body image in young people with chronic illness, an overlooked population. A review of risk and protective factors of body dissatisfaction in this population and suggested treatment strategies/interventions in the prevention of body dissatisfaction are also considered. Reported findings may help health care providers become more aware of body image issues their young patients with chronic illness face, and posit the importance of regularly monitoring their psychosocial well-being in the efforts to curtail development of body dissatisfaction and consequential poor health outcomes. JF - American Journal of Lifestyle Medicine AU - Quick, Virginia AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development/National Institutes of Health, Division of Intramural Population Health Research, Bethesda, Maryland Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 15 EP - 20 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 8 IS - 1 SN - 1559-8276, 1559-8276 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Prevention KW - Health care KW - Risk factors KW - Reviews KW - Intervention KW - H 0500:General KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496883676?accountid=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+Lifestyle+Medicine&rft.atitle=Social+Theory+Applied+to+Body+Image+and+Chronic+Illness+in+Youth&rft.au=Quick%2C+Virginia&rft.aulast=Quick&rft.aufirst=Virginia&rft.date=2014-02-01&rft.volume=8&rft.issue=1&rft.spage=15&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Lifestyle+Medicine&rft.issn=15598276&rft_id=info:doi/10.1177%2F1559827613505408 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Number of references - 45 N1 - Last updated - 2014-06-26 N1 - SubjectsTermNotLitGenreText - Prevention; Health care; Reviews; Risk factors; Intervention DO - http://dx.doi.org/10.1177/1559827613505408 ER - TY - JOUR T1 - Circulating estrogens and estrogens within the breast among postmenopausal BRCA1/2 mutation carriers. AN - 1493798895; 24442642 AB - Accurately quantifying parent estrogens (PE) estrone (E1) and estradiol (E2) and their metabolites (EM) within breast tissue and serum may permit detailed investigations of their contributions to breast carcinogenesis among BRCA1/2 mutation carriers. We conducted a study of PE/EM in serum, nipple aspirate fluid (NAF), and ductal lavage supernatant (DLS) among postmenopausal BRCA1/2 mutation carriers. PE/EM (conjugated and unconjugated) were measured in paired serum/NAF (n = 22 women) and paired serum/DLS samples (n = 24 women) using quantitative liquid chromatography-tandem mass spectrometry (LC/MS/MS). The relationships between serum and tissue-specific PE/EM were measured using Pearson's correlation coefficients. Conjugated forms of PE/EM constituted the majority of estrogen in serum (88 %), NAF (59 %) and DLS (69 %). PE/EM in NAF and serum were highly correlated [E1 (r = 0.97, p < 0.0001), E2 (r = 0.90, p < 0.0001) and estriol (E3) (r = 0.74, p < 0.0001)] as they were in DLS and serum [E1 (r = 0.92, p < 0.0001; E2 (r = 0.70, p = 0.0001; E3 (r = 0.67, p = 0.0004)]. Analyses of paired total estrogen values for NAF and serum, and DLS and serum yielded ratios of 0.22 (95 % CI 0.19-0.25) and 0.28 (95 % CI 0.24-0.32), respectively. This report is the first to employ LC/MS/MS to quantify PE/EM in novel breast tissue-derived biospecimens (i.e., NAF and DLS). We demonstrate that circulating PE and EM are strongly and positively correlated with tissue-specific PE and EM measured in NAF and DLS among postmenopausal BRCA1/2 mutation carriers. If confirmed, future etiologic studies could utilize the more readily obtainable serum hormone levels as a reliable surrogate measure of exposure at the tissue level. JF - Breast cancer research and treatment AU - Loud, Jennifer T AU - Gierach, Gretchen L AU - Veenstra, Timothy D AU - Falk, Roni T AU - Nichols, Kathryn AU - Guttmann, Allison AU - Xu, Xia AU - Greene, Mark H AU - Gail, Mitchell H AD - Clinical Genetics Branch (CGB), Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 9609 Medical Center Drive, Room 6E536, Bethesda, MD, 20850-9772, USA, loudj@mail.nih.gov. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 517 EP - 529 VL - 143 IS - 3 KW - BRCA1 Protein KW - 0 KW - BRCA1 protein, human KW - BRCA2 Protein KW - BRCA2 protein, human KW - Estrone KW - 2DI9HA706A KW - Estradiol KW - 4TI98Z838E KW - Index Medicus KW - Nipple Aspirate Fluid KW - Carcinogenesis -- metabolism KW - Carcinogenesis -- genetics KW - Postmenopause KW - Premenopause KW - Humans KW - Heterozygote KW - Adult KW - Middle Aged KW - Tandem Mass Spectrometry KW - Mutation KW - Female KW - Breast Neoplasms -- genetics KW - Estradiol -- blood KW - BRCA1 Protein -- genetics KW - Breast Neoplasms -- metabolism KW - Estrone -- blood KW - Estrone -- metabolism KW - Breast Neoplasms -- blood KW - BRCA2 Protein -- genetics KW - Estradiol -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1493798895?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Circulating+estrogens+and+estrogens+within+the+breast+among+postmenopausal+BRCA1%2F2+mutation+carriers.&rft.au=Loud%2C+Jennifer+T%3BGierach%2C+Gretchen+L%3BVeenstra%2C+Timothy+D%3BFalk%2C+Roni+T%3BNichols%2C+Kathryn%3BGuttmann%2C+Allison%3BXu%2C+Xia%3BGreene%2C+Mark+H%3BGail%2C+Mitchell+H&rft.aulast=Loud&rft.aufirst=Jennifer&rft.date=2014-02-01&rft.volume=143&rft.issue=3&rft.spage=517&rft.isbn=&rft.btitle=&rft.title=Breast+cancer+research+and+treatment&rft.issn=1573-7217&rft_id=info:doi/10.1007%2Fs10549-013-2821-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-19 N1 - Date created - 2014-01-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: JAMA. 2000 Jan 26;283(4):485-91 [10659874] Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2779-84 [10688907] J Natl Cancer Inst. 2012 Feb 22;104(4):326-39 [22232133] J Natl Cancer Inst Monogr. 2000;(27):95-112 [10963622] J Endocrinol. 2000 Nov;167(2):281-7 [11054642] J Natl Cancer Inst. 2001 Nov 7;93(21):1624-32 [11698566] JAMA. 2002 Jul 17;288(3):321-33 [12117397] Lancet. 2002 Sep 21;360(9337):942-4 [12354487] Clin Cancer Res. 2002 Oct;8(10):3146-55 [12374682] Cancer Res. 2003 May 15;63(10):2425-33 [12750262] J Natl Cancer Inst. 2003 Aug 20;95(16):1218-26 [12928347] J Steroid Biochem Mol Biol. 2003 Aug;86(2):159-66 [14568567] J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):477-86 [14623547] JAMA. 2004 Apr 14;291(14):1701-12 [15082697] J Natl Cancer Inst. 1987 Nov;79(5):949-60 [3479643] Proc Natl Acad Sci U S A. 1995 Apr 25;92(9):3650-7 [7731959] Annu Rev Pharmacol Toxicol. 1996;36:203-32 [8725388] Carcinogenesis. 1998 Jan;19(1):1-27 [9472688] Lancet. 1997 Oct 11;350(9084):1047-59 [10213546] J Endocrinol. 2004 Oct;183(1):91-9 [15525577] J Clin Endocrinol Metab. 2005 Mar;90(3):1686-91 [15572416] Endocr Relat Cancer. 2005 Sep;12(3):497-510 [16172189] Cancer Epidemiol Biomarkers Prev. 2005 Nov;14(11 Pt 1):2620-7 [16284387] N Engl J Med. 2006 Jan 19;354(3):270-82 [16421368] Anal Chem. 2007 Oct 15;79(20):7813-21 [17848096] Curr Opin Obstet Gynecol. 2008 Feb;20(1):68-73 [18197009] Future Oncol. 2008 Feb;4(1):23-39 [18240998] Int J Cancer. 2008 May 1;122(9):1949-57 [18098283] Int J Biol Sci. 2009;5(1):20-7 [19119312] Cancer Epidemiol Biomarkers Prev. 2009 Apr;18(4):1243-51 [19336560] Nat Med. 2009 Aug;15(8):907-13 [19648928] BMC Womens Health. 2009;9:20 [19602282] Cancer Epidemiol Biomarkers Prev. 2010 Jan;19(1):275-9 [20056648] Cancer Epidemiol Biomarkers Prev. 2010 Jan;19(1):292-300 [20056650] Breast Cancer Res Treat. 2010 Aug;123(1):245-55 [20130984] J Steroid Biochem Mol Biol. 2010 Aug;121(3-5):538-45 [20382222] Reprod Biol Endocrinol. 2010;8:93 [20678202] Cancer Causes Control. 2011 Apr;22(4):529-40 [21286801] J Steroid Biochem Mol Biol. 2011 Jul;125(3-5):169-80 [21397019] Horm Cancer. 2010 Aug;1(4):197-204 [21533003] Breast Cancer Res Treat. 2012 Jan;131(1):287-94 [21870130] Nat Rev Cancer. 2012 Jan;12(1):68-78 [22193408] Comment In: Breast Cancer Res Treat. 2014 Dec;148(3):685 [25385178] Breast Cancer Res Treat. 2014 Dec;148(3):691-2 [25403808] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10549-013-2821-6 ER - TY - JOUR T1 - Cixutumumab for patients with recurrent or refractory advanced thymic epithelial tumours: a multicentre, open-label, phase 2 trial. AN - 1493797390; 24439931 AB - No standard treatment exists for refractory or relapsed advanced thymic epithelial tumours. We investigated the efficacy of cixutumumab, a fully human IgG1 monoclonal antibody targeting the insulin-like growth factor 1 receptor in thymic epithelial tumours after failure of previous chemotherapy. Between Aug 25, 2009, and March 27, 2012, we did a multicentre, open-label, phase 2 trial in patients aged 18 years or older with histologically confirmed recurrent or refractory thymic epithelial tumours. We enrolled individuals who had progressed after at least one previous regimen of platinum-containing chemotherapy, had an Eastern Cooperative Oncology Group performance status of 0 or 1, and had measurable disease and adequate organ function. Eligible patients received intravenous cixutumumab (20 mg/kg) every 3 weeks until disease progression or development of intolerable toxic effects. The primary endpoint was the frequency of response, analysed on an intention-to-treat basis. We also did pharmacodynamic studies. This trial is registered with ClinicalTrials.gov, number NCT00965250. 49 patients were enrolled (37 with thymomas and 12 with thymic carcinomas) who received a median of eight cycles of cixutumumab (range 1-46). At the final actuarial analysis when follow-up data were updated (Nov 30, 2012), median potential follow-up (from on-study date to most current follow-up date) was 24·0 months (IQR 17·3-36·9). In the thymoma cohort, five (14%) of 37 patients (95% CI 5-29) achieved a partial response, 28 had stable disease, and four had progressive disease. In the thymic carcinoma cohort, none of 12 patients (95% CI 0-26) had a partial response, five had stable disease, and seven had progressive disease. The most common grade 3-4 adverse events in both cohorts combined were hyperglycaemia (five [10%]), lipase elevation (three [6%]), and weight loss, tumour pain, and hyperuricaemia (two each [4%]). Nine (24%) of 37 patients with thymoma developed autoimmune conditions during treatment (five were new-onset disorders), the most common of which was pure red-cell aplasia. Two (4%) patients died; one was attributed to disease progression and the other to disease-related complications (respiratory failure, myositis, and an acute coronary event), which could have been precipitated by treatment with cixutumumab. Cixutumumab monotherapy is well-tolerated and active in relapsed thymoma. Development of autoimmunity during treatment needs further investigation. Division of Cancer Treatment and Diagnosis at the National Cancer Institute (National Institutes of Health), ImClone Systems. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - The Lancet. Oncology AU - Rajan, Arun AU - Carter, Corey A AU - Berman, Arlene AU - Cao, Liang AU - Kelly, Ronan J AU - Thomas, Anish AU - Khozin, Sean AU - Chavez, Ariel Lopez AU - Bergagnini, Isabella AU - Scepura, Barbara AU - Szabo, Eva AU - Lee, Min-Jung AU - Trepel, Jane B AU - Browne, Sarah K AU - Rosen, Lindsey B AU - Yu, Yunkai AU - Steinberg, Seth M AU - Chen, Helen X AU - Riely, Gregory J AU - Giaccone, Giuseppe AD - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Memorial Sloan-Kettering Cancer Center, New York, NY, USA. ; National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; Biostatistics and Data Management Section, Office of the Clinical Director, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: gg496@Georgetown.edu. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 191 EP - 200 VL - 15 IS - 2 KW - Antibodies, Monoclonal KW - 0 KW - Antineoplastic Agents KW - anti-IGF-1R antibody A12 KW - Receptor, IGF Type 1 KW - EC 2.7.10.1 KW - Index Medicus KW - Receptor, IGF Type 1 -- immunology KW - Disease-Free Survival KW - Humans KW - Disease Progression KW - Aged KW - Kaplan-Meier Estimate KW - Aged, 80 and over KW - Adult KW - Intention to Treat Analysis KW - Treatment Outcome KW - Autoimmunity -- drug effects KW - Receptor, IGF Type 1 -- antagonists & inhibitors KW - Middle Aged KW - Time Factors KW - Female KW - Male KW - Neoplasms, Glandular and Epithelial -- mortality KW - Thymus Neoplasms -- immunology KW - Thymus Neoplasms -- pathology KW - Antibodies, Monoclonal -- therapeutic use KW - Antineoplastic Agents -- adverse effects KW - Neoplasms, Glandular and Epithelial -- pathology KW - Neoplasm Recurrence, Local -- immunology KW - Neoplasms, Glandular and Epithelial -- drug therapy KW - Neoplasm Recurrence, Local -- drug therapy KW - Neoplasms, Glandular and Epithelial -- immunology KW - Antibodies, Monoclonal -- adverse effects KW - Thymus Neoplasms -- drug therapy KW - Antineoplastic Agents -- therapeutic use KW - Thymus Neoplasms -- mortality KW - Neoplasm Recurrence, Local -- mortality KW - Neoplasm Recurrence, Local -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1493797390?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Oncology&rft.atitle=Cixutumumab+for+patients+with+recurrent+or+refractory+advanced+thymic+epithelial+tumours%3A+a+multicentre%2C+open-label%2C+phase+2+trial.&rft.au=Rajan%2C+Arun%3BCarter%2C+Corey+A%3BBerman%2C+Arlene%3BCao%2C+Liang%3BKelly%2C+Ronan+J%3BThomas%2C+Anish%3BKhozin%2C+Sean%3BChavez%2C+Ariel+Lopez%3BBergagnini%2C+Isabella%3BScepura%2C+Barbara%3BSzabo%2C+Eva%3BLee%2C+Min-Jung%3BTrepel%2C+Jane+B%3BBrowne%2C+Sarah+K%3BRosen%2C+Lindsey+B%3BYu%2C+Yunkai%3BSteinberg%2C+Seth+M%3BChen%2C+Helen+X%3BRiely%2C+Gregory+J%3BGiaccone%2C+Giuseppe&rft.aulast=Rajan&rft.aufirst=Arun&rft.date=2014-02-01&rft.volume=15&rft.issue=2&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Oncology&rft.issn=1474-5488&rft_id=info:doi/10.1016%2FS1470-2045%2813%2970596-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-03-27 N1 - Date created - 2014-01-31 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00965250; ClinicalTrials.gov N1 - SuppNotes - Cited By: Clin Cancer Res. 2003 Jan;9(1):377-82 [12538491] Clin Exp Immunol. 2003 Apr;132(1):128-36 [12653847] Clin Cancer Res. 2013 Aug 1;19(15):4282-9 [23741071] Invest New Drugs. 2012 Aug;30(4):1548-56 [21748299] J Clin Oncol. 2012 May 20;30(15):1849-56 [22508822] J Clin Immunol. 2012 Apr;32(2):238-45 [22170314] Clin Cancer Res. 2012 Mar 15;18(6):1808-17 [22287600] Nat Rev Cancer. 2012 Mar;12(3):159-69 [22337149] J Clin Oncol. 2012 Jan 20;30(3):256-62 [22184397] J Clin Oncol. 2011 May 20;29(15):2052-9 [21502553] Cancer. 2010 Oct 15;116(20):4686-95 [20597130] Ann Oncol. 2010 Jun;21(6):1168-72 [19880439] Pharmacol Rev. 2010 Jun;62(2):199-236 [20392809] Mol Cancer Ther. 2010 Feb;9(2):410-8 [20124453] Cancer Res. 2009 Oct 1;69(19):7662-71 [19789339] Cancer Lett. 2009 Sep 8;282(1):14-24 [19345478] Expert Opin Investig Drugs. 2009 Jul;18(7):1025-33 [19548856] Curr Treat Options Oncol. 2008 Dec;9(4-6):277-87 [19381821] Cancer Res. 2008 Oct 1;68(19):8039-48 [18829562] Blood. 2008 Oct 1;112(7):2836-46 [18658030] Clin Cancer Res. 2007 Oct 1;13(19):5834-40 [17908976] J Neurol. 2007 Jun;254(6):756-62 [17325820] J Clin Oncol. 2005 Sep 1;23(25):6043-53 [16087944] Control Clin Trials. 1989 Mar;10(1):1-10 [2702835] Ann Thorac Surg. 2004 May;77(5):1860-9 [15111216] J Clin Oncol. 2004 Jan 15;22(2):293-9 [14722038] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/S1470-2045(13)70596-5 ER - TY - JOUR T1 - Methylarsonous acid causes oxidative DNA damage in cells independent of the ability to biomethylate inorganic arsenic. AN - 1493797081; 24091636 AB - Inorganic arsenic (iAs) and its toxic methylated metabolite, methylarsonous acid (MMA(III)), both have carcinogenic potential. Prior study shows iAs-induced malignant transformation in both arsenic methylation-proficient (liver) and methylation-deficient (prostate) cells, but only methylation-proficient cells show oxidative DNA damage (ODD) during this transformation. To further define whether arsenic methylation is necessary for transformation or ODD induction, here we chronically exposed these same liver or prostate cell lines to MMA(III) (0.25-1.0 μM) and tested for acquired malignant phenotype. Various metrics of oncogenic transformation were periodically assessed along with ODD during chronic MMA(III) exposure. Methylation-deficient and methylation-proficient cells both acquired a cancer phenotype with MMA(III) exposure at about 20 weeks, based on increased matrix metalloproteinase secretion, colony formation, and invasion. In contrast, prior work showed iAs-induced transformation took longer in biomethylation-deficient cells (~30 weeks) than in biomethylation-proficient cells (~18 weeks). In the present study, MMA(III) caused similar peak ODD levels at similar concentrations and at similar exposure times (18-22 weeks) in both cell types. At the approximate peak of ODD production, both cell types showed similar alterations in arsenic and oxidative stress adaptation factors (i.e., ABCC1, ABCC2, GST-π, SOD-1). Thus, MMA(III) causes oncogenic transformation associated with ODD in methylation-deficient cells, indicating that further methylation is not required to induce ODD. Together, these results show that MMA(III) and iAs cause an acquired malignant phenotype in methylation-deficient cells, yet iAs does not induce ODD. This indicates iAs likely has both genotoxic and non-genotoxic mechanisms dictated by the target cell's ability to methylate arsenic. JF - Archives of toxicology AU - Tokar, Erik J AU - Kojima, Chikara AU - Waalkes, Michael P AD - National Toxicology Program (NTP) Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences (NIEHS), 111 Alexander Drive, MD E1-07, P.O. Box 12233, Research Triangle Park, NC, 27709, USA. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 249 EP - 261 VL - 88 IS - 2 KW - Arsenicals KW - 0 KW - PTEN Phosphohydrolase KW - EC 3.1.3.67 KW - PTEN protein, human KW - Pten protein, rat KW - monomethylarsonic acid KW - J37VJ5709S KW - Index Medicus KW - Animals KW - Arsenic Poisoning -- pathology KW - Liver -- cytology KW - Cell Line -- drug effects KW - Humans KW - Prostate -- metabolism KW - PTEN Phosphohydrolase -- genetics KW - Rats KW - Oxidation-Reduction KW - Adaptation, Physiological -- drug effects KW - Adaptation, Physiological -- physiology KW - Liver -- drug effects KW - Toxicity Tests, Chronic KW - Prostate -- cytology KW - Methylation KW - Male KW - Cell Transformation, Neoplastic -- chemically induced KW - Arsenicals -- pharmacology KW - DNA Damage -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1493797081?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+toxicology&rft.atitle=Methylarsonous+acid+causes+oxidative+DNA+damage+in+cells+independent+of+the+ability+to+biomethylate+inorganic+arsenic.&rft.au=Tokar%2C+Erik+J%3BKojima%2C+Chikara%3BWaalkes%2C+Michael+P&rft.aulast=Tokar&rft.aufirst=Erik&rft.date=2014-02-01&rft.volume=88&rft.issue=2&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Archives+of+toxicology&rft.issn=1432-0738&rft_id=info:doi/10.1007%2Fs00204-013-1141-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-30 N1 - Date created - 2014-01-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Toxicol Appl Pharmacol. 2012 Jun 1;261(2):204-16 [22521957] Nat Methods. 2006 Feb;3(2):123-7 [16432522] Arch Toxicol. 2012 Jun;86(6):975-82 [22398986] Trends Mol Med. 2012 Sep;18(9):509-15 [22795735] Mol Pharmacol. 2001 Aug;60(2):302-9 [11455017] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74 [11553815] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585] Chem Res Toxicol. 2002 Dec;15(12):1627-34 [12482246] J Natl Cancer Inst. 2002 Dec 18;94(24):1888-91 [12488483] J Biol Chem. 2003 Apr 4;278(14):12029-38 [12556532] Carcinogenesis. 2003 May;24(5):967-74 [12771042] Toxicol Pathol. 2004 Jan-Feb;32(1):64-72 [14713550] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6770-3 [15096609] J Biol Chem. 2004 Jul 30;279(31):32700-8 [15161912] Nature. 2004 Oct 21;431(7011):997-1002 [15496926] Cell. 1991 Apr 5;65(1):25-35 [2013093] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10907-12 [9380733] Toxicol Appl Pharmacol. 2005 Aug 15;206(3):288-98 [16039940] Clin Exp Metastasis. 2005;22(3):275-84 [16158255] Chem Biol Interact. 2006 Mar 10;160(1):1-40 [16430879] Toxicol Appl Pharmacol. 2006 Oct 1;216(1):69-79 [16806342] Exp Biol Med (Maywood). 2007 Jan;232(1):3-13 [17202581] Nat Protoc. 2007;2(3):512-22 [17406615] Environ Health Perspect. 2007 May;115(5):734-42 [17520061] Toxicol Appl Pharmacol. 2007 Aug 1;222(3):271-80 [17306315] Free Radic Biol Med. 2008 Sep 1;45(5):651-8 [18572023] Cancer Res. 2008 Oct 15;68(20):8278-85 [18922899] Nature. 2009 Apr 9;458(7239):780-3 [19194462] J Natl Cancer Inst. 2009 Dec 16;101(24):1670-81 [19933942] Environ Health Perspect. 2010 Jan;118(1):108-15 [20056578] Chem Res Toxicol. 2010 Feb 15;23(2):327-35 [20035570] Cell. 2010 Apr 2;141(1):52-67 [20371345] J Natl Cancer Inst. 2010 May 5;102(9):638-49 [20339138] Cancer Res. 2010 Jun 15;70(12):5127-35 [20516118] Cell. 2000 Feb 18;100(4):387-90 [10693755] Toxicol Sci. 2000 Apr;54(2):500-8 [10774833] Arch Toxicol. 2000 Aug;74(6):289-99 [11005674] J Biol Chem. 2000 Oct 27;275(43):33404-8 [10938093] Chem Res Toxicol. 2001 Apr;14(4):355-61 [11304123] Toxicol Sci. 2010 Jul;116(1):44-57 [20375083] Crit Rev Toxicol. 2010 Nov;40(10):912-27 [20812815] Toxicol Sci. 2011 Jan;119(1):73-83 [20937726] Environ Health Perspect. 2011 Feb;119(2):182-8 [21247820] Toxicol Lett. 2011 Feb 25;201(1):62-71 [21167264] Cell. 2011 Mar 4;144(5):646-74 [21376230] Mutat Res. 2011 Jun 3;711(1-2):193-201 [21216256] Toxicol Appl Pharmacol. 2011 Jul 15;254(2):86-99 [21296097] Toxicol Appl Pharmacol. 2011 Sep 15;255(3):242-50 [21820459] J Cell Physiol. 2011 Dec;226(12):3225-32 [21344382] Toxicol Appl Pharmacol. 2011 Nov 15;257(1):1-13 [21925530] Toxicol Sci. 2012 Jan;125(1):20-9 [22011395] Cancer Lett. 2012 Jun 28;319(2):125-9 [22266095] Biol Trace Elem Res. 2005 Winter;108(1-3):115-26 [16327065] J Cell Biochem. 2006 Jan 1;97(1):18-32 [16216007] Environ Health Perspect. 2012 Jun;120(6):865-71 [22472196] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00204-013-1141-2 ER - TY - JOUR T1 - Arsenic-induced cancer cell phenotype in human breast epithelia is estrogen receptor-independent but involves aromatase activation. AN - 1493795270; 24068038 AB - Accumulating data suggest arsenic may be an endocrine disruptor and tentatively linked to breast cancer by some studies. Therefore, we tested the effects of chronic inorganic arsenic exposure on the normal estrogen receptor (ER)-negative breast epithelial cell line, MCF-10A. Cells were chronically exposed to a low-level arsenite (500 nM) for up to 24 weeks. Markers of cancer cell phenotype and the expression of critical genes relevant to breast cancer or stem cells (SCs) were examined. After 24 weeks, chronic arsenic-exposed breast epithelial (CABE) cells showed increases in secreted MMP activity, colony formation, invasion, and proliferation rate, indicating an acquired cancer cell phenotype. These CABE cells presented with basal-like breast cancer characteristics, including ER-α, HER-2, and progesterone receptor negativity, and overexpression of K5 and p63. Putative CD44(+)/CD24(-/low) breast SCs were increased to 80 % over control in CABE cells. CABE cells also formed multilayer cell mounds, indicative of loss of contact inhibition. These mounds showed high levels of K5 and p63, indicating the potential presence of cancer stem cells (CSCs). Epithelial-to-mesenchymal transition occurred during arsenic exposure. Overexpression of aromatase, a key rate-limiting enzyme in estrogen synthesis, occurred with arsenic starting early on in exposure. Levels of 17β-estradiol increased in CABE cells and their conditioned medium. The aromatase inhibitor letrozole abolished arsenic-induced increases in 17β-estradiol production and reversed cancer cell phenotype. Thus, chronic arsenic exposure drives human breast epithelia into a cancer cell phenotype with an apparent overabundance of putative CSCs. Arsenic appears to transform breast epithelia through overexpression of aromatase, thereby activating oncogenic processes independent of ER. JF - Archives of toxicology AU - Xu, Yuanyuan AU - Tokar, Erik J AU - Waalkes, Michael P AD - National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 263 EP - 274 VL - 88 IS - 2 KW - Estrogen Receptor alpha KW - 0 KW - Receptors, Estrogen KW - estrogen receptor alpha, human KW - Estradiol KW - 4TI98Z838E KW - Aromatase KW - EC 1.14.14.1 KW - Matrix Metalloproteinase 2 KW - EC 3.4.24.24 KW - Matrix Metalloproteinase 9 KW - EC 3.4.24.35 KW - Arsenic KW - N712M78A8G KW - Index Medicus KW - Cell Line -- drug effects KW - Humans KW - Epithelial-Mesenchymal Transition -- drug effects KW - Estrogen Receptor alpha -- metabolism KW - Matrix Metalloproteinase 2 -- metabolism KW - Estradiol -- metabolism KW - Neoplastic Stem Cells -- drug effects KW - Matrix Metalloproteinase 9 -- metabolism KW - Epithelial Cells -- drug effects KW - Epithelial Cells -- pathology KW - Toxicity Tests, Chronic KW - Cell Transformation, Neoplastic -- chemically induced KW - Female KW - Mammary Glands, Human -- cytology KW - Arsenic -- toxicity KW - Breast Neoplasms -- pathology KW - Aromatase -- metabolism KW - Breast Neoplasms -- metabolism KW - Receptors, Estrogen -- metabolism KW - Breast Neoplasms -- chemically induced KW - Mammary Glands, Human -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1493795270?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+toxicology&rft.atitle=Arsenic-induced+cancer+cell+phenotype+in+human+breast+epithelia+is+estrogen+receptor-independent+but+involves+aromatase+activation.&rft.au=Xu%2C+Yuanyuan%3BTokar%2C+Erik+J%3BWaalkes%2C+Michael+P&rft.aulast=Xu&rft.aufirst=Yuanyuan&rft.date=2014-02-01&rft.volume=88&rft.issue=2&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Archives+of+toxicology&rft.issn=1432-0738&rft_id=info:doi/10.1007%2Fs00204-013-1131-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-30 N1 - Date created - 2014-01-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Environ Health Perspect. 2010 Jan;118(1):108-15 [20056578] Environ Health Perspect. 2009 Dec;117(12):1847-52 [20049202] Crit Rev Toxicol. 2010 Nov;40(10):912-27 [20812815] Toxicol Sci. 2011 Jan;119(1):73-83 [20937726] J Steroid Biochem Mol Biol. 2011 May;125(1-2):13-22 [21335088] Cancer Res. 2011 Aug 15;71(16):5477-87 [21840986] Biol Trace Elem Res. 2011 Dec;144(1-3):360-79 [21660533] Cancer Res. 2012 Mar 15;72(6):1459-66 [22422990] PLoS One. 2012;7(4):e35957 [22558281] PLoS Genet. 2012;8(5):e1002723 [22654675] Environ Health Perspect. 2012 Jun;120(6):865-71 [22472196] Arch Toxicol. 2012 Jun;86(6):825-30 [22638732] Steroids. 2013 Feb;78(2):161-70 [23178278] J Mammary Gland Biol Neoplasia. 2013 Mar;18(1):25-42 [23392570] Oncogene. 2013 Oct 31;32(44):5233-40 [23178495] N Engl J Med. 2000 Jul 13;343(2):78-85 [10891514] Endocrinology. 2000 Oct;141(10):3595-602 [11014213] Cancer Res. 2001 Mar 1;61(5):1910-8 [11280746] APMIS. 2001 May;109(5):321-32 [11478680] Nat Rev Cancer. 2002 Jun;2(6):442-54 [12189386] J Natl Cancer Inst. 2002 Dec 18;94(24):1888-91 [12488483] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218] Endocrinology. 2003 Jun;144(6):2425-36 [12746304] Cancer Res. 2003 Aug 15;63(16):5041-5 [12941832] J Natl Cancer Inst. 2004 Mar 17;96(6):466-74 [15026472] Chem Res Toxicol. 2004 Aug;17(8):1064-76 [15310238] Jpn J Clin Oncol. 1993 Feb;23(1):1-13 [8459638] J Steroid Biochem Mol Biol. 1997 Apr;61(3-6):281-6 [9365202] Anticancer Res. 2005 Jan-Feb;25(1A):369-75 [15816560] Histopathology. 2005 Nov;47(5):458-66 [16241993] Chem Res Toxicol. 2006 Dec;19(12):1619-29 [17173375] Toxicol Sci. 2007 Feb;95(2):313-20 [17077188] Cancer. 2007 Jun 15;109(12 Suppl):2667-711 [17503436] Toxicol Sci. 2007 Jul;98(1):75-86 [17283378] Toxicol Appl Pharmacol. 2007 Aug 1;222(3):271-80 [17306315] Nat Clin Pract Oncol. 2008 Mar;5(3):149-59 [18212769] Cell. 2008 May 16;133(4):704-15 [18485877] PLoS One. 2008;3(8):e2888 [18682804] Cancer Res. 2008 Oct 15;68(20):8278-85 [18922899] Environ Sci Technol. 2008 Oct 1;42(19):7187-92 [18939545] Nat Rev Cancer. 2009 Apr;9(4):265-73 [19262571] Cancer Res. 2009 Apr 1;69(7):2887-95 [19276366] Biol Trace Elem Res. 2009 Summer;129(1-3):28-35 [19043675] Nature. 2010 Jun 10;465(7299):798-802 [20383121] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00204-013-1131-4 ER - TY - JOUR T1 - S-(-)equol producing status not associated with breast cancer risk among low isoflavone-consuming US postmenopausal women undergoing a physician-recommended breast biopsy. AN - 1492703557; 24461312 AB - Soy foods are the richest sources of isoflavones, mainly daidzein and genistein. Soy isoflavones are structurally similar to the steroid hormone 17β-estradiol and may protect against breast cancer. S-(-)equol, a metabolite of the soy isoflavone daidzein, has a higher bioavailability and greater affinity for estrogen receptor β than daidzein. Approximately one-third of the Western population is able to produce S-(-)equol, and the ability is linked to certain gut microbes. We hypothesized that the prevalence of breast cancer, ductal hyperplasia, and overall breast pathology will be lower among S-(-)equol producing, as compared with nonproducing, postmenopausal women undergoing a breast biopsy. We tested our hypothesis using a cross-sectional study design. Usual diets of the participants were supplemented with 1 soy bar per day for 3 consecutive days. Liquid chromatography-multiple reaction ion monitoring mass spectrometry analysis of urine from 143 subjects revealed 25 (17.5%) as S-(-)equol producers. We found no statistically significant associations between S-(-)equol producing status and overall breast pathology (odds ratio [OR], 0.68; 95% confidence interval [CI], 0.23-1.89), ductal hyperplasia (OR, 0.84; 95% CI, 0.20-3.41), or breast cancer (OR, 0.56; 95% CI, 0.16-1.87). However, the mean dietary isoflavone intake was much lower (0.3 mg/d) than in previous reports. Given that the amount of S-(-)equol produced in the gut depends on the amount of daidzein exposure, the low soy intake coupled with lower prevalence of S-(-)equol producing status in the study population favors toward null associations. Findings from our study could be used for further investigations on S-(-)equol producing status and disease risk. Published by Elsevier Inc. JF - Nutrition research (New York, N.Y.) AU - Virk-Baker, Mandeep K AU - Barnes, Stephen AU - Krontiras, Helen AU - Nagy, Tim R AD - Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: mandeep.virk-baker@nih.gov. ; Department of Pharmacology and Toxicology, University of Alabama at Birmingham, Birmingham, AL, USA; The UAB Comprehensive Cancer Center, Birmingham, AL, USA. Electronic address: sbarnes@uab.edu. ; The UAB Comprehensive Cancer Center, Birmingham, AL, USA; Department of Surgery, Surgical Oncology, University of Alabama at Birmingham, Birmingham, AL, USA. Electronic address: helen.krontiras@ccc.uab.edu. ; Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL, USA; The UAB Comprehensive Cancer Center, Birmingham, AL, USA. Electronic address: tnagy@uab.edu. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 116 EP - 125 VL - 34 IS - 2 KW - Estrogen Receptor beta KW - 0 KW - Isoflavones KW - Phytoestrogens KW - Equol KW - 531-95-3 KW - Index Medicus KW - ER+ KW - Soy Screen Questionnaire KW - liquid chromatography–multiple reaction ion monitoring mass spectrometry KW - Dietary soy isoflavones KW - body mass index KW - estrogen receptor positive KW - Ductal hyperplasia KW - University of Alabama at Birmingham. KW - BMI KW - Food Frequency Questionnaire KW - estrogen receptor negative KW - UAB KW - S-(−)equol status KW - ER– KW - Breast biopsy KW - AS KW - FFQ KW - confidence interval KW - OR KW - African American KW - estrogen receptor KW - CI KW - Postmenopausal women KW - AA KW - odds ratio KW - ER KW - LC-MRM-MS KW - SSQ KW - Asian American KW - Breast cancer KW - United States KW - Cross-Sectional Studies KW - Odds Ratio KW - Postmenopause KW - Humans KW - Soy Foods KW - Aged KW - Middle Aged KW - Dietary Supplements KW - Biopsy KW - Estrogen Receptor beta -- metabolism KW - Feeding Behavior KW - Female KW - Biological Availability KW - Isoflavones -- pharmacology KW - Phytoestrogens -- pharmacology KW - Isoflavones -- administration & dosage KW - Soybeans -- chemistry KW - Breast Neoplasms -- etiology KW - Equol -- urine KW - Breast Neoplasms -- metabolism KW - Breast -- pathology KW - Diet KW - Phytoestrogens -- administration & dosage KW - Equol -- metabolism KW - Equol -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492703557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nutrition+research+%28New+York%2C+N.Y.%29&rft.atitle=S-%28-%29equol+producing+status+not+associated+with+breast+cancer+risk+among+low+isoflavone-consuming+US+postmenopausal+women+undergoing+a+physician-recommended+breast+biopsy.&rft.au=Virk-Baker%2C+Mandeep+K%3BBarnes%2C+Stephen%3BKrontiras%2C+Helen%3BNagy%2C+Tim+R&rft.aulast=Virk-Baker&rft.aufirst=Mandeep&rft.date=2014-02-01&rft.volume=34&rft.issue=2&rft.spage=116&rft.isbn=&rft.btitle=&rft.title=Nutrition+research+%28New+York%2C+N.Y.%29&rft.issn=1879-0739&rft_id=info:doi/10.1016%2Fj.nutres.2013.12.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-11 N1 - Date created - 2014-01-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lancet. 1997 Oct 4;350(9083):990-4 [9329514] Proc Soc Exp Biol Med. 1998 Mar;217(3):335-9 [9492344] J Nutr. 2006 Jan;136(1):45-51 [16365057] J Nutr. 2006 May;136(5):1347-51 [16614428] Eur J Cancer Prev. 2006 Jun;15(3):225-32 [16679865] J Nutr. 2006 Aug;136(8):2188-93 [16857839] Nutr Cancer. 2006;55(1):1-12 [16965235] Cancer Causes Control. 2006 Dec;17(10):1253-61 [17111256] J Clin Oncol. 2007 Feb 20;25(6):648-55 [17200150] J Appl Microbiol. 2007 Aug;103(2):445-53 [17650205] Menopause. 2007 Sep-Oct;14(5):866-74 [17464237] Br J Nutr. 2005 Dec;94(6):873-6 [16351761] Cancer Epidemiol Biomarkers Prev. 2008 Jan;17(1):33-42 [18199709] Breast Cancer Res. 2008;10(2):R32 [18419813] Biosci Biotechnol Biochem. 2008 Oct;72(10):2660-6 [18838805] J Clin Oncol. 2008 Dec 20;26(36):5923-9 [19018085] Cancer Epidemiol Biomarkers Prev. 2009 Apr;18(4):1050-9 [19318430] Am J Clin Nutr. 2009 May;89(5):1664S-1667S [19357217] Breast Cancer Res Treat. 2009 Aug;116(3):587-94 [18821061] Nutr Cancer. 2009;61(6):792-8 [20155618] Wei Sheng Yan Jiu. 2010 Jan;39(1):59-64 [20364591] J Chromatogr B Analyt Technol Biomed Life Sci. 2010 Apr 15;878(13-14):994-1002 [20346741] Am J Clin Nutr. 1998 Dec;68(6 Suppl):1333S-1346S [9848496] Nutr Cancer. 1999;33(1):3-19 [10227038] J Natl Cancer Inst. 1999 Jun 16;91(12):1067-72 [10379970] Cancer Epidemiol Biomarkers Prev. 2005 Jan;14(1):221-6 [15668498] Exp Biol Med (Maywood). 2005 Mar;230(3):155-70 [15734719] Am J Clin Nutr. 2005 May;81(5):1072-9 [15883431] J Nutr. 2005 Jun;135(6):1400-6 [15930444] Breast Cancer Res Treat. 2011 Jan;125(2):315-23 [21113655] Proc Nutr Soc. 2011 Feb;70(1):10-8 [21092366] Food Funct. 2011 May;2(5):235-44 [21779561] J Bacteriol. 2011 Oct;193(19):5570-1 [21914883] Nutrients. 2010 Mar;2(3):340-54 [22254026] Br J Nutr. 2012 Apr;107(8):1201-6 [21920062] J Nutr Biochem. 2012 Jun;23(6):573-9 [21775122] Appl Environ Microbiol. 2013 Jun;79(11):3494-502 [23542626] Int J Food Sci Nutr. 2013 Dec;64(8):936-43 [23869769] J Epidemiol. 2000 Mar;10(2):127-35 [10778038] Nutr Cancer. 2000;36(1):27-32 [10798213] Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):581-6 [10868692] Cancer Epidemiol Biomarkers Prev. 2001 Mar;10(3):223-8 [11303591] Cancer Epidemiol Biomarkers Prev. 2001 May;10(5):483-8 [11352858] Br J Cancer. 2001 Aug 3;85(3):372-8 [11487268] Am J Epidemiol. 2001 Sep 1;154(5):434-41 [11532785] Cancer Causes Control. 2002 Jun;13(5):407-15 [12146845] Carcinogenesis. 2002 Sep;23(9):1491-6 [12189192] J Nutr. 2002 Dec;132(12):3577-84 [12468591] Food Chem Toxicol. 2003 May;41(5):631-6 [12659715] Am J Clin Nutr. 2003 Jun;77(6):1459-65 [12791624] J Natl Cancer Inst. 2003 Jun 18;95(12):906-13 [12813174] J Steroid Biochem Mol Biol. 2003 Jul;86(1):71-7 [12943746] Carcinogenesis. 2004 Jan;25(1):77-81 [14555615] Am J Clin Nutr. 2004 Feb;79(2):282-8 [14749235] Bioorg Med Chem. 2004 Mar 15;12(6):1559-67 [15018930] Int J Cancer. 2004 Jun 10;110(2):284-90 [15069695] Breast Cancer Res. 2004;6(3):119-27 [15084232] Cancer Epidemiol Biomarkers Prev. 2004 Jul;13(7):1156-62 [15247126] J Nutr. 2004 Oct;134(10):2623-7 [15465757] FEBS Lett. 1981 Jan 26;123(2):337-42 [6262113] Proc Soc Exp Biol Med. 1995 Jan;208(1):40-3 [7892293] J Am Diet Assoc. 1995 May;95(5):545-51 [7722188] Br J Cancer. 1995 Jun;71(6):1353-8 [7779738] Obstet Gynecol. 1996 May;87(5 Pt 2):897-904 [8677131] Nutr Cancer. 1996;26(2):123-48 [8875551] Cancer Epidemiol Biomarkers Prev. 1996 Nov;5(11):901-6 [8922298] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.nutres.2013.12.002 ER - TY - JOUR T1 - Endometrial thickness and risk of breast and endometrial carcinomas in the prostate, lung, colorectal and ovarian cancer screening trial AN - 1492633661; 18888730 AB - Postmenopausal women with higher circulating estrogen levels are at increased risk of developing breast and endometrial carcinomas. In the endometrium, excess estrogen relative to progesterone produces a net proliferative stimulus, which may result in endometrial thickening. Therefore, the hypothesis that endometrial thickness is a biological marker of excess estrogen stimulation that is associated with risk of breast and endometrial carcinomas was tested. Endometrial thickness was measured in 1,272 postmenopausal women, aged 55-74 years, who underwent transvaginal ultrasound (TVU) screening as part of the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Serial endometrial thickness measurements were available for a subset of women at 1 year (n=1,018), 2 years (n=869) and 3 years (n=641) after baseline. The associations between endometrial thickness and breast (n=91) and endometrial (n=14) carcinoma were evaluated by estimating relative risks (RRs) and 95% confidence intervals (CIs) using Cox proportional hazards regression with age as the time metric. Models incorporating baseline endometrial thickness and as a time-varying covariate using all measurements were examined. Median follow-up among study participants was 12.5 years (range: 0.3-13.8 years). Compared to baseline endometrial thickness of 1.0-2.99 mm, women with baseline endometrial thickness greater than or equal to 5.0 mm had an increased risk of breast (RR=2.00, 95% CI=1.15-3.48) and endometrial (RR=5.02, 95% CI=0.96-26.36) carcinomas in models adjusted for menopausal hormone use and BMI. These data suggest that increased endometrial thickness as assessed by TVU was associated with increased risk of breast and endometrial carcinomas. What's new? Endometrial thickness is related to obesity and menopausal hormone use, factors associated with a higher incidence of breast and endometrial carcinomas. Given these associations, the authors of this study investigated whether endometrial thickness was independently associated with incident breast or endometrial carcinoma risk. In a cohort of 1,272 women, an endometrial thickness greater than five millimeters was associated with a two-fold increase in risk for breast carcinoma and a five-fold increase in risk for endometrial carcinoma. JF - International Journal of Cancer AU - Felix, Ashley S AU - Weissfeld, Joel L AU - Pfeiffer, Ruth M AU - Modugno, Francesmary AU - Black, Amanda AU - Hill, Lyndon M AU - Martin, Jerry AU - Sit, Anita S AU - Sherman, Mark E AU - Brinton, Louise A AD - Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Rockville, MD. Y1 - 2014/02// PY - 2014 DA - Feb 2014 SP - 954 EP - 960 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 134 IS - 4 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Age KW - Risk assessment 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/1492633661?accountid=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=Endometrial+thickness+and+risk+of+breast+and+endometrial+carcinomas+in+the+prostate%2C+lung%2C+colorectal+and+ovarian+cancer+screening+trial&rft.au=Felix%2C+Ashley+S%3BWeissfeld%2C+Joel+L%3BPfeiffer%2C+Ruth+M%3BModugno%2C+Francesmary%3BBlack%2C+Amanda%3BHill%2C+Lyndon+M%3BMartin%2C+Jerry%3BSit%2C+Anita+S%3BSherman%2C+Mark+E%3BBrinton%2C+Louise+A&rft.aulast=Felix&rft.aufirst=Ashley&rft.date=2014-02-01&rft.volume=134&rft.issue=4&rft.spage=954&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.28404 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-01-01 N1 - Last updated - 2014-02-11 N1 - SubjectsTermNotLitGenreText - Risk assessment DO - http://dx.doi.org/10.1002/ijc.28404 ER - TY - JOUR T1 - Role of Myc in hepatocellular proliferation and hepatocarcinogenesis. AN - 1490900417; 24096051 AB - Myc is involved in cell growth, proliferation, apoptosis, energy metabolism, and differentiation. Whether it is essential for hepatocellular proliferation and carcinogenesis is unclear due to a lack of an efficient hepatocyte-specific Myc disruption model. This study used a novel genetic model to investigate the involvement of Myc in hepatocellular proliferation and hepatocarcinogenesis in mice. Temporal hepatocyte-specific Myc disruption was achieved by use of the tamoxifen-inducible Cre-ER(T2) recombinase system under control of the serum albumin promoter. Hepatocyte proliferation was assessed by administering peroxisome proliferator-activated receptor α (PPARα) agonist Wy-14,643. A diethylnitrosamine-induced liver cancer model was used to evaluate the role of Myc in hepatocarcinogenesis. Tamoxifen administration induced recombination of Myc specifically in hepatocytes of Myc(fl/fl,ERT2-Cre) mice. When treated with a known hepatocellular proliferative stimulus Wy-14,643, Myc(fl/fl,ERT2-Cre) mice showed a lower liver/body weight ratio and suppressed hepatocyte proliferation as compared to Myc(fl/fl) mice. Hepatic expression of cell cycle control genes, DNA repair genes, and Myc target gene miRNAs were upregulated in Wy-14,643-treated Myc(fl/fl) mouse livers, but not in Wy-14,643-treated Myc(fl/fl,ERT2-Cre) livers. However, no differences were observed in the lipid-lowering effect of Wy-14,643 between Myc(fl/fl,ERT2-Cre) and Myc(fl/fl) mice, consistent with no differences in the expression of several PPARα target genes involved in fatty acid β-oxidation. Moreover, when subjected to the diethylnitrosamine liver cancer bioassay, Myc(fl/fl,ERT2-Cre) mice exhibited a markedly lower incidence of tumor formation compared with Myc(fl/fl) mice. Myc plays an essential role in hepatocellular proliferation and liver tumorigenesis. Published by Elsevier B.V. JF - Journal of hepatology AU - Qu, Aijuan AU - Jiang, Changtao AU - Cai, Yan AU - Kim, Jung-Hwan AU - Tanaka, Naoki AU - Ward, Jerrold M AU - Shah, Yatrik M AU - Gonzalez, Frank J AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States. ; Global VetPathology, Montgomery Village, MD 20866, United States. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States; Department of Molecular and Integrative Physiology and Internal Medicine, Division of Gastroenterology, University of Michigan School of Medicine, Ann Arbor, MI 48109, United States. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States. Electronic address: gonzalef@mail.nih.gov. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 331 EP - 338 VL - 60 IS - 2 KW - Fatty Acids KW - 0 KW - MIRN17-92 microRNA, mouse KW - MicroRNAs KW - PPAR alpha KW - Pyrimidines KW - RNA, Messenger KW - pirinixic acid KW - 86C4MRT55A KW - Index Medicus KW - peroxisome proliferator-activated receptor α KW - Cyp4a10 and Cyp4a14 KW - diethynitrosamine KW - Rad51 KW - cre recombinase, tamoxifen-inducible estrogen receptor ligand-binding domain fusion protein KW - minichromosome maintenance KW - DEN KW - α/β interferon-inducible Mx-promoter driving Cre recombinase KW - floxed Myc allele KW - cytochromes P450 4a10 and 4a14 KW - bromodeoxyuridine KW - CDK KW - RAD51 homolog (S. cerevisiae) KW - bHLH KW - acyl-CoA oxidase KW - cyclin-dependent kinase KW - Myc(fl/fl) KW - Myc KW - inducible liver-specific Myc knockout mouse KW - Tumorigenesis KW - Mcm KW - Myc(fl/fl,ERT2-Cre) KW - PPARα KW - Cre-ER(T2) KW - serum albumin promoter KW - BrdU KW - Acox1 KW - checkpoint kinase 1 homologue KW - Chek1 KW - Cell cycle control KW - basic helix-loop-helix leucine zipper KW - Cell proliferation KW - Myc(fl/fl)Mx-Cre KW - SA KW - Cell Proliferation -- drug effects KW - Animals KW - MicroRNAs -- genetics KW - Pyrimidines -- pharmacology KW - Mice KW - RNA, Messenger -- genetics KW - PPAR alpha -- agonists KW - Fatty Acids -- metabolism KW - Mice, Knockout KW - Gene Knockout Techniques KW - MicroRNAs -- metabolism KW - RNA, Messenger -- metabolism KW - Models, Genetic KW - Male KW - Liver Neoplasms, Experimental -- genetics KW - Hepatocytes -- drug effects KW - Liver Neoplasms, Experimental -- pathology KW - Liver Neoplasms, Experimental -- etiology KW - Genes, myc KW - Hepatocytes -- pathology KW - Hepatocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490900417?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+Myc+in+hepatocellular+proliferation+and+hepatocarcinogenesis.&rft.au=Qu%2C+Aijuan%3BJiang%2C+Changtao%3BCai%2C+Yan%3BKim%2C+Jung-Hwan%3BTanaka%2C+Naoki%3BWard%2C+Jerrold+M%3BShah%2C+Yatrik+M%3BGonzalez%2C+Frank+J&rft.aulast=Qu&rft.aufirst=Aijuan&rft.date=2014-02-01&rft.volume=60&rft.issue=2&rft.spage=331&rft.isbn=&rft.btitle=&rft.title=Journal+of+hepatology&rft.issn=1600-0641&rft_id=info:doi/10.1016%2Fj.jhep.2013.09.024 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-26 N1 - Date created - 2014-01-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Diabetes. 2005 Aug;54(8):2460-70 [16046315] BMC Physiol. 2012;12:1 [22397685] Science. 2000 Jun 2;288(5471):1643-7 [10834843] Genes Dev. 2000 Jun 15;14(12):1448-59 [10859164] Annu Rev Cell Dev Biol. 2000;16:653-99 [11031250] Science. 2000 Dec 22;290(5500):2271-3 [11188727] Immunity. 2001 Jan;14(1):45-55 [11163229] Biochem J. 2002 Dec 15;368(Pt 3):931-7 [12230428] Genesis. 2004 Jul;39(3):167-72 [15282742] Nature. 2004 Oct 28;431(7012):1112-7 [15475948] Mod Treat. 1969 Nov;6(6):1341-51 [5377637] Ann N Y Acad Sci. 1982;386:81-110 [7046570] Cancer Res. 1983 Sep;43(9):4253-9 [6871863] Cell. 1983 Dec;35(3 Pt 2):603-10 [6606489] Mol Cell Biol. 1985 Apr;5(4):780-6 [2581126] Nature. 1990 Oct 18;347(6294):645-50 [2129546] Genes Dev. 1993 Apr;7(4):671-82 [8458579] Cancer Res. 1993 Apr 15;53(8):1719-23 [8467484] Mol Cell Biol. 1995 Jun;15(6):3012-22 [7539101] Carcinogenesis. 1997 Nov;18(11):2029-33 [9395198] J Biol Chem. 1999 Jan 1;274(1):305-15 [9867845] Oncogene. 1999 May 13;18(19):2934-41 [10378690] Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7324-9 [10377413] Nat Cell Biol. 2005 Mar;7(3):215-7 [15738972] Proc Natl Acad Sci U S A. 2005 May 17;102(20):7286-91 [15857952] Nature. 2005 Jun 9;435(7043):839-43 [15944709] Mol Cell Biol. 2007 Jun;27(12):4238-47 [17438130] Eur J Cancer. 2007 Nov;43(16):2413-22 [17826980] Nat Genet. 2008 Jan;40(1):43-50 [18066065] Toxicology. 2008 Apr 3;246(1):2-8 [18006136] Proc Natl Acad Sci U S A. 2008 Jun 10;105(23):8079-84 [18524952] Genes Dev. 2008 Oct 15;22(20):2755-66 [18923074] Nat Rev Cancer. 2008 Dec;8(12):976-90 [19029958] Clin Cancer Res. 2009 Nov 1;15(21):6479-83 [19861459] Toxicol Sci. 2010 Dec;118(2):404-10 [20813756] Proc Natl Acad Sci U S A. 2010 Nov 23;107(47):20471-6 [21059911] Cell Metab. 2011 Jul 6;14(1):131-42 [21723511] Hepatology. 2011 Aug;54(2):472-83 [21538443] Clin Cancer Res. 2011 Nov 15;17(22):7067-79 [21933891] Semin Cell Dev Biol. 2011 Oct;22(8):898-905 [21821141] Cancer Res. 2005 Nov 1;65(21):9628-32 [16266980] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jhep.2013.09.024 ER - TY - JOUR T1 - The potential of hyperpolarized (13)C MRI in assessing signaling pathways in cancer. AN - 1490899543; 24439335 AB - Advances in genomics are enabling integration of various -omics to reveal the complexities underneath carcinogenesis. Multivariate signaling pathways are deregulated and evolve spatially and temporally depending on the tumor microenvironment. This finding shifts the focus of cancer research from "one disease-one target and drug" to "one disease-multiple pathway targets and combinational therapy" and imposes new challenges on the imaging community in terms of imaging targets, scales and information levels. In current clinical settings, most imaging modalities assess cancer risk through alternations in anatomy, function, metabolism, cellularity, or limited molecular events. Few clinical-translatable imaging modalities are capable of detecting aberrations in signaling pathways at the level of tissue biology. An exception to this is hyperpolarized (13)C magnetic resonance spectroscopic imaging (HP (13)C MRI), which is capable of imaging the molecular signatures of special metabolic enzymes using HP (13)C-labeled substrates. HP (13)C MRI can identify multiple metabolites including intermediates and products simultaneously to allow extraction of critical parameters such as flux alterations for multiple metabolic pathways. Meanwhile, recent progress in cancer metabolism research affirms that metabolic alterations are directly controlled by signaling pathways. Thus, in vivo assessment of aberrations occurring in signaling pathways becomes feasible through HP (13)C imaging. This report briefly reviews the connections between signaling pathways and cancer metabolic phenotypes, the current status of HP (13)C MRI in assessing signal pathways, and recent advances in HP (13)C MRI techniques. Integrated with cancer genomics and animal models, HP (13)C MRI may hold high promise in exploring important issues in cancer that are linked to functionality of signaling pathways. Examples include genomic-driven therapy, intratumoral heterogeneity, and drug resistances. Published by Elsevier Inc. JF - Academic radiology AU - Zhang, Huiming AD - Division of Cancer Treatment and Diagnosis, Cancer Imaging Program, National Cancer Institute, National Institutes of Health, Bethesda, MD. Electronic address: zhanghui@mail.nih.gov. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 215 EP - 222 VL - 21 IS - 2 KW - Carbon Isotopes KW - 0 KW - Neoplasm Proteins KW - Index Medicus KW - cancer genomics–driven approach KW - cancer metabolism KW - signaling pathways KW - metabolic imaging KW - Hyperpolarized (13)C MRI KW - Image Interpretation, Computer-Assisted -- methods KW - Animals KW - Feasibility Studies KW - Humans KW - Molecular Imaging -- methods KW - Carbon Isotopes -- pharmacokinetics KW - Magnetic Resonance Spectroscopy -- methods KW - Magnetic Resonance Imaging -- methods KW - Algorithms KW - Neoplasm Proteins -- metabolism KW - Signal Transduction KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490899543?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Academic+radiology&rft.atitle=The+potential+of+hyperpolarized+%2813%29C+MRI+in+assessing+signaling+pathways+in+cancer.&rft.au=Zhang%2C+Huiming&rft.aulast=Zhang&rft.aufirst=Huiming&rft.date=2014-02-01&rft.volume=21&rft.issue=2&rft.spage=215&rft.isbn=&rft.btitle=&rft.title=Academic+radiology&rft.issn=1878-4046&rft_id=info:doi/10.1016%2Fj.acra.2013.11.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-06 N1 - Date created - 2014-01-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.acra.2013.11.015 ER - TY - JOUR T1 - A phase II study of cixutumumab (IMC-A12, NSC742460) in advanced hepatocellular carcinoma. AN - 1490899263; 24045151 AB - IGF-IR is implicated in hepatic carcinogenesis. This and preliminary evidence of biological activity of anti-IGF-1R monoclonal antibody cixutumumab in phase I trials prompted this phase II study. Patients with advanced HCC, Child-Pugh A-B8, received cixutumumab 6mg/kg weekly, in a Simon two-stage design study, with the primary endpoints being 4-month PFS and RECIST-defined response rate. Tissue and circulating markers plus different HCC scoring systems were evaluated for correlation with PFS and OS. As a result of pre-specified futility criteria, only stage 1 was accrued: N=24: median age 67.5 years (range 49-83), KPS 80% (70-90%), 20 males (83%), 9 stage III (37%)/15 stage IV (63%), 18 Child-Pugh A (75%), 11 HBV (46%)/10 HCV (42%)/11 alcoholic cirrhosis (46%)/2 NASH (8%), 11 (46%) diabetic. Median number of doses: 7 (range 1-140). Grade 3/4 toxicities >10% included: diabetes, elevated liver function tests, hyponatremia, and lymphopenia. Four-month PFS was 30% (95% CI 13-48), and there were no objective responses. Median overall survival was 8 months (95% CI 5.8-14). IGF-R1 staining did not correlate with outcome. Elevated IGFBP-1 correlated with improved PFS (1.2 [95% CI 1-1.4]; p 0.009) and OS (1.2 [95% CI 1.1-1.4]; p 0.003). Cixutumumab monotherapy did not have clinically meaningful activity in this unselected HCC population. Grade 3-4 hyperglycemia occurred in 46% of patients. Elevated IGFBP-1 correlated with improved PFS and OS. Copyright © 2013 European Association for the Study of the Liver. All rights reserved. JF - Journal of hepatology AU - Abou-Alfa, Ghassan K AU - Capanu, Marinela AU - O'Reilly, Eileen M AU - Ma, Jennifer AU - Chou, Joanne F AU - Gansukh, Bolorsukh AU - Shia, Jinru AU - Kalin, Marcia AU - Katz, Seth AU - Abad, Leslie AU - Reidy-Lagunes, Diane L AU - Kelsen, David P AU - Chen, Helen X AU - Saltz, Leonard B AD - Department of Internal Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, United States; Department of Internal Medicine, Weill Medical College at Cornell University, New York, NY, United States. Electronic address: abou-alg@mskcc.org. ; Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY, United States. ; Department of Internal Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, United States; Department of Internal Medicine, Weill Medical College at Cornell University, New York, NY, United States. ; Department of Internal Medicine, Memorial Sloan-Kettering Cancer Center, New York, NY, United States. ; Department of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, United States. ; Department of Radiology, Memorial Sloan-Kettering Cancer Center, New York, NY, United States. ; Research Department, ImClone Systems, a wholly-owned subsidiary of Eli Lilly & Company, New York, NY, United States. ; Cancer Therapy Evaluation Program (CTEP), National Cancer Institute, Bethesda, MD, United States. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 319 EP - 324 VL - 60 IS - 2 KW - Antibodies, Monoclonal KW - 0 KW - Biomarkers, Tumor KW - IGFBP1 protein, human KW - IGFBP3 protein, human KW - Insulin-Like Growth Factor Binding Protein 1 KW - Insulin-Like Growth Factor Binding Protein 3 KW - anti-IGF-1R antibody A12 KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Insulin-Like Growth Factor II KW - 67763-97-7 KW - Receptor, IGF Type 1 KW - EC 2.7.10.1 KW - Index Medicus KW - HR KW - LOH KW - CTEP/NCI KW - Units/Liter KW - Insulin growth factor 1 receptor KW - Cell conditioning 1 KW - Insulin-like growth factor binding protein 1 KW - ELISA KW - progression free survival KW - Insulin-like growth factor binding protein 3 KW - mcl KW - IGFBP 1 KW - Enzyme-linked immunosorbent assay KW - RECIST KW - Mitogen activated protein KW - ALT KW - Insulin growth factor 2 KW - ADCC KW - IGFBP 3 KW - Loss of heterozygosity KW - Insulin growth factor 1 KW - Karnofsky performance status KW - Free IGF1 KW - Cixutumumab (IMC-A12, NSC742460) KW - PFS KW - mg/kg KW - Milliliter per minute KW - Alanine aminotransferase KW - HIV KW - Response evaluation criteria in solid tumors KW - Antibody-dependent complement-mediated cytotoxicity KW - Aspartate aminotransferase KW - Insulin growth factor 2 receptor KW - CALGB KW - AJCC KW - IRB KW - milligram/kilogram KW - Overall urvival KW - American Joint Committee on Cancer KW - IGF-1R KW - mg/dl KW - IgG1 KW - CTCAE KW - PT/INR KW - CDC KW - Hepatocellular Carcinoma KW - Complement-dependent cytotoxicity KW - Prothrombin time/International normalized ratio KW - Non-alcoholic steatohepatitis KW - Immunoglobulin 1 KW - Hepatocellular carcinoma KW - units/L KW - KPS KW - OS KW - Cells per microliter KW - IGF2 KW - Institutional Review Board KW - Cancer Leukemia Group B KW - IGF-IR KW - IGF-2 KW - ml/min KW - IGF-1 KW - MAP KW - Diabetes KW - Hazard ratio KW - Common terminology criteria for adverse events KW - Milligram/deciliter KW - Human immunodeficiency virus KW - AST KW - IGF-2R KW - CC1 KW - Cancer Therapy Evaluation Program (CTEP)/National Cancer Institute KW - NASH KW - HCC KW - Receptor, IGF Type 1 -- metabolism KW - Humans KW - Aged KW - Insulin-Like Growth Factor I -- metabolism KW - Insulin-Like Growth Factor II -- metabolism KW - Biomarkers, Tumor -- metabolism KW - Kaplan-Meier Estimate KW - Aged, 80 and over KW - Middle Aged KW - Insulin-Like Growth Factor Binding Protein 1 -- blood KW - Biomarkers, Tumor -- blood KW - Insulin-Like Growth Factor Binding Protein 3 -- blood KW - Female KW - Male KW - Liver Neoplasms -- pathology KW - Liver Neoplasms -- therapy KW - Carcinoma, Hepatocellular -- therapy KW - Carcinoma, Hepatocellular -- blood KW - Carcinoma, Hepatocellular -- pathology KW - Liver Neoplasms -- blood KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490899263?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+phase+II+study+of+cixutumumab+%28IMC-A12%2C+NSC742460%29+in+advanced+hepatocellular+carcinoma.&rft.au=Abou-Alfa%2C+Ghassan+K%3BCapanu%2C+Marinela%3BO%27Reilly%2C+Eileen+M%3BMa%2C+Jennifer%3BChou%2C+Joanne+F%3BGansukh%2C+Bolorsukh%3BShia%2C+Jinru%3BKalin%2C+Marcia%3BKatz%2C+Seth%3BAbad%2C+Leslie%3BReidy-Lagunes%2C+Diane+L%3BKelsen%2C+David+P%3BChen%2C+Helen+X%3BSaltz%2C+Leonard+B&rft.aulast=Abou-Alfa&rft.aufirst=Ghassan&rft.date=2014-02-01&rft.volume=60&rft.issue=2&rft.spage=319&rft.isbn=&rft.btitle=&rft.title=Journal+of+hepatology&rft.issn=1600-0641&rft_id=info:doi/10.1016%2Fj.jhep.2013.09.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-26 N1 - Date created - 2014-01-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] J Clin Oncol. 2011 Jul 20;29(21):e638-40 [21606420] Dig Dis Sci. 2001 Jun;46(6):1313-20 [11414310] Cell Growth Differ. 2002 Mar;13(3):115-22 [11959812] Curr Cancer Drug Targets. 2002 Sep;2(3):191-207 [12188907] Br J Cancer. 2003 Mar 10;88(5):733-9 [12618883] Mol Cell Endocrinol. 2003 May 30;203(1-2):51-63 [12782403] Cancer Res. 2003 Dec 15;63(24):8912-21 [14695208] Oncogene. 1995 May 4;10(9):1725-9 [7753549] Clin Cancer Res. 2005 Apr 15;11(8):3065-74 [15837762] J Hepatol. 2005 Oct;43(4):630-6 [16024131] Biochem Pharmacol. 2006 May 14;71(10):1435-48 [16530734] World J Gastroenterol. 2006 Jul 7;12(25):3977-82 [16810743] N Engl J Med. 2008 Jul 24;359(4):378-90 [18650514] Curr Oncol Rep. 2008 May;10(3):199-205 [18765149] J Hepatol. 2010 Apr;52(4):550-9 [20206398] Br J Cancer. 2011 Jan 4;104(1):68-74 [21102589] Cell Mol Life Sci. 2000 Jul;57(7):1050-93 [10961344] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jhep.2013.09.008 ER - TY - JOUR T1 - Pain-related depression of the mesolimbic dopamine system in rats: expression, blockade by analgesics, and role of endogenous κ-opioids. AN - 1490758611; 24008352 AB - Pain is often associated with depression of behavior and mood, and relief of pain-related depression is a common goal of treatment. This study tested the hypothesis that pain-related behavioral depression is mediated by activation of endogenous κ-opioid systems and subsequent depression of mesolimbic dopamine release. Adult male Sprague-Dawley rats were implanted with electrodes targeting the medial forebrain bundle (for behavior studies of intracranial self-stimulation (ICSS)) or with cannulae for microdialysis measures of nucleus accumbens dopamine (NAc DA). Changes in ICSS and NAc DA were examined after treatment with a visceral noxious stimulus (intraperitoneal injection of dilute lactic acid) or an exogenous κ-agonist (U69593). Additional studies examined the sensitivity of acid and U69593 effects to blockade by two analgesics (the nonsteroidal antiinflammatory drug ketoprofen and the μ-opioid agonist morphine) or by the κ-antagonist norbinaltorphimine (norBNI). The effects of acid were also examined on mRNA expression for prodynorphin (PDYN) and κ-opioid receptors (KORs) in mesocorticolimbic brain regions. Both acid and U69593 depressed ICSS and extracellular levels of NAc DA. Pain-related acid effects were blocked by ketoprofen and morphine but not by norBNI. The U69593 effects were blocked by norBNI but not by ketoprofen, and were only attenuated by morphine. Acid did not significantly alter PDYN or KOR in NAc, but it produced a delayed increase in PDYN in prefrontal cortex. These results support a key role for the mesolimbic DA system, but a more nuanced role for endogenous κ-opioid systems, in mediating acute pain-related behavioral depression in rats. JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology AU - Leitl, Michael D AU - Onvani, Sara AU - Bowers, M Scott AU - Cheng, Kejun AU - Rice, Kenner C AU - Carlezon, William A AU - Banks, Matthew L AU - Negus, S Stevens AD - Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, VA, USA. ; Behavioral Genetics Laboratory, McLean Hospital, Harvard Medical School, Belmont, MA, USA. ; Department of Psychiatry, Virginia Commonwealth University, Richmond, VA, USA. ; Chemical Biology Research Branch, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 614 EP - 624 VL - 39 IS - 3 KW - Analgesics, Opioid KW - 0 KW - Benzeneacetamides KW - Narcotic Antagonists KW - Pyrrolidines KW - Receptors, Opioid, kappa KW - Lactic Acid KW - 33X04XA5AT KW - norbinaltorphimine KW - 36OOQ86QM1 KW - Naltrexone KW - 5S6W795CQM KW - Morphine KW - 76I7G6D29C KW - Ketoprofen KW - 90Y4QC304K KW - U 69593 KW - J5S4K6TKTG KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Benzeneacetamides -- pharmacology KW - Self Stimulation KW - Medial Forebrain Bundle -- drug effects KW - Medial Forebrain Bundle -- physiology KW - Naltrexone -- analogs & derivatives KW - Disease Models, Animal KW - Ketoprofen -- pharmacology KW - Morphine -- pharmacology KW - Rats KW - Rats, Sprague-Dawley KW - Analgesics, Opioid -- pharmacology KW - Naltrexone -- pharmacology KW - Pyrrolidines -- pharmacology KW - Time Factors KW - Narcotic Antagonists -- pharmacology KW - Lactic Acid -- pharmacology KW - Male KW - Pain -- complications KW - Pain -- drug therapy KW - Depression -- pathology KW - Receptors, Opioid, kappa -- genetics KW - Nucleus Accumbens -- drug effects KW - Depression -- etiology KW - Depression -- metabolism KW - Receptors, Opioid, kappa -- metabolism KW - Nucleus Accumbens -- metabolism KW - Dopamine -- metabolism KW - Gene Expression Regulation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490758611?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.atitle=Pain-related+depression+of+the+mesolimbic+dopamine+system+in+rats%3A+expression%2C+blockade+by+analgesics%2C+and+role+of+endogenous+%CE%BA-opioids.&rft.au=Leitl%2C+Michael+D%3BOnvani%2C+Sara%3BBowers%2C+M+Scott%3BCheng%2C+Kejun%3BRice%2C+Kenner+C%3BCarlezon%2C+William+A%3BBanks%2C+Matthew+L%3BNegus%2C+S+Stevens&rft.aulast=Leitl&rft.aufirst=Michael&rft.date=2014-02-01&rft.volume=39&rft.issue=3&rft.spage=614&rft.isbn=&rft.btitle=&rft.title=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.issn=1740-634X&rft_id=info:doi/10.1038%2Fnpp.2013.236 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-10 N1 - Date created - 2014-01-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Pharmacol Exp Ther. 2012 Nov;343(2):389-400 [22892341] Pain. 2012 Apr;153(4):744-54 [22386471] Br J Pharmacol. 2013 Feb;168(4):850-62 [22978626] J Neurosci. 2013 May 8;33(19):8202-15 [23658159] Neuropsychopharmacology. 2013 Aug;38(9):1770-9 [23542927] Lab Anim (NY). 2013 Aug;42(8):292-300 [23877610] Ann Neurol. 2013 Aug;74(2):257-65 [23686557] J Neurosci. 2001 Sep 15;21(18):7397-403 [11549750] J Neurosci. 2003 Jul 2;23(13):5674-83 [12843270] Arch Intern Med. 2003 Nov 10;163(20):2433-45 [14609780] Psychopharmacology (Berl). 2004 Apr;172(4):463-70 [14727002] Anesthesiology. 2004 Jul;101(1):191-203 [15220791] Science. 1982 Jan 22;215(4531):413-5 [6120570] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5274-8 [2899326] J Pharmacol Exp Ther. 1988 Mar;244(3):1067-80 [2855239] Arch Int Pharmacodyn Ther. 1992 Mar-Apr;316:30-42 [1326932] Ann Acad Med Singapore. 1994 Mar;23(2):129-38 [8080219] J Pharmacol Exp Ther. 1994 Dec;271(3):1216-22 [7996429] Eur J Pharmacol. 1995 Feb 24;275(1):9-16 [7774666] Brain Res. 1995 Mar 27;675(1-2):325-8 [7796146] J Comp Physiol Psychol. 1954 Dec;47(6):419-27 [13233369] Neuropsychopharmacology. 2005 May;30(5):864-70 [15562294] Psychopharmacology (Berl). 2005 May;179(3):551-8 [15682306] J Pharmacol Exp Ther. 2006 Jan;316(1):440-7 [16223871] Science. 2006 Feb 10;311(5762):864-8 [16469931] J Pain. 2006 Jun;7(6):408-16 [16750797] Eur J Pain. 2007 Jan;11(1):7-20 [16495096] J Neurochem. 2007 Oct;103(2):487-99 [17666048] J Biol Chem. 2007 Oct 12;282(41):29803-11 [17702750] Nat Protoc. 2007;2(11):2987-95 [18007634] Expert Rev Neurother. 2008 May;8(5):781-97 [18457535] Eur J Pain. 2008 Oct;12(7):866-9 [18226937] Neurotox Res. 2008 Oct;14(2-3):169-83 [19073424] Mol Pharmacol. 2009 Mar;75(3):704-12 [19106229] Pain. 2009 Jul;144(1-2):170-7 [19435650] Life Sci. 2009 Aug 12;85(7-8):309-15 [19559034] Brain Res. 2010 Feb 16;1314:44-55 [19716811] Brain Res. 2010 Feb 16;1314:56-73 [19782055] Methods Mol Biol. 2010;617:79-91 [20336415] Psychopharmacology (Berl). 2010 Jun;210(2):149-59 [20101391] Psychopharmacology (Berl). 2010 Jun;210(2):121-35 [20352414] Pharmacol Ther. 2010 Dec;128(3):549-58 [20807551] J Neurosci. 2011 Feb 23;31(8):3095-103 [21414930] Behav Pharmacol. 2011 Oct;22(7):663-73 [21921839] Int J Neuropsychopharmacol. 2011 Nov;14(10):1327-39 [21281560] J Clin Pharmacol. 2012 Jan;52(1):6-17 [21415285] J Pharmacol Exp Ther. 2012 Mar;340(3):501-9 [22128346] Eur J Pain. 2012 Apr;16(4):485-95 [22396078] Pain. 2012 Apr;153(4):876-84 [22341563] Proc Natl Acad Sci U S A. 2012 Dec 11;109(50):20709-13 [23184995] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/npp.2013.236 ER - TY - JOUR T1 - Approaches and considerations for the assessment of immunotoxicity for environmental chemicals: a workshop summary. AN - 1490704678; 24280359 AB - As experience is gained with toxicology testing and as new assays and technologies are developed, it is critical for stakeholders to discuss opportunities to advance our overall testing strategies. To facilitate these discussions, a workshop on practices for assessing immunotoxicity for environmental chemicals was held with the goal of sharing perspectives on immunotoxicity testing strategies and experiences, developmental immunotoxicity (DIT), and integrated and alternative approaches to immunotoxicity testing. Experiences across the chemical and pharmaceutical industries suggested that standard toxicity studies, combined with triggered-based testing approaches, represent an effective and efficient approach to evaluate immunotoxic potential. Additionally, discussions on study design, critical windows, and new guideline approaches and experiences identified important factors to consider before initiating DIT evaluations including assay choice and timing and the impact of existing adult data. Participants agreed that integrating endpoints into standard repeat-dose studies should be considered for fulfilling any immunotoxicity testing requirements, while also maximizing information and reducing animal use. Participants also acknowledged that in vitro evaluation of immunosuppression is complex and may require the use of multiple assays that are still being developed. These workshop discussions should contribute to developing an effective but more resource and animal efficient approach for evaluating chemical immunotoxicity. Copyright © 2013 Elsevier Inc. All rights reserved. JF - Regulatory toxicology and pharmacology : RTP AU - Boverhof, Darrell R AU - Ladics, Greg AU - Luebke, Bob AU - Botham, Jane AU - Corsini, Emanuela AU - Evans, Ellen AU - Germolec, Dori AU - Holsapple, Michael AU - Loveless, Scott E AU - Lu, Haitian AU - van der Laan, Jan Willem AU - White, Kimber L AU - Yang, Yung AD - The Dow Chemical Company, Midland, MI, United States. Electronic address: rboverhof@dow.com. ; DuPont Pioneer, Wilmington, DE, United States. ; Cardiopulmonary and Immunotoxicology Branch, US Environmental Protection Agency, Research Triangle Park, NC, United States. ; Syngenta Ltd., Macclesfield, UK. ; Laboratory of Toxicology, Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy. ; Pfizer, Inc., Groton, CT, United States. ; National Toxicology Program, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, United States. ; Battelle Memorial Institute, Columbus, OH, United States. ; DuPont Haskell Global Centers for Health and Environmental Sciences, Newark, DE, United States. ; Dow AgroSciences, Indianapolis, IN, United States. ; Medicines Evaluation Board, Utrecht, The Netherlands. ; ImmunoTox® Inc., Richmond, VA, United States. ; Office of Pesticides Programs, US Environmental Protection Agency, Washington, DC, United States. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 96 EP - 107 VL - 68 IS - 1 KW - Environmental Pollutants KW - 0 KW - Index Medicus KW - AFC KW - keyhole limpet hemocyanin KW - agricultural chemical safety assessment KW - NIEHS KW - European union KW - developmental and reproductive toxicology KW - NOAEL KW - NIOSH KW - T-cell dependent antibody reaction KW - PND KW - Environmental chemicals KW - ELISA KW - RIVM KW - national institute of environmental health sciences KW - US KW - STS KW - DART KW - antibody forming cell KW - EU KW - weight-of-evidence KW - SRBC KW - allergic contact dermatitis KW - EPA KW - national institute for occupational safety and health KW - standard toxicology studies KW - WoE KW - NK KW - FDA KW - HESI KW - ACSA KW - EOGRTS KW - developmental immunotoxicity KW - international life sciences institute KW - United States KW - 2,4-D KW - postnatal day KW - no observed adverse effect level KW - national toxicology program KW - organisation for economic cooperation and development KW - natural killer KW - environmental protection agency KW - Testing KW - local lymph node assay KW - enzyme linked immunosorbent assay KW - cyclophosphamide KW - ACD KW - 2,4-dichlorophenoxyacetic acid KW - international conference on harmonization KW - NRC KW - national research council KW - KLH KW - sheep red blood cells KW - CT KW - DIT KW - food and drug administration KW - ICH KW - health and environmental sciences institute KW - carbon tetrachloride KW - Immunotoxicity KW - NTP KW - extended one-generation reproductive toxicity study KW - TDAR KW - OECD KW - LLNA KW - CP KW - dutch national institute of public health and the environment KW - ILSI KW - Animals KW - Humans KW - Toxicity Tests KW - Environmental Exposure -- adverse effects KW - Female KW - Risk Assessment KW - Prenatal Exposure Delayed Effects KW - Pregnancy KW - Immune System -- drug effects KW - Environmental Pollutants -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490704678?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Regulatory+toxicology+and+pharmacology+%3A+RTP&rft.atitle=Approaches+and+considerations+for+the+assessment+of+immunotoxicity+for+environmental+chemicals%3A+a+workshop+summary.&rft.au=Boverhof%2C+Darrell+R%3BLadics%2C+Greg%3BLuebke%2C+Bob%3BBotham%2C+Jane%3BCorsini%2C+Emanuela%3BEvans%2C+Ellen%3BGermolec%2C+Dori%3BHolsapple%2C+Michael%3BLoveless%2C+Scott+E%3BLu%2C+Haitian%3Bvan+der+Laan%2C+Jan+Willem%3BWhite%2C+Kimber+L%3BYang%2C+Yung&rft.aulast=Boverhof&rft.aufirst=Darrell&rft.date=2014-02-01&rft.volume=68&rft.issue=1&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Regulatory+toxicology+and+pharmacology+%3A+RTP&rft.issn=1096-0295&rft_id=info:doi/10.1016%2Fj.yrtph.2013.11.012 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-04 N1 - Date created - 2014-01-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.yrtph.2013.11.012 ER - TY - JOUR T1 - Targeting notch signaling pathway in cancer: clinical development advances and challenges. AN - 1490702251; 24076266 AB - Notch signaling plays an important role in development and cell fate determination, and it is deregulated in human hematologic malignancies and solid tumors. This review includes a brief introduction of the relevant pathophysiology of Notch signaling pathway and primarily focuses on the clinical development of promising agents that either obstruct Notch receptor cleavages such as γ-secretase inhibitors (GSIs) or interfere with the Notch ligand-receptor interaction by monoclonal antibodies (mAbs). Antitumor activity by GSIs and mAbs administered as single agent in early phases of clinical trials has been observed in advanced or metastatic thyroid cancer, non-small cell lung cancer, intracranial tumors, sarcoma or desmoid tumors, colorectal cancer with neuroendocrine features, melanoma and ovarian cancer. A number of mechanism-based adverse events particularly gastrointestinal toxicities emerged and mitigation strategies are developed after testing multiple GSIs and Notch targeting mAbs. We also discuss pharmacodynamic biomarkers in conjunction with methods of assessment of the molecular target inhibition validation. Biomarkers of efficacy or benefit may be of importance for a successful development of this class of drugs. Published by Elsevier Inc. JF - Pharmacology & therapeutics AU - Takebe, Naoko AU - Nguyen, Dat AU - Yang, Sherry X AD - Cancer Therapy Evaluation Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, United States. Electronic address: takeben@mail.nih.gov. ; National Clinical Target Validation Laboratory, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, United States. ; National Clinical Target Validation Laboratory, Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, United States. Electronic address: Sherry.Yang@nih.gov. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 140 EP - 149 VL - 141 IS - 2 KW - Antineoplastic Agents KW - 0 KW - Biomarkers KW - Receptors, Notch KW - Index Medicus KW - JAG KW - cancer stem cells KW - MSFE KW - T-LL KW - Clinical trials KW - a disintegrin and metalloproteases KW - MTD KW - partial response KW - ethylenediaminetetraacetic acid KW - dose limiting toxicity KW - stable disease KW - maximum tolerated dose KW - T-cell lymphoblastic lymphoma KW - TICs KW - tumor initiating cells KW - mAb KW - RECIST KW - Diarrhea KW - Jagged KW - Monoclonal antibodies (mAbs) KW - GSI KW - metalloproteinase tumor necrosis factor-α-converting enzyme KW - mammosphere-forming efficiency KW - TACE KW - PR KW - MAML KW - Notch intracellular domain KW - T-cell acute lymphoblastic leukemia KW - DLT KW - DLL KW - GBM KW - EDTA KW - response evaluation criteria in solid tumors KW - pharmacodynamics KW - γ-Secretase inhibitors KW - CSCs KW - NICD KW - γ-secretase inhibitor KW - SD KW - mastermind-like KW - non-small cell lung cancer KW - glioblastoma multiforme KW - ADAM KW - T-ALL KW - NSCLC KW - Delta-like ligand KW - PK KW - PD KW - Notch signaling KW - CR KW - pharmacokinetics KW - complete response KW - monoclonal antibody KW - Animals KW - Humans KW - Biomarkers -- metabolism KW - Neovascularization, Pathologic KW - Antineoplastic Agents -- therapeutic use KW - Signal Transduction KW - Neoplastic Stem Cells -- metabolism KW - Neoplasms -- drug therapy KW - Receptors, Notch -- metabolism KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490702251?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=Targeting+notch+signaling+pathway+in+cancer%3A+clinical+development+advances+and+challenges.&rft.au=Takebe%2C+Naoko%3BNguyen%2C+Dat%3BYang%2C+Sherry+X&rft.aulast=Takebe&rft.aufirst=Naoko&rft.date=2014-02-01&rft.volume=141&rft.issue=2&rft.spage=140&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=1879-016X&rft_id=info:doi/10.1016%2Fj.pharmthera.2013.09.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-24 N1 - Date created - 2014-01-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Cancer Res. 2010 Jun 15;16(12):3141-52 [20530696] Nat Rev Drug Discov. 2010 Nov;9(11):843-56 [21031001] Anticancer Res. 2010 Oct;30(10):3853-67 [21036696] Clin Cancer Res. 2010 Dec 15;16(24):6060-70 [21169257] Clin Cancer Res. 2011 Jan 15;17(2):372-81 [21224365] Nat Rev Clin Oncol. 2011 Feb;8(2):97-106 [21151206] PLoS One. 2011;6(3):e16633 [21415927] Nat Rev Cancer. 2011 May;11(5):338-51 [21508972] Mol Oncol. 2011 Jun;5(3):292-301 [21315665] J Immunol. 2011 Sep 1;187(5):2803-13 [21788444] Cancer Res. 2011 Sep 1;71(17):5626-34 [21795476] J Clin Oncol. 2011 Sep 10;29(26):3529-34 [21825264] Cancer Res. 2011 Sep 15;71(18):6030-9 [21795478] Thyroid. 2011 Dec;21(12):1323-30 [22066479] Oncogene. 2012 Feb 9;31(6):787-98 [21725355] J Clin Oncol. 2012 Jul 1;30(19):2348-53 [22529266] J Clin Oncol. 2012 Jul 1;30(19):2307-13 [22547604] J Clin Oncol. 2012 Jul 1;30(19):2291-3 [22564999] J Clin Oncol. 2012 Jul 1;30(19):2418-20 [22585704] Mol Cancer Ther. 2012 Jul;11(7):1565-75 [22504949] Clin Cancer Res. 2012 Sep 15;18(18):5008-19 [22806875] Clin Cancer Res. 2012 Oct 1;18(19):5188-95 [22773520] Proc Natl Acad Sci U S A. 2012 Oct 9;109(41):16558-63 [23012411] Clin Cancer Res. 2012 Nov 15;18(22):6101-9 [23065428] BMC Med. 2012;10:141 [23158439] Mod Pathol. 2013 Jan;26(1):139-47 [22918166] Stem Cells Transl Med. 2013 Mar;2(3):233-42 [23408105] Clin Cancer Res. 2013 Mar 15;19(6):1512-24 [23340294] Clin Cancer Res. 2013 Apr 15;19(8):1972-80 [23444212] Clin Cancer Res. 2013 Jul 1;19(13):3485-94 [23649002] Br J Cancer. 2013 Aug 20;109(4):943-9 [23868004] Invest New Drugs. 2013 Oct;31(5):1182-91 [23860641] Invest New Drugs. 2014 Apr;32(2):243-9 [23645447] Cancer Res. 2006 Feb 1;66(3):1517-25 [16452208] Genes Dev. 2006 Aug 1;20(15):2096-109 [16847353] Nature. 2006 Aug 17;442(7104):823-6 [16799564] Nature. 2006 Dec 21;444(7122):1032-7 [17183313] Nature. 2006 Dec 21;444(7122):1083-7 [17183323] Development. 2007 Mar;134(5):839-44 [17251261] Nature. 2007 Feb 15;445(7129):781-4 [17259972] Nature. 2007 Feb 15;445(7129):776-80 [17259973] Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2803-8 [17296934] Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3219-24 [17296940] Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3225-30 [17296941] Circ Res. 2007 Jun 8;100(11):1556-68 [17556669] J Neurosurg. 2007 Jul;107(1):185-9 [17639893] Stem Cell Rev. 2007 Jun;3(2):169-75 [17873349] Mol Cell Biol. 2000 Mar;20(5):1825-35 [10669757] EMBO J. 2001 Jul 2;20(13):3427-36 [11432830] Mol Cell Biol. 2001 Sep;21(17):5925-34 [11486031] Mech Dev. 2001 Oct;108(1-2):161-4 [11578869] J Immunol. 2001 Oct 15;167(8):4458-67 [11591772] Cancer Res. 2002 Feb 1;62(3):665-8 [11830517] Cell Death Differ. 2002 Aug;9(8):842-55 [12107827] Nat Med. 2002 Sep;8(9):979-86 [12185362] Nat Rev Mol Cell Biol. 2002 Sep;3(9):673-84 [12209127] Oncogene. 2003 Sep 29;22(42):6598-608 [14528285] Am J Physiol Heart Circ Physiol. 2003 Nov;285(5):H1917-38 [12842817] Cancer Cell. 2003 Dec;4(6):451-61 [14706337] Genes Dev. 2004 Jan 1;18(1):99-115 [14701881] Nat Rev Mol Cell Biol. 2004 Jun;5(6):499-504 [15173829] Semin Cancer Biol. 2004 Oct;14(5):357-64 [15288261] Cancer Res. 2004 Oct 1;64(19):6854-7 [15466172] Science. 2004 Oct 8;306(5694):269-71 [15472075] Cell. 1987 Jul 3;50(1):107-17 [3036364] Cell. 1991 Aug 23;66(4):649-61 [1831692] Proc Natl Acad Sci U S A. 1995 Jul 3;92(14):6414-8 [7604005] J Biol Chem. 1997 May 30;272(22):14110-4 [9162037] J Biol Chem. 1997 Nov 21;272(47):29729-34 [9368042] Genes Dev. 1998 Aug 1;12(15):2269-77 [9694793] Nature. 1999 Apr 8;398(6727):518-22 [10206645] Gene Expr Patterns. 2004 Nov;5(1):123-7 [15533827] Breast Cancer Res. 2004;6(6):R605-15 [15535842] J Mammary Gland Biol Neoplasia. 2005 Jan;10(1):75-86 [15886888] Nature. 2005 Jun 16;435(7044):959-63 [15959515] Nature. 2005 Jun 16;435(7044):964-8 [15959516] J Exp Med. 2005 Jul 4;202(1):157-68 [15998794] Cancer Cell. 2005 Jul;8(1):1-3 [16023591] J Biol Chem. 2005 Sep 16;280(37):32133-40 [15994302] Cancer Res. 2005 Sep 15;65(18):8530-7 [16166334] Nature. 2006 Jan 26;439(7075):470-4 [16340960] J Gastroenterol. 2007 Sep;42(9):705-10 [17876539] Cancer Res. 2008 Jun 15;68(12):4727-35 [18559519] Oncogene. 2008 Sep 1;27(38):5132-7 [18758482] Cell Stem Cell. 2007 Nov;1(5):555-67 [18371393] Nat Med. 2009 Jan;15(1):50-8 [19098907] Nat Cell Biol. 2009 Feb;11(2):162-71 [19136966] Dev Cell. 2009 Feb;16(2):196-208 [19217422] Front Biosci (Landmark Ed). 2009;14:3094-110 [19273260] Cell Cycle. 2009 Jun 15;8(12):1860-4 [19440048] Nature. 2009 Nov 12;462(7270):182-8 [19907488] Stem Cells. 2010 Jan;28(1):5-16 [19904829] Stem Cells. 2010 Jan;28(1):17-28 [19921751] Nature. 2010 Feb 11;463(7282):E6-7 [20147986] Nature. 2010 Apr 15;464(7291):1052-7 [20393564] Curr Drug Targets. 2010 Jun;11(6):745-51 [20041844] Mol Cancer Ther. 2010 Jun;9(6):1618-28 [20530712] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.pharmthera.2013.09.005 ER - TY - JOUR T1 - Prevalence and predictors of elevated aspartate aminotransferase-to-platelet ratio index in Latin American perinatally HIV-infected children. AN - 1490694003; 23799515 AB - Chronic liver disease has emerged as an important problem in adults with longstanding HIV infection, but data are lacking for children. We characterized elevated aspartate aminotransferase-to-platelet ratio index (APRI), a marker of possible liver fibrosis, in perinatally HIV-infected children. The National Institute of Child Health and Human Development International Site Development Initiative enrolled HIV-infected children (ages 0.1-20.1 years) from 5 Latin American countries in an observational cohort from 2002 to 2009. Twice yearly visits included medical history, physical examination and laboratory evaluations. The prevalence (95% confidence interval) of APRI > 1.5 was calculated, and associations with demographic, HIV-related and liver-related variables were investigated in bivariate analyses. APRI was available for 1012 of 1032 children. APRI was >1.5 in 32 (3.2%, 95% confidence interval: 2.2%-4.4%) including 2 of 4 participants with hepatitis B virus infection. Factors significantly associated with APRI > 1.5 (P 1.5 varied significantly by current ARV regimen (P = 0.0002), from 8.0% for no ARV to 3.2% for non-protease inhibitor regimens to 1.5% for protease inhibitor-based regimens. Elevated APRI occurred in approximately 3% of perinatally HIV-infected children. Protease inhibitor-based ARVs appeared protective whereas inadequate HIV control appeared to increase risk of elevated APRI. Additional investigations are needed to better assess potential subclinical, chronic liver disease in HIV-infected children. JF - The Pediatric infectious disease journal AU - Siberry, George K AU - Cohen, Rachel A AU - Harris, D Robert AU - Cruz, Maria Leticia Santos AU - Oliveira, Ricardo AU - Peixoto, Mario F AU - Cervi, Maria Celia AU - Hazra, Rohan AU - Pinto, Jorge A AU - NISDI PLACES Protocol AD - From the *Maternal and Pediatric Infectious Disease Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda; †Westat, Rockville, MD; ‡Department of Infectious Diseases, Hospital Federal dos Servidores do Estado; §Instituto de Puericultura e Pediatria Martagão Gesteira, Universidade Federal do Rio de Janeiro, Rio de Janeiro; ¶Vertical Transmission Unit, Femina Hospital, Porto Alegre; ‖Department of Pediatrics, University of São Paulo Faculty of Medicine of Ribeirão Preto, Ribeirão Preto; and **Department of Pediatrics, Federal University of Minas Gerais, Belo Horizonte, Brazil. ; NISDI PLACES Protocol Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 177 EP - 182 VL - 33 IS - 2 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Index Medicus KW - Sensitivity and Specificity KW - Infectious Disease Transmission, Vertical KW - Liver Cirrhosis -- virology KW - Latin America -- epidemiology KW - Humans KW - Child KW - Liver Cirrhosis -- blood KW - Liver Cirrhosis -- enzymology KW - Child, Preschool KW - Infant KW - Female KW - Male KW - Prevalence KW - Platelet Count KW - Aspartate Aminotransferases -- blood KW - HIV Infections -- blood KW - HIV Infections -- enzymology KW - Blood Platelets -- cytology KW - HIV Infections -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490694003?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Pediatric+infectious+disease+journal&rft.atitle=Prevalence+and+predictors+of+elevated+aspartate+aminotransferase-to-platelet+ratio+index+in+Latin+American+perinatally+HIV-infected+children.&rft.au=Siberry%2C+George+K%3BCohen%2C+Rachel+A%3BHarris%2C+D+Robert%3BCruz%2C+Maria+Leticia+Santos%3BOliveira%2C+Ricardo%3BPeixoto%2C+Mario+F%3BCervi%2C+Maria+Celia%3BHazra%2C+Rohan%3BPinto%2C+Jorge+A%3BNISDI+PLACES+Protocol&rft.aulast=Siberry&rft.aufirst=George&rft.date=2014-02-01&rft.volume=33&rft.issue=2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=The+Pediatric+infectious+disease+journal&rft.issn=1532-0987&rft_id=info:doi/10.1097%2FINF.0b013e3182a01dfb LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-25 N1 - Date created - 2014-01-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Hepatol. 2005 Jul;43(1):78-84 [15894397] J Pediatr Gastroenterol Nutr. 2010 Aug;51(2):198-202 [20531020] J Acquir Immune Defic Syndr. 2005 Dec 15;40(5):538-44 [16284529] Hepatology. 2006 Jun;43(6):1317-25 [16729309] AIDS. 2007 Nov 30;21(18):2483-91 [18025885] J Pediatr Gastroenterol Nutr. 2007 Oct;45(4):443-50 [18030211] BMC Public Health. 2007;7:338 [18031586] PLoS One. 2009;4(2):e4517 [19223976] PLoS Med. 2009 Apr 28;6(4):e1000066 [19399157] Clin Infect Dis. 2009 Aug 15;49(4):626-35 [19589079] Int J Epidemiol. 2009 Oct;38(5):1207-14 [19036797] Virol J. 2009;6:181 [19878552] J Pediatr Gastroenterol Nutr. 2010 Mar;50(3):340-3 [19841596] J Pediatr Gastroenterol Nutr. 2010 Mar;50(3):344-6 [20118806] Pediatrics. 2010 May;125(5):e1039-47 [20385636] BMC Infect Dis. 2010;10:116 [20465840] J Acquir Immune Defic Syndr. 2010 Jun;54(2):191-6 [20032784] AIDS. 2010 Jun 19;24(10):1537-48 [20453631] J Pediatr Surg. 2010 Jun;45(6):1266-73 [20620330] Clin Gastroenterol Hepatol. 2010 Dec;8(12):1002-12 [20851211] Clin Infect Dis. 2011 Mar 1;52(5):674-80 [21248367] Clin Infect Dis. 2011 May;52(9):1164-73 [21467023] J Infect Dis. 2012 Mar 15;205(6):1005-13 [22291196] AIDS. 2012 Mar 13;26(5):599-607 [22156972] Pediatr Infect Dis J. 2012 Sep;31(9):943-7 [22592516] HIV Med. 2005 Nov;6(6):375-8 [16268817] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/INF.0b013e3182a01dfb ER - TY - JOUR T1 - Blockade of D3 receptors by YQA14 inhibits cocaine's rewarding effects and relapse to drug-seeking behavior in rats. AN - 1469214824; 24176392 AB - Preclinical studies suggest that dopamine D3 receptor (D3R) antagonists are promising for the treatment of drug abuse and addiction. However, few D3R antagonists have potential to be tested in humans due to short half-life, toxicity or limited preclinical research into pharmacotherapeutic efficacy. Here, we report on a novel D3R antagonist YQA14, which has improved half-life and pharmacokinetic profile and which displays potent pharmacotherapeutic efficacy in attenuating cocaine reward and relapse to drug-seeking behavior. Electrical brain-stimulation reward (BSR) in laboratory animals is a highly sensitive experimental approach to evaluate a drug's rewarding effects. We found that cocaine (2 mg/kg) significantly enhanced electrical BSR in rats (i.e., decreased stimulation threshold for BSR), while YQA14 alone had no effect on BSR. Pretreatment with YQA14 significantly and dose-dependently attenuated cocaine-enhanced BSR. YQA14 also facilitated extinction from drug-seeking behavior in rats during early behavioral extinction, and attenuated cocaine- or contextual cue-induced relapse to drug-seeking behavior. YQA14 alone did not maintain self-administration in either naïve rats or in rats experienced at cocaine self-administration. YQA14 also inhibited expression of repeated cocaine-induced behavioral sensitization. These findings suggest that YQA14 may have pharmacotherapeutic potential in attenuating cocaine-taking and cocaine-seeking behavior. Thus, YQA14 deserves further investigation as a promising agent for treatment of cocaine addiction. Published by Elsevier Ltd. JF - Neuropharmacology AU - Song, Rui AU - Bi, Guo-Hua AU - Zhang, Hai-Ying AU - Yang, Ri-Fang AU - Gardner, Eliot L AU - Li, Jin AU - Xi, Zheng-Xiong AD - Intramural Research Program, National Institute on Drug Abuse, Baltimore, MD 21224, USA; Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. ; Intramural Research Program, National Institute on Drug Abuse, Baltimore, MD 21224, USA. ; Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. ; Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. Electronic address: jinli9802@163.com. ; Intramural Research Program, National Institute on Drug Abuse, Baltimore, MD 21224, USA. Electronic address: zxi@intra.nida.nih.gov. Y1 - 2014/02// PY - 2014 DA - February 2014 SP - 398 EP - 405 VL - 77 KW - Benzoxazoles KW - 0 KW - Dopamine Antagonists KW - Dopamine Uptake Inhibitors KW - Piperazines KW - Receptors, Dopamine D3 KW - YQA14 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Dopamine KW - Reward KW - Reinstatement KW - D3 receptors KW - Rats KW - Behavior, Animal -- drug effects KW - Animals KW - Rats, Long-Evans KW - Dose-Response Relationship, Drug KW - Brain -- drug effects KW - Cocaine-Related Disorders -- drug therapy KW - Behavior, Addictive -- drug therapy KW - Electric Stimulation KW - Recurrence KW - Male KW - Drug-Seeking Behavior -- drug effects KW - Benzoxazoles -- pharmacology KW - Benzoxazoles -- therapeutic use KW - Piperazines -- therapeutic use KW - Dopamine Antagonists -- pharmacology KW - Receptors, Dopamine D3 -- antagonists & inhibitors KW - Piperazines -- pharmacology KW - Cocaine -- pharmacology KW - Dopamine Uptake Inhibitors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1469214824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropharmacology&rft.atitle=Blockade+of+D3+receptors+by+YQA14+inhibits+cocaine%27s+rewarding+effects+and+relapse+to+drug-seeking+behavior+in+rats.&rft.au=Song%2C+Rui%3BBi%2C+Guo-Hua%3BZhang%2C+Hai-Ying%3BYang%2C+Ri-Fang%3BGardner%2C+Eliot+L%3BLi%2C+Jin%3BXi%2C+Zheng-Xiong&rft.aulast=Song&rft.aufirst=Rui&rft.date=2014-02-01&rft.volume=77&rft.issue=&rft.spage=398&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=1873-7064&rft_id=info:doi/10.1016%2Fj.neuropharm.2013.10.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-26 N1 - Date created - 2013-12-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Int J Neuropsychopharmacol. 2006 Oct;9(5):585-602 [16942635] Neuropsychopharmacology. 2006 Jul;31(7):1393-405 [16205781] Nat Neurosci. 2007 Aug;10(8):1020-8 [17603481] Neuropsychopharmacology. 2008 Jan;33(1):56-72 [17882236] Neuroimage. 2008 Feb 1;39(3):1266-73 [18024160] Neuropsychopharmacology. 2008 Jun;33(7):1735-45 [17728698] Pharmacol Biochem Behav. 2008 Aug;90(2):261-72 [17928041] Neuropharmacology. 2009 Mar;56(4):752-60 [19136017] Neuropharmacology. 2010 Jan;58(1):304-13 [19559037] Eur J Neurosci. 2009 Nov;30(10):1889-99 [19912327] Ann N Y Acad Sci. 2010 Feb;1187:4-34 [20201845] Neuroscience. 2010 Aug 11;169(1):182-94 [20435100] J Psychopharmacol. 2011 Feb;25(2):263-73 [20142301] Neuron. 2011 Feb 24;69(4):650-63 [21338877] Pharmacol Biochem Behav. 2011 Aug;99(2):229-44 [21295059] Addict Biol. 2012 Mar;17(2):259-73 [21507153] Science. 2012 Apr 13;336(6078):241-5 [22499948] Hum Genet. 2012 Jun;131(6):803-22 [22350797] Proc Natl Acad Sci U S A. 2012 Oct 23;109(43):17675-80 [23045656] Addict Biol. 2013 Jul;18(4):665-77 [22913325] Neuropharmacology. 2013 Sep;72:82-7 [23643749] Eur J Neurosci. 2005 Jun;21(12):3427-38 [16026480] J Psychiatry Neurosci. 2000 Mar;25(2):125-36 [10740986] Psychopharmacology (Berl). 2000 Jun;150(3):337-46 [10923762] J Pharmacol Exp Ther. 2000 Sep;294(3):1154-65 [10945872] J Neurosci. 2000 Oct 1;20(19):7489-95 [11007908] Pharmacol Rev. 2002 Mar;54(1):1-42 [11870259] J Neurosci. 2002 Nov 1;22(21):9595-603 [12417684] Biol Psychiatry. 2002 Nov 15;52(10):976-86 [12437938] J Neurosci. 2003 Feb 1;23(3):742-7 [12574402] Psychopharmacology (Berl). 2003 Jul;168(1-2):75-83 [12545331] Psychopharmacology (Berl). 2003 Jul;168(1-2):44-56 [12652346] J Med Chem. 2003 Nov 6;46(23):4952-64 [14584946] Neuropsychopharmacology. 2004 Aug;29(8):1479-87 [15100700] Neuropharmacology. 2004;47 Suppl 1:214-26 [15464139] Brain Res Bull. 1982 Jul-Dec;9(1-6):321-53 [6816390] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5274-8 [2899326] Brain Res. 1991 Nov 15;564(2):203-19 [1839781] Arzneimittelforschung. 1992 Feb;42(2A):224-30 [1586393] Psychopharmacology (Berl). 1994 Apr;114(3):523-7 [7855213] Neuroscience. 1995 Apr;65(3):731-45 [7609872] Curr Opin Neurobiol. 1996 Apr;6(2):243-51 [8725967] J Neurosci. 1996 Oct 1;16(19):6100-6 [8815892] Bioorg Med Chem Lett. 1998 Oct 6;8(19):2715-8 [9873609] Nature. 1999 Jul 22;400(6742):371-5 [10432116] Psychopharmacologia. 1960 Feb 12;1:251-6 [13834123] J Med Chem. 2005 Feb 10;48(3):839-48 [15689168] Brain Res Brain Res Rev. 2005 Jul;49(1):77-105 [15960988] Drug Alcohol Depend. 2006 Jan 4;81(1):63-70 [16005579] J Neurosci. 2006 Jun 14;26(24):6583-8 [16775146] CNS Drug Rev. 2007 Summer;13(2):240-59 [17627675] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.neuropharm.2013.10.010 ER - TY - JOUR T1 - Simultaneous quantification of 20 synthetic cannabinoids and 21 metabolites, and semi-quantification of 12 alkyl hydroxy metabolites in human urine by liquid chromatography-tandem mass spectrometry. AN - 1492681123; 24418231 AB - Clandestine laboratories constantly produce new synthetic cannabinoids to circumvent legislative efforts, complicating toxicological analysis. No extensive synthetic cannabinoid quantitative urinary methods are reported in the literature. We developed and validated a liquid chromatography-tandem mass spectrometric (LC-MS/MS) method for simultaneously quantifying JWH-018, JWH-019, JWH-073, JWH-081, JWH-122, JWH-200, JWH-210, JWH-250, JWH-398, RCS-4, AM-2201, MAM-2201, UR-144, CP 47,497-C7, CP 47,497-C8 and their metabolites, and JWH-203, AM-694, RCS-8, XLR-11 and HU-210 parent compounds in urine. Non-chromatographically resolved alkyl hydroxy metabolite isomers were considered semi-quantitative. β-Glucuronidase hydrolyzed urine was extracted with 1ml Biotage SLE+ columns. Specimens were reconstituted in 150μL mobile phase consisting of 50% A (0.01% formic acid in water) and 50% B (0.01% formic acid in 50:50 methanol:acetonitrile). 4 and 25μL injections were performed to acquire data in positive and negative ionization modes, respectively. The LC-MS/MS instrument consisted of a Shimadzu UFLCxr system and an ABSciex 5500 Qtrap mass spectrometer with an electrospray source. Gradient chromatographic separation was achieved utilizing a Restek Ultra Biphenyl column with a 0.5ml/min flow rate and an overall run time of 19.5 and 11.4min for positive and negative mode methods, respectively. Quantification was by multiple reaction monitoring with CP 47,497 compounds and HU-210 ionized via negative polarity; all other analytes were acquired in positive mode. Lower and upper limits of linearity were 0.1-1.0 and 50-100μg/l (r(2)>0.994). Validation parameters were evaluated at three concentrations spanning linear dynamic ranges. Inter-day analytical recovery (bias) and imprecision (N=20) were 88.3-112.2% and 4.3-13.5% coefficient of variation, respectively. Extraction efficiencies and matrix effect (N=10) were 44-110 and -73 to 52%, respectively. We present a novel LC-MS/MS method for simultaneously quantifying 20 synthetic cannabinoids and 21 metabolites, and semi-quantifying 12 alkyl hydroxy metabolites in urine. Published by Elsevier B.V. JF - Journal of chromatography. A AU - Scheidweiler, Karl B 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. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, USA. Electronic address: mhuestis@intra.nida.nih.gov. Y1 - 2014/01/31/ PY - 2014 DA - 2014 Jan 31 SP - 105 EP - 117 VL - 1327 KW - Cannabinoids KW - 0 KW - Index Medicus KW - Urine KW - Analytical method KW - Synthetic cannabinoids KW - Metabolites KW - LC–MS/MS KW - Sensitivity and Specificity KW - Chromatography, Liquid -- methods KW - Humans KW - Tandem Mass Spectrometry -- methods KW - Cannabinoids -- metabolism KW - Cannabinoids -- urine KW - Substance Abuse Detection -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492681123?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chromatography.+A&rft.atitle=Simultaneous+quantification+of+20+synthetic+cannabinoids+and+21+metabolites%2C+and+semi-quantification+of+12+alkyl+hydroxy+metabolites+in+human+urine+by+liquid+chromatography-tandem+mass+spectrometry.&rft.au=Scheidweiler%2C+Karl+B%3BHuestis%2C+Marilyn+A&rft.aulast=Scheidweiler&rft.aufirst=Karl&rft.date=2014-01-31&rft.volume=1327&rft.issue=&rft.spage=105&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography.+A&rft.issn=1873-3778&rft_id=info:doi/10.1016%2Fj.chroma.2013.12.067 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-07-15 N1 - Date created - 2014-01-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Anal Chem. 2003 Jul 1;75(13):3019-30 [12964746] Fed Regist. 2013 May 16;78(95):28735-9 [23678676] Anal Chem. 2011 Jun 1;83(11):4228-36 [21506519] Anal Bioanal Chem. 2011 Jul;400(10):3481-9 [21533799] Anal Bioanal Chem. 2011 Aug;401(2):493-505 [21455647] Anal Chem. 2011 Aug 15;83(16):6381-8 [21740038] J Anal Toxicol. 2011 Sep;35(7):487-95 [21871158] J Chromatogr B Analyt Technol Biomed Life Sci. 2012 May 15;897:22-31 [22521213] Am J Emerg Med. 2012 Sep;30(7):1320.e5-7 [21802885] Clin Chim Acta. 2012 Nov 20;413(23-24):1839-47 [22771478] Clin Toxicol (Phila). 2012 Sep;50(8):733-42 [22888997] Ther Drug Monit. 2012 Dec;34(6):615-21 [23131695] J Chromatogr B Analyt Technol Biomed Life Sci. 2012 Nov 15;909:42-50 [23153643] Fed Regist. 2013 Jan 4;78(3):664-6 [23289157] J Anal Toxicol. 2013 Jan-Feb;37(1):43-6 [23111916] J Anal Toxicol. 2013 Jan-Feb;37(1):17-24 [23118149] Anal Chem. 2013 Apr 2;85(7):3730-8 [23458260] J Mass Spectrom. 2011 Feb;46(2):163-71 [21259394] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.chroma.2013.12.067 ER - TY - JOUR T1 - Biomarkers and neurodevelopment in perinatally HIV-infected or exposed youth: a structural equation model analysis AN - 1765970385; PQ0002559384 AB - Objective: To examine the relationship between markers of vascular dysfunction and neurodevelopmental outcomes in perinatally HIV-infected (PHIV+) and perinatally HIV-exposed but uninfected (PHEU) youth. Design: Cross-sectional design within a prospective, 15-site US-based cohort study. Methods: Neurodevelopmental outcomes were evaluated in relation to nine selected vascular biomarkers in 342 youth (212 PHIV+, 130 PHEU). Serum levels were assessed for adiponectin, C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), soluble vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-selectin), monocyte chemoattractant protein (sMCP-1), intercellular adhesion molecule-1 (slCAM-1), and P-selectin (sP-selectin). The Wechsler Intelligence Scale for Children-Fourth Edition (WISC-IV) was administered at entry, yielding a Full-Scale IQ score, and four index scores. Factor analysis was conducted to reduce the biomarkers to fewer factors with related biological roles. Structural equation models (SEMs) were used to measure associations between resulting factors and WISC-IV scores. Results: Mean participant age was 11.4 years, 54% were female, 70% black. The nine biomarkers were clustered into three factor groups: F1 (fibrinogen, CRP, and IL-6); F2 (slCAM-1 and sVCAM-1); and F3 (MCP-1, sP-selectin, and sE-selectin). Adiponectin showed little correlation with any factor. SEMs revealed significant negative association of F1 with WISC-IV processing speed score in the total cohort. This effect remained significant after adjusting for HIV status and other potential confounders. A similar association was observed when restricted to PHIV+ participants in both unadjusted and adjusted SEMs. Conclusion: Aggregate measures of fibrinogen, CRP, and IL-6 may serve as a latent biomarker associated with relatively decreased processing speed in both PHIV+ and PHEU youth. JF - AIDS AU - Kapetanovic, Suad AU - Griner, Ray AU - Zeldow, Bret AU - Nichols, Sharon AU - Leister, Erin AU - Gelbard, Harris A AU - Miller, Tracie L AU - Hazra, Rohan AU - Mendez, Armando J AU - Malee, Kathleen AU - Kammerer, Betsy AU - Williams, Paige L AD - National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, suad.kapetanovic@nih.gov Y1 - 2014/01/28/ PY - 2014 DA - 2014 Jan 28 SP - 355 EP - 364 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 IS - 3 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - HIV-affected children KW - inflammatory markers KW - neurodevelopmental outcomes KW - perinatal HIV infection KW - Bioindicators KW - Interleukin 6 KW - Acquired immune deficiency syndrome KW - Age KW - Monocyte chemoattractant protein 1 KW - Mathematical models KW - Factor analysis KW - Fibrinogen KW - P-selectin KW - Adhesion KW - biomarkers KW - Monocyte chemoattractant protein KW - Serum levels KW - Intelligence KW - vascular cell adhesion molecule 1 KW - Human immunodeficiency virus KW - intercellular adhesion molecule 1 KW - Proteins KW - Adiponectin KW - E-selectin KW - C-reactive protein KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765970385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Biomarkers+and+neurodevelopment+in+perinatally+HIV-infected+or+exposed+youth%3A+a+structural+equation+model+analysis&rft.au=Kapetanovic%2C+Suad%3BGriner%2C+Ray%3BZeldow%2C+Bret%3BNichols%2C+Sharon%3BLeister%2C+Erin%3BGelbard%2C+Harris+A%3BMiller%2C+Tracie+L%3BHazra%2C+Rohan%3BMendez%2C+Armando+J%3BMalee%2C+Kathleen%3BKammerer%2C+Betsy%3BWilliams%2C+Paige+L&rft.aulast=Kapetanovic&rft.aufirst=Suad&rft.date=2014-01-28&rft.volume=28&rft.issue=3&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000072 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Interleukin 6; Age; Mathematical models; Monocyte chemoattractant protein 1; Factor analysis; Fibrinogen; P-selectin; Monocyte chemoattractant protein; biomarkers; Serum levels; vascular cell adhesion molecule 1; Intelligence; intercellular adhesion molecule 1; Adiponectin; E-selectin; C-reactive protein; Bioindicators; Acquired immune deficiency syndrome; Human immunodeficiency virus; Proteins; Adhesion DO - http://dx.doi.org/10.1097/QAD.0000000000000072 ER - TY - JOUR T1 - Factors associated with survival among patients with AIDS-related primary central nervous system lymphoma AN - 1765970192; PQ0002559388 AB - Objective: AIDS-related primary central nervous system lymphoma (AR-PCNSL) has a poor prognosis. Improved understanding of specific patient, infectious, diagnostic, and treatment-related factors that affect overall survival (OS) is required to improve outcomes. Design: Population-based registry linkage study. Methods: Adult cases from the San Francisco AIDS registry (1990-2000) were matched with the California Cancer Registry (1985-2002) to ascertain AR-PCNSL data. Survival time was assessed through 31 December 2007. Risk factors and temporal trends for death were measured using two-sided Kaplan-Meier and Cox analyses. Results: Two hundred and seven AR-PCNSL patients were identified: 68% were white, 20% Hispanic, 10% African-American, and 2% Asian. Nineteen percent of patients had central nervous system (CNS) opportunistic infections diagnosed prior to AR-PCNSL. Fifty-seven percent of patients received radiation and/or chemotherapy and 12% used HAART prior to or within 30 days of AR-PCNSL diagnosis. One hundred and ninety-nine patients died (34 deaths/100 person-years). In adjusted analysis, prior CNS opportunistic infection diagnosis increased risk of death (hazard ratio 1.9, P = 0.0006) whereas radiation and/or chemotherapy decreased risk (hazard ratio 0.6, P < 0.0001). AR-PCNSL diagnosis 1999-2002 had a lower mortality risk (hazard ratio = 0.4, P = 0.02) compared to 1990-1995. African-Americans had an increased risk of death compared to whites or Asians (hazard ratio = 2.0, P = 0.007). Conclusion: OS among AR-PCNSL patients improved over time but remains poor, especially among African-Americans. Prospective evaluation of curative therapy in AR-PCNSL is urgently needed. Accurate diagnosis of CNS mass lesions in patients with AIDS is required and for those with AR-PCNSL, antiretroviral therapy with concomitant AR-PCNSL therapy, and antimicrobial supportive care may improve OS. JF - AIDS AU - Uldrick, Thomas S AU - Pipkin, Sharon AU - Scheer, Susan AU - Hessol, Nancy A AD - HIV & AIDS Malignancy Branch, Center for Cancer Research, National Cancer Institute at the National Institutes of Health, Bethesda, Maryland, uldrickts@mail.nih.gov Y1 - 2014/01/28/ PY - 2014 DA - 2014 Jan 28 SP - 397 EP - 405 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 IS - 3 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - AIDS KW - AIDS-related lymphoma KW - brain neoplasms KW - HAART KW - prognosis KW - risk factors KW - time factors KW - Risk assessment KW - Central nervous system KW - Acquired immune deficiency syndrome KW - Chemotherapy KW - Survival KW - Infection KW - Radiation KW - Risk factors KW - Lesions KW - Lymphoma KW - Ethnic groups KW - Mortality KW - Data processing KW - Prognosis KW - Antiretroviral agents KW - Cancer KW - Antimicrobial agents KW - Opportunist infection KW - Health risks KW - highly active antiretroviral therapy KW - INE, USA, California, San Francisco KW - V 22360:AIDS and HIV KW - H 8000:Radiation Safety/Electrical Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765970192?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Factors+associated+with+survival+among+patients+with+AIDS-related+primary+central+nervous+system+lymphoma&rft.au=Uldrick%2C+Thomas+S%3BPipkin%2C+Sharon%3BScheer%2C+Susan%3BHessol%2C+Nancy+A&rft.aulast=Uldrick&rft.aufirst=Thomas&rft.date=2014-01-28&rft.volume=28&rft.issue=3&rft.spage=397&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000030 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Central nervous system; Mortality; Acquired immune deficiency syndrome; Data processing; Chemotherapy; Prognosis; Survival; Cancer; Opportunist infection; Antimicrobial agents; Radiation; highly active antiretroviral therapy; Risk factors; Lymphoma; Risk assessment; Infection; Antiretroviral agents; Health risks; Lesions; Ethnic groups; INE, USA, California, San Francisco DO - http://dx.doi.org/10.1097/QAD.0000000000000030 ER - TY - JOUR T1 - The role of a Schiff base scaffold, N-(2-hydroxy acetophenone) glycinate-in overcoming multidrug resistance in cancer. AN - 1459563804; 24044945 AB - Drug resistance is a problem that hinders the numerous successes of chemotherapeutic intervention of cancer and continues to be a major obstacle for cures. Till date, several attempts have been made to develop suitable multidrug resistance (MDR) reversing agents. But, throughout the clinical development of MDR reversing agents, patients repeatedly suffer from toxicities. So far, some anticancer activity of Schiff bases which are the condensation products of carbonyl compounds and primary amines and their metal complexes has been described. But, overcoming multidrug resistance, by the use of such small molecules still remain unexplored. Under this backdrop, in search of less toxic and more effective MDR reversing agents our laboratory has developed the different metal chelates of Schiff base N-(2-hydroxy acetophenone)glycinate (NG) which is structurally similar to azatyrosine [L-β-(5-hydroxy-2-pyridyl)-alanine] that inhibits tumor formation by deactivating the c-Raf-1 kinase and c-Ha-ras signalling pathway. A decade-long research proposes possible strategies to overcome MDR by exploiting the chemical nature of such metal chelates. In this review we have catalogued the success of metal chelates of NG to overcome MDR in cancer. The review depict that the problem of MDR can be circumvent by synchronized activation of immunogenic cell death pathways that utilize the components of a host's immune system to kill cancer cells in combination with other conventional strategies. The current wealth of preclinical information promises better understanding of the cellular processes underlying MDR reversing activity of metal derivatives of NG and thus exposes several cellular targets for rational designing of new generation of Schiff base metal chelates as MDR reversing agents. Copyright © 2013 Elsevier B.V. All rights reserved. JF - European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences AU - Ganguly, Avishek AU - Chakraborty, Paramita AU - Banerjee, Kaushik AU - Choudhuri, Soumitra Kumar AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, Kolkata, India. Y1 - 2014/01/23/ PY - 2014 DA - 2014 Jan 23 SP - 96 EP - 109 VL - 51 KW - Chelating Agents KW - 0 KW - Coordination Complexes KW - Schiff Bases KW - Index Medicus KW - N-(2-hydroxy acetophenone)glycinate KW - MAPK KW - MDR KW - FoxP3 KW - Apoptosis KW - ROS KW - Glutathione KW - EAC/Dox KW - Reactive oxygen species KW - CuNG KW - Schiff base metal chelates KW - Multidrug Resistance-associated Protein 1 KW - Myeloid derived suppressor cell KW - Iron N-(2-hydroxy acetophenone)glycinate KW - ABC transporter KW - reactive oxygen species KW - GSH KW - ZnNG KW - TAM KW - FeNG KW - Zn N-(2-hydroxyacetophenone)glycinate. KW - T regulatory cell (CD4(+)CD25(+)FoxP3(+)) KW - NG KW - MDSC KW - Tumor-associated macrophage KW - MAP kinase signalling KW - Forkhead box P3 KW - Copper N-(2-hydroxyacetophenone)glycinate KW - Multidrug resistance KW - T(Reg) KW - Mitogen-activated protein kinase KW - Doxorubicin resistant Ehrlich ascites carcinoma cells KW - MRP1 KW - Animals KW - Humans KW - Chelating Agents -- metabolism KW - Coordination Complexes -- metabolism KW - Schiff Bases -- therapeutic use KW - Drug Resistance, Multiple -- drug effects KW - Schiff Bases -- pharmacology KW - Drug Resistance, Neoplasm -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1459563804?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmaceutical+sciences+%3A+official+journal+of+the+European+Federation+for+Pharmaceutical+Sciences&rft.atitle=The+role+of+a+Schiff+base+scaffold%2C+N-%282-hydroxy+acetophenone%29+glycinate-in+overcoming+multidrug+resistance+in+cancer.&rft.au=Ganguly%2C+Avishek%3BChakraborty%2C+Paramita%3BBanerjee%2C+Kaushik%3BChoudhuri%2C+Soumitra+Kumar&rft.aulast=Ganguly&rft.aufirst=Avishek&rft.date=2014-01-23&rft.volume=51&rft.issue=&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmaceutical+sciences+%3A+official+journal+of+the+European+Federation+for+Pharmaceutical+Sciences&rft.issn=1879-0720&rft_id=info:doi/10.1016%2Fj.ejps.2013.09.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-06-23 N1 - Date created - 2013-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ejps.2013.09.003 ER - TY - JOUR T1 - 4-(3-Chloro-5-(trifluoromethyl)pyridin-2-yl)-N-(4-methoxypyridin-2 -yl) piperazine-1-carbothioamide (ML267), a Potent Inhibitor of Bacterial Phosphopantetheinyl Transferase That Attenuates Secondary Metabolism and Thwarts Bacterial Growth AN - 1660395444; PQ0001015742 AB - 4'-Phosphopantetheinyl transferases (PPTases) catalyze a post-translational modification essential to bacterial cell viability and virulence. We present the discovery and medicinal chemistry optimization of 2-pyridinyl-N-(4-aryl)piperazine-1-carbothioamides, which exhibit submicromolar inhibition of bacterial Sfp-PPTase with no activity toward the human orthologue. Moreover, compounds within this class possess antibacterial activity in the absence of a rapid cytotoxic response in human cells. An advanced analogue of this series, ML267 (55), was found to attenuate production of an Sfp-PPTase-dependent metabolite when applied to Bacillus subtilis at sublethal doses. Additional testing revealed antibacterial activity against methicillin-resistant Staphylococcus aureus, and chemical genetic studies implicated efflux as a mechanism for resistance in Escherichia coli. Additionally, we highlight the in vitro absorption, distribution, metabolism, and excretion and in vivo pharmacokinetic profiles of compound 55 to further demonstrate the potential utility of this small-molecule inhibitor. JF - Journal of Medicinal Chemistry AU - Foley, Timothy L AU - Rai, Ganesha AU - Yasgar, Adam AU - Daniel, Thomas AU - Baker, Heather L AU - Attene-Ramos, Matias AU - Kosa, Nicolas M AU - Leister, William AU - Burkart, Michael D AU - Jadhav, Ajit AU - Simeonov, Anton AU - Maloney, David J AD - National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, Maryland 20850, United States Y1 - 2014/01/22/ PY - 2014 DA - 2014 Jan 22 SP - 1063 EP - 1078 PB - American Chemical Society, P.O. Box 182426 Columbus OH 43218-2426 United States VL - 57 IS - 3 SN - 0022-2623, 0022-2623 KW - Microbiology Abstracts B: Bacteriology KW - Bacillus subtilis KW - Antibacterial activity KW - Drug resistance KW - Metabolites KW - Pharmacokinetics KW - Virulence KW - Cytotoxicity KW - Post-translation KW - Escherichia coli KW - Excretion KW - Staphylococcus aureus KW - Metabolism KW - J 02340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660395444?accountid=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+Medicinal+Chemistry&rft.atitle=4-%283-Chloro-5-%28trifluoromethyl%29pyridin-2-yl%29-N-%284-methoxypyridin-2+-yl%29+piperazine-1-carbothioamide+%28ML267%29%2C+a+Potent+Inhibitor+of+Bacterial+Phosphopantetheinyl+Transferase+That+Attenuates+Secondary+Metabolism+and+Thwarts+Bacterial+Growth&rft.au=Foley%2C+Timothy+L%3BRai%2C+Ganesha%3BYasgar%2C+Adam%3BDaniel%2C+Thomas%3BBaker%2C+Heather+L%3BAttene-Ramos%2C+Matias%3BKosa%2C+Nicolas+M%3BLeister%2C+William%3BBurkart%2C+Michael+D%3BJadhav%2C+Ajit%3BSimeonov%2C+Anton%3BMaloney%2C+David+J&rft.aulast=Foley&rft.aufirst=Timothy&rft.date=2014-01-22&rft.volume=57&rft.issue=3&rft.spage=1063&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medicinal+Chemistry&rft.issn=00222623&rft_id=info:doi/10.1021%2Fjm401752p LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Virulence; Cytotoxicity; Post-translation; Antibacterial activity; Drug resistance; Metabolites; Excretion; Pharmacokinetics; Metabolism; Bacillus subtilis; Escherichia coli; Staphylococcus aureus DO - http://dx.doi.org/10.1021/jm401752p ER - TY - JOUR T1 - Cytolethal distending toxin B as a cell-killing component of tumor-targeted anthrax toxin fusion proteins. AN - 1490706502; 24434511 AB - Cytolethal distending toxin (Cdt) is produced by Gram-negative bacteria of several species. It is composed of three subunits, CdtA, CdtB, and CdtC, with CdtB being the catalytic subunit. We fused CdtB from Haemophilus ducreyi to the N-terminal 255 amino acids of Bacillus anthracis toxin lethal factor (LFn) to design a novel, potentially potent antitumor drug. As a result of this fusion, CdtB was transported into the cytosol of targeted cells via the efficient delivery mechanism of anthrax toxin. The fusion protein efficiently killed various human tumor cell lines by first inducing a complete cell cycle arrest in the G2/M phase, followed by induction of apoptosis. The fusion protein showed very low toxicity in mouse experiments and impressive antitumor effects in a Lewis Lung carcinoma model, with a 90% cure rate. This study demonstrates that efficient drug delivery by a modified anthrax toxin system combined with the enzymatic activity of CdtB has great potential as anticancer treatment and should be considered for the development of novel anticancer drugs. JF - Cell death & disease AU - Bachran, C AU - Hasikova, R AU - Leysath, C E AU - Sastalla, I AU - Zhang, Y AU - Fattah, R J AU - Liu, S AU - Leppla, S H AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. Y1 - 2014/01/16/ PY - 2014 DA - 2014 Jan 16 SP - 1 VL - 5 KW - Antigens, Bacterial KW - 0 KW - Bacterial Toxins KW - Recombinant Fusion Proteins KW - anthrax toxin KW - cytolethal distending toxin KW - Index Medicus KW - Recombinant Fusion Proteins -- metabolism KW - Animals KW - Humans KW - Apoptosis -- drug effects KW - Recombinant Fusion Proteins -- genetics KW - Mice, Inbred C57BL KW - Cell Cycle Checkpoints -- drug effects KW - Recombinant Fusion Proteins -- pharmacology KW - Mice KW - Cell Line, Tumor KW - Male KW - Female KW - Bacterial Toxins -- genetics KW - Neoplasms -- drug therapy KW - Bacterial Toxins -- metabolism KW - Antigens, Bacterial -- metabolism KW - Neoplasms -- physiopathology KW - Bacterial Toxins -- pharmacology KW - Antigens, Bacterial -- pharmacology KW - Antigens, Bacterial -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490706502?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytolethal+distending+toxin+B+as+a+cell-killing+component+of+tumor-targeted+anthrax+toxin+fusion+proteins.&rft.au=Bachran%2C+C%3BHasikova%2C+R%3BLeysath%2C+C+E%3BSastalla%2C+I%3BZhang%2C+Y%3BFattah%2C+R+J%3BLiu%2C+S%3BLeppla%2C+S+H&rft.aulast=Bachran&rft.aufirst=C&rft.date=2014-01-16&rft.volume=5&rft.issue=&rft.spage=e1003&rft.isbn=&rft.btitle=&rft.title=Cell+death+%26+disease&rft.issn=2041-4889&rft_id=info:doi/10.1038%2Fcddis.2013.540 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-02 N1 - Date created - 2014-01-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2001 May 25;276(21):17976-84 [11278833] Biochem J. 1986 Jul 1;237(1):123-30 [3800873] J Biol Chem. 1993 Feb 15;268(5):3334-41 [8429009] Infect Immun. 1994 Nov;62(11):4955-61 [7927776] Science. 1997 Jan 17;275(5298):343-9 [8994024] Nat Biotechnol. 2005 Jun;23(6):725-30 [15895075] Microbes Infect. 2005 May;7(5-6):867-74 [15876546] Proteins. 2006 Feb 1;62(2):421-34 [16304641] Nat Methods. 2006 Apr;3(4):259-61 [16554829] J Control Release. 2007 Feb 26;117(3):342-50 [17207883] Cell Microbiol. 2007 Apr;9(4):977-87 [17381430] J Immunol. 2007 Apr 15;178(8):5099-108 [17404292] Vaccine. 2007 May 4;25(18):3606-14 [17289219] J Biol Chem. 2008 Jan 4;283(1):529-40 [17974567] FEMS Microbiol Lett. 2009 Feb;291(2):222-31 [19087203] Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12424-9 [19617532] J Mol Biol. 2009 Sep 25;392(3):614-29 [19627991] PLoS One. 2009;4(11):e7946 [19956758] Science. 2009 Nov 27;326(5957):1231-5 [19965467] Mol Cancer Ther. 2010 Jul;9(7):2007-15 [20587662] Mol Immunol. 2010 Nov-Dec;48(1-3):203-10 [20863570] J Dent Res. 2011 May;90(5):638-45 [21220361] Microbiology. 2011 Jul;157(Pt 7):1851-75 [21565933] Protein Expr Purif. 2011 Nov;80(1):80-90 [21827967] Infect Immun. 2012 Aug;80(8):2761-70 [22645284] Nature. 2012 Oct 4;490(7418):107-11 [22902502] J Biol Chem. 2013 Mar 29;288(13):9058-65 [23393143] Mol Oncol. 2013 Jun;7(3):440-51 [23290417] Mol Microbiol. 2000 Aug;37(4):952-63 [10972814] Cancer Res. 2000 Nov 1;60(21):6061-7 [11085528] J Biol Chem. 2001 Dec 7;276(49):46326-32 [11574549] Proc Natl Acad Sci U S A. 2003 Jan 21;100(2):657-62 [12525700] J Biol Chem. 2003 Dec 12;278(50):50671-81 [12947116] Pediatr Infect Dis J. 1987 Dec;6(12):1135-6 [3324043] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/cddis.2013.540 ER - TY - JOUR T1 - Testing multiple biological mediators simultaneously AN - 1496895174; 19037923 AB - Motivation:Modern biomedical and epidemiological studies often measure hundreds or thousands of biomarkers, such as gene expression or metabolite levels. Although there is an extensive statistical literature on adjusting for 'multiple comparisons' when testing whether these biomarkers are directly associated with a disease, testing whether they are biological mediators between a known risk factor and a disease requires a more complex null hypothesis, thus offering additional methodological challenges.Results:We propose a permutation approach that tests multiple putative mediators and controls the family wise error rate. We demonstrate that, unlike when testing direct associations, replacing the Bonferroni correction with a permutation approach that focuses on the maximum of the test statistics can significantly improve the power to detect mediators even when all biomarkers are independent. Through simulations, we show the power of our method is 2-5 larger than the power achieved by Bonferroni correction. Finally, we apply our permutation test to a case-control study of dietary risk factors and colorectal adenoma to show that, of 149 test metabolites, docosahexaenoate is a possible mediator between fish consumption and decreased colorectal adenoma risk. JF - Bioinformatics AU - Boca, Simina M AU - Sinha, Rashmi AU - Cross, Amanda J AU - Moore, Steven C AU - Sampson, Joshua N AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, USA Y1 - 2014/01/15/ PY - 2014 DA - 2014 Jan 15 SP - 214 EP - 220 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 30 IS - 2 SN - 1367-4803, 1367-4803 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Gene expression KW - Statistics KW - Risk factors KW - Colorectal cancer KW - Metabolites KW - Bioinformatics KW - biomarkers KW - Adenoma KW - Internet KW - N 14810:Methods KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496895174?accountid=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=Testing+multiple+biological+mediators+simultaneously&rft.au=Boca%2C+Simina+M%3BSinha%2C+Rashmi%3BCross%2C+Amanda+J%3BMoore%2C+Steven+C%3BSampson%2C+Joshua+N&rft.aulast=Boca&rft.aufirst=Simina&rft.date=2014-01-15&rft.volume=30&rft.issue=2&rft.spage=214&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtt633 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Gene expression; Statistics; Risk factors; Colorectal cancer; Metabolites; Bioinformatics; Adenoma; biomarkers; Internet DO - http://dx.doi.org/10.1093/bioinformatics/btt633 ER - TY - CPAPER T1 - Microbiome and Intestinal Farnesoid X Receptor in the Control of Obesity T2 - 2014 Keystone Symposia on Obesity: A Multisystems Perspective AN - 1518609723; 6280460 JF - 2014 Keystone Symposia on Obesity: A Multisystems Perspective AU - Gonzalez, Frank Y1 - 2014/01/12/ PY - 2014 DA - 2014 Jan 12 KW - Obesity KW - farnesoid X receptors KW - Intestine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1518609723?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2014+Keystone+Symposia+on+Obesity%3A+A+Multisystems+Perspective&rft.atitle=Microbiome+and+Intestinal+Farnesoid+X+Receptor+in+the+Control+of+Obesity&rft.au=Gonzalez%2C+Frank&rft.aulast=Gonzalez&rft.aufirst=Frank&rft.date=2014-01-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2014+Keystone+Symposia+on+Obesity%3A+A+Multisystems+Perspective&rft.issn=&rft_id=info:doi/ L2 - http://www.keystonesymposia.org/index.cfm?e=web.Meeting.Program&meetingid=1294 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-23 N1 - Last updated - 2014-04-24 ER - TY - JOUR T1 - High-Resolution Structures and Orientations of Antimicrobial Peptides Piscidin 1 and Piscidin 3 in Fluid Bilayers Reveal Tilting, Kinking, and Bilayer Immersion AN - 1660399658; PQ0001052602 AB - While antimicrobial peptides (AMPs) have been widely investigated as potential therapeutics, high-resolution structures obtained under biologically relevant conditions are lacking. Here, the high-resolution structures of the homologous 22-residue long AMPs piscidin 1 (p1) and piscidin 3 (p3) are determined in fluid-phase 3:1 phosphatidylcholine/phosphatidylglycerol (PC/PG) and 1:1 phosphatidylethanolamine/phosphatidylglycerol (PE/PG) bilayers to identify molecular features important for membrane destabilization in bacterial cell membrane mimics. Structural refinement of 1H-15N dipolar couplings and 15N chemical shifts measured by oriented sample solid-state NMR and all-atom molecular dynamics (MD) simulations provide structural and orientational information of high precision and accuracy about these interfacially bound alpha -helical peptides. The tilt of the helical axis, tau , is between 83 degree and 93 degree with respect to the bilayer normal for all systems and analysis methods. The average azimuthal rotation, rho , is 235 degree , which results in burial of hydrophobic residues in the bilayer. The refined NMR and MD structures reveal a slight kink at G13 that delineates two helical segments characterized by a small difference in their tau angles (<10 degree ) and significant difference in their rho angles ( similar to 25 degree ). Remarkably, the kink, at the end of a G(X)4G motif highly conserved among members of the piscidin family, allows p1 and p3 to adopt rho angles that maximize their hydrophobic moments. Two structural features differentiate the more potent p1 from p3: p1 has a larger rho angle and less N-terminal fraying. The peptides have comparable depths of insertion in PC/PG, but p3 is 1.2 Aa more deeply inserted than p1 in PE/PG. In contrast to the ideal alpha -helical structures typically assumed in mechanistic models of AMPs, p1 and p3 adopt disrupted alpha -helical backbones that correct for differences in the amphipathicity of their N- and C-ends, and their centers of mass lie similar to 1.2-3.6 Aa below the plane defined by the C2 atoms of the lipid acyl chains. JF - Journal of the American Chemical Society AU - Perrin, BScott AU - Tian, Ye AU - Fu, Riqiang AU - Grant, Christopher V AU - Chekmenev, Eduard Y AU - Wieczorek, William E AU - Dao, Alexander E AU - Hayden, Robert M AU - Burzynski, Caitlin M AU - Venable, Richard M AU - Sharma, Mukesh AU - Opella, Stanley J AU - Pastor, Richard W AU - Cotten, Myriam L AD - Laboratory of Computational Biology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, United States Y1 - 2014/01/10/ PY - 2014 DA - 2014 Jan 10 SP - 3491 EP - 3504 PB - American Chemical Society, P.O. Box 182426 Columbus OH 43218-2426 United States VL - 136 IS - 9 SN - 0002-7863, 0002-7863 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - Cell membranes KW - Lipids KW - phosphatidylglycerol KW - Lecithin KW - Immersion KW - Hydrophobicity KW - N.M.R. KW - phosphatidylethanolamine KW - Antimicrobial peptides KW - A 01340:Antibiotics & Antimicrobials KW - J 02330:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660399658?accountid=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+the+American+Chemical+Society&rft.atitle=High-Resolution+Structures+and+Orientations+of+Antimicrobial+Peptides+Piscidin+1+and+Piscidin+3+in+Fluid+Bilayers+Reveal+Tilting%2C+Kinking%2C+and+Bilayer+Immersion&rft.au=Perrin%2C+BScott%3BTian%2C+Ye%3BFu%2C+Riqiang%3BGrant%2C+Christopher+V%3BChekmenev%2C+Eduard+Y%3BWieczorek%2C+William+E%3BDao%2C+Alexander+E%3BHayden%2C+Robert+M%3BBurzynski%2C+Caitlin+M%3BVenable%2C+Richard+M%3BSharma%2C+Mukesh%3BOpella%2C+Stanley+J%3BPastor%2C+Richard+W%3BCotten%2C+Myriam+L&rft.aulast=Perrin&rft.aufirst=BScott&rft.date=2014-01-10&rft.volume=136&rft.issue=9&rft.spage=3491&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Chemical+Society&rft.issn=00027863&rft_id=info:doi/10.1021%2Fja411119m LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Cell membranes; Lipids; phosphatidylglycerol; Immersion; Lecithin; N.M.R.; Hydrophobicity; phosphatidylethanolamine; Antimicrobial peptides DO - http://dx.doi.org/10.1021/ja411119m ER - TY - JOUR T1 - An Insight into the Transcriptome of the Digestive Tract of the Bloodsucking Bug, Rhodnius prolixus AN - 1496881099; 19022519 AB - The bloodsucking hemipteran Rhodnius prolixus is a vector of Chagas' disease, which affects 7-8 million people today in Latin America. In contrast to other hematophagous insects, the triatomine gut is compartmentalized into three segments that perform different functions during blood digestion. Here we report analysis of transcriptomes for each of the segments using pyrosequencing technology. Comparison of transcript frequency in digestive libraries with a whole-body library was used to evaluate expression levels. All classes of digestive enzymes were highly expressed, with a predominance of cysteine and aspartic proteinases, the latter showing a significant expansion through gene duplication. Although no protein digestion is known to occur in the anterior midgut (AM), protease transcripts were found, suggesting secretion as pro-enzymes, being possibly activated in the posterior midgut (PM). As expected, genes related to cytoskeleton, protein synthesis apparatus, protein traffic, and secretion were abundantly transcribed. Despite the absence of a chitinous peritrophic membrane in hemipterans - which have instead a lipidic perimicrovillar membrane lining over midgut epithelia - several gut-specific peritrophin transcripts were found, suggesting that these proteins perform functions other than being a structural component of the peritrophic membrane. Among immunity-related transcripts, while lysozymes and lectins were the most highly expressed, several genes belonging to the Toll pathway - found at low levels in the gut of most insects - were identified, contrasting with a low abundance of transcripts from IMD and STAT pathways. Analysis of transcripts related to lipid metabolism indicates that lipids play multiple roles, being a major energy source, a substrate for perimicrovillar membrane formation, and a source for hydrocarbons possibly to produce the wax layer of the hindgut. Transcripts related to amino acid metabolism showed an unanticipated priority for degradation of tyrosine, phenylalanine, and tryptophan. Analysis of transcripts related to signaling pathways suggested a role for MAP kinases, GTPases, and LKBP1/AMP kinases related to control of cell shape and polarity, possibly in connection with regulation of cell survival, response of pathogens and nutrients. Together, our findings present a new view of the triatomine digestive apparatus and will help us understand trypanosome interaction and allow insights into hemipteran metabolic adaptations to a blood-based diet. The bloodsucking bug Rhodnius prolixus is a vector of Chagas' disease, which affects 7-8 million people in Latin America. In contrast to other insects, the digestive tract of Rhodnius has three segments that perform different functions during blood digestion. Here we report analysis of transcriptomes for each of these segments using pyrosequencing technology amounting to several million sequences. Comparison of transcript frequency in digestive libraries with a whole-body library was used to evaluate expression levels, leading to the discovery of several families of enzymes associated with the digestion of proteins, carbohydrates, and lipids, as well as proteins involved in immunity, signal transduction, amino-acid metabolism, and detoxification. Together, our findings present a new view of the triatomine digestive apparatus and will help us understand the mechanism of blood digestion by Rhodnius and its interaction with the agent of Chagas' disease, Trypanosoma cruzi, a parasite that grows within the insect's digestive system. JF - PLoS Neglected Tropical Diseases AU - Ribeiro, Jose MC AU - Genta, Fernando A AU - Sorgine, Marcos HF AU - Logullo, Raquel AU - Mesquita, Rafael D AU - Paiva-Silva, Gabriela O AU - Majerowicz, David AU - Medeiros, Marcelo AU - Koerich, Leonardo AU - Terra, Walter R AU - Ferreira, Clelia AU - Pimentel, Andre C AU - Bisch, Paulo M AU - Leite, Daniel C AU - Diniz, Michelle MP AU - Junior, Joao Lidio da SGV AU - Da Silva, Manuela L AU - Araujo, Ricardo N AU - Gandara, Ana Caroline P AU - Brosson, Sebastien AU - Salmon, Didier AU - Bousbata, Sabrina AU - Gonzalez-Caballero, Natalia AU - Silber, Ariel Mariano AU - Alves-Bezerra, Michele AU - Gondim, Katia C AU - Silva-Neto, Mario Alberto C AU - Atella, Georgia C AU - Araujo, Helena AU - Dias, Felipe A AU - Polycarpo, Carla AU - Vionette-Amaral, Raquel J AU - Fampa, Patricia AU - Melo, Ana Claudia A AU - Tanaka, Aparecida S AU - Balczun, Carsten AU - Oliveira, Jose Henrique M AU - Goncalves, Renata LS AU - Lazoski, Cristiano AU - Rivera-Pomar, Rolando AU - Diambra, Luis AU - Schaub, Guenter A AU - Garcia, Eloi S AU - Azambuja, Patricia AU - Braz, Gloria RC AU - Oliveira, Pedro L AD - Section of Vector Biology, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America Y1 - 2014/01/09/ PY - 2014 DA - 2014 Jan 09 PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States VL - 8 IS - 1 SN - 1935-2727, 1935-2727 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Entomology Abstracts KW - Cell survival KW - Parasites KW - Secretion KW - Peritrophic membrane KW - Hosts KW - Rhodnius prolixus KW - gene duplication KW - Public health KW - Disease transmission KW - Gene expression KW - Digestion KW - Midgut KW - Aquatic insects KW - Trypanosoma cruzi KW - Protein biosynthesis KW - Amino acids KW - Hydrocarbons KW - Latin America KW - Transcription KW - Pest control KW - Immunity KW - Lipid metabolism KW - Blood KW - Rhodnius KW - Digestive tract KW - Aspartic proteinase KW - Digestive system KW - Signal transduction KW - Chagas' disease KW - Guanosinetriphosphatase KW - Z 05300:General 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/1496881099?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+Neglected+Tropical+Diseases&rft.atitle=An+Insight+into+the+Transcriptome+of+the+Digestive+Tract+of+the+Bloodsucking+Bug%2C+Rhodnius+prolixus&rft.au=Ribeiro%2C+Jose+MC%3BGenta%2C+Fernando+A%3BSorgine%2C+Marcos+HF%3BLogullo%2C+Raquel%3BMesquita%2C+Rafael+D%3BPaiva-Silva%2C+Gabriela+O%3BMajerowicz%2C+David%3BMedeiros%2C+Marcelo%3BKoerich%2C+Leonardo%3BTerra%2C+Walter+R%3BFerreira%2C+Clelia%3BPimentel%2C+Andre+C%3BBisch%2C+Paulo+M%3BLeite%2C+Daniel+C%3BDiniz%2C+Michelle+MP%3BJunior%2C+Joao+Lidio+da+SGV%3BDa+Silva%2C+Manuela+L%3BAraujo%2C+Ricardo+N%3BGandara%2C+Ana+Caroline+P%3BBrosson%2C+Sebastien%3BSalmon%2C+Didier%3BBousbata%2C+Sabrina%3BGonzalez-Caballero%2C+Natalia%3BSilber%2C+Ariel+Mariano%3BAlves-Bezerra%2C+Michele%3BGondim%2C+Katia+C%3BSilva-Neto%2C+Mario+Alberto+C%3BAtella%2C+Georgia+C%3BAraujo%2C+Helena%3BDias%2C+Felipe+A%3BPolycarpo%2C+Carla%3BVionette-Amaral%2C+Raquel+J%3BFampa%2C+Patricia%3BMelo%2C+Ana+Claudia+A%3BTanaka%2C+Aparecida+S%3BBalczun%2C+Carsten%3BOliveira%2C+Jose+Henrique+M%3BGoncalves%2C+Renata+LS%3BLazoski%2C+Cristiano%3BRivera-Pomar%2C+Rolando%3BDiambra%2C+Luis%3BSchaub%2C+Guenter+A%3BGarcia%2C+Eloi+S%3BAzambuja%2C+Patricia%3BBraz%2C+Gloria+RC%3BOliveira%2C+Pedro+L&rft.aulast=Ribeiro&rft.aufirst=Jose&rft.date=2014-01-09&rft.volume=8&rft.issue=1&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0002594 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Secretion; Pest control; Hosts; Aquatic insects; Digestive system; Disease transmission; Public health; Cell survival; Parasites; Amino acids; Protein biosynthesis; Hydrocarbons; Transcription; Peritrophic membrane; Immunity; gene duplication; Lipid metabolism; Digestion; Gene expression; Blood; Digestive tract; Aspartic proteinase; Midgut; Guanosinetriphosphatase; Chagas' disease; Signal transduction; Trypanosoma cruzi; Rhodnius; Rhodnius prolixus; Latin America DO - http://dx.doi.org/10.1371/journal.pntd.0002594 ER - TY - JOUR T1 - Cigarette smoking, alcohol intake, and risk of glioma in the NIH-AARP Diet and Health Study AN - 1496885998; 18984786 AB - Background: Although cigarette smoking and alcohol drinking increase the risk of several cancers and certain components of cigarette smoke and alcohol can penetrate the blood-brain barrier, it remains unclear whether these exposures influence the risk of glioma. Methods: We examined the associations between cigarette smoking, alcohol intake, and risk of glioma in the National Institutes of Health-AARP Diet and Health Study, a prospective study of 477 095 US men and women ages 50-71 years at baseline. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using models with age as the time metric and adjusted for sex, race/ethnicity, education, and marital status. Results: During a median 10.5 person-years of follow-up, 492 men and 212 women were diagnosed with first primary glioma. Among men, current, heavier smoking was associated with a reduced risk of glioma compared with never smoking, but this was based on only nine cases. No associations were observed between smoking behaviours and glioma risk in women. Greater alcohol consumption was associated with a decreased risk of glioma, particularly among men (>2 drinks per day vs <1 drink per week: HR=0.67, 95% CI=0.51-0.90). Conclusion: Smoking and alcohol drinking do not appear to increase the risk of glioma. JF - British Journal of Cancer AU - Braganza, M Z AU - Rajaraman, P AU - Park, Y AU - Inskip, P D AU - Freedman, N D AU - Hollenbeck, A R AU - de Gonzalez, A Berrington AU - Kitahara, C M AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 9609 Medical Center Drive, Bethesda, MD 20892, USA Y1 - 2014/01/07/ PY - 2014 DA - 2014 Jan 07 SP - 242 EP - 248 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 110 IS - 1 SN - 0007-0920, 0007-0920 KW - Toxicology Abstracts; Health & Safety Science Abstracts; Risk Abstracts KW - Age KW - Cigarettes KW - Blood-brain barrier KW - Cigarette smoke KW - Risk reduction KW - Models KW - Cigarette smoking KW - Glioma KW - Ethnic groups KW - Ethanol KW - Diets KW - Alcohol KW - Alcoholic beverages KW - Beverages KW - Marriage KW - Cancer KW - Smoke KW - Brain tumors KW - Health risks KW - Education KW - Drinking behavior KW - X 24380:Social Poisons & Drug Abuse 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/1496885998?accountid=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=Cigarette+smoking%2C+alcohol+intake%2C+and+risk+of+glioma+in+the+NIH-AARP+Diet+and+Health+Study&rft.au=Braganza%2C+M+Z%3BRajaraman%2C+P%3BPark%2C+Y%3BInskip%2C+P+D%3BFreedman%2C+N+D%3BHollenbeck%2C+A+R%3Bde+Gonzalez%2C+A+Berrington%3BKitahara%2C+C+M&rft.aulast=Braganza&rft.aufirst=M&rft.date=2014-01-07&rft.volume=110&rft.issue=1&rft.spage=242&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2013.611 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Last updated - 2014-07-24 N1 - SubjectsTermNotLitGenreText - Diets; Age; Beverages; Alcoholic beverages; Blood-brain barrier; Cigarette smoke; Models; Brain tumors; Cigarette smoking; Drinking behavior; Glioma; Ethnic groups; Ethanol; Smoke; Health risks; Alcohol; Education; Cigarettes; Marriage; Risk reduction; Cancer DO - http://dx.doi.org/10.1038/bjc.2013.611 ER - TY - JOUR T1 - Graves' disease as immune reconstitution disease in HIV-positive patients is associated with naive and primary thymic emigrant CD4 super(+) T-cell recovery AN - 1768579437; PQ0002676661 AB - Objective: Immune restoration disease (IRD) can develop in HIV-infected patients following antiretroviral therapy (ART) initiation as unmasking or paradoxical worsening of opportunistic infections and, rarely, autoimmune phenomena. Although IRD usually occurs in the first months of ART during memory CD4 super(+) T-cell recovery, Graves' disease occurs as a distinctive late-onset IRD and its pathogenesis is unclear. Design: Seven patients who developed Graves' disease following ART initiation from the primary HIV care clinic at the National Institutes of Health were retrospectively identified and each was matched with two HIV-infected controls based on age, sex, and baseline CD4 super(+) T-cell count. Laboratory evaluations on stored cryopreserved samples were performed. Methods: Immunophenotyping of peripheral blood mononuclear cells (PBMCs), T-cell receptor excision circle (TREC) analysis in PBMCs, measurement of serum cytokines, and luciferase immunoprecipitation systems (LIPS) analysis for autoimmune antibodies were performed on stored samples for cases and controls at baseline and longitudinally following ART initiation. TSH/thyrotropin receptor (TSH-R) antibody testing was performed on serum from cases. Data were analyzed using nonparametric testing. Results: In comparison with controls, the proportion of naive CD4 super(+) T cells increased significantly (P = 0.0027) in the Graves' disease-IRD patients. TREC/10 super(6) PBMCs also increased significantly following ART in Graves' disease-IRD patients compared with controls (P = 0.0071). Similarly, LIPS analysis demonstrated increases in nonthyroid-related autoantibody titers over time following ART in cases compared with controls. Conclusion: Our data suggest that Graves' disease-IRD, in contrast to early-onset IRD, is associated with naive and primary thymic emigrant CD4 super(+) T-cell recovery and inappropriate autoantibody production. JF - AIDS AU - Sheikh, Virginia AU - Dersimonian, Rebecca AU - Richterman, Aaron G AU - Porter, Brian O AU - Natarajan AU - Burbelo, Peter D AU - Rupert, Adam AU - Santich, Brian H AU - Kardava, Lela AU - Mican, Joann M AU - Moir, Susan AU - Sereti, Irini AD - National Institute of Allergy and Infectious Diseases (NIAID), sheikhv@niaid.nih.gov Y1 - 2014/01/02/ PY - 2014 DA - 2014 Jan 02 SP - 31 EP - 39 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 28 IS - 1 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - Graves' disease KW - immune reconstitution inflammatory syndrome KW - immune restoration disease KW - naive T cells KW - T-cell receptor excision circles KW - Acquired immune deficiency syndrome KW - T-cell receptor KW - Age KW - Data processing KW - Thymus KW - antiretroviral therapy KW - Immunoprecipitation KW - Immunological memory KW - Infection KW - Antiretroviral agents KW - Cryopreservation KW - Opportunist infection KW - Immune reconstitution KW - CD4 antigen KW - Peripheral blood mononuclear cells KW - thyrotropin receptors KW - Autoantibodies KW - Human immunodeficiency virus KW - Lymphocytes T KW - Cytokines KW - Sex KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma KW - F 06930:Autoimmunity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768579437?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Graves%27+disease+as+immune+reconstitution+disease+in+HIV-positive+patients+is+associated+with+naive+and+primary+thymic+emigrant+CD4+super%28%2B%29+T-cell+recovery&rft.au=Sheikh%2C+Virginia%3BDersimonian%2C+Rebecca%3BRichterman%2C+Aaron+G%3BPorter%2C+Brian+O%3BNatarajan%3BBurbelo%2C+Peter+D%3BRupert%2C+Adam%3BSantich%2C+Brian+H%3BKardava%2C+Lela%3BMican%2C+Joann+M%3BMoir%2C+Susan%3BSereti%2C+Irini&rft.aulast=Sheikh&rft.aufirst=Virginia&rft.date=2014-01-02&rft.volume=28&rft.issue=1&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000006 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Age; T-cell receptor; Data processing; antiretroviral therapy; Thymus; Immunological memory; Immunoprecipitation; Graves' disease; Cryopreservation; Opportunist infection; Immune reconstitution; Peripheral blood mononuclear cells; CD4 antigen; Autoantibodies; thyrotropin receptors; Lymphocytes T; Cytokines; Sex; Acquired immune deficiency syndrome; Human immunodeficiency virus; Infection; Antiretroviral agents DO - http://dx.doi.org/10.1097/QAD.0000000000000006 ER - TY - JOUR T1 - An efficient algorithm coupled with synthetic minority over-sampling technique to classify imbalanced PubChem BioAssay data AN - 1524412397; 19788022 AB - It is common that imbalanced datasets are often generated from high-throughput screening (HTS). For a given dataset without taking into account the imbalanced nature, most classification methods tend to produce high predictive accuracy for the majority class, but significantly poor performance for the minority class. In this work, an efficient algorithm, GLMBoost. coupled with Synthetic Minority Over-sampling TEchnique (SMOTE) is developed and utilized to overcome the problem for several imbalanced datasets from PubChem BioAssay. By applying the proposed combinatorial method, those data of rare samples (active compounds), for which usually poor results are generated, can be detected apparently with high balanced accuracy (Gmean). As a comparison with GLMBoost, Random Forest (RF) combined with SMOTE is also adopted to classify the same datasets. Our results show that the former (GLMBoost + SMOTE) not only exhibits higher performance as measured by the percentage of correct classification for the rare samples (Sensitivity) and Gmean, but also demonstrates greater computational efficiency than the latter (RF + SMOTE). Therefore, we hope that the proposed combinatorial algorithm based on GLMBoost and SMOTE could be extensively used to tackle the imbalanced classification problem. JF - Analytica Chimica Acta AU - Hao, Ming AU - Wang, Yanli AU - Bryant, Stephen H AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894, USA, ywang@ncbi.nlm.nih.gov Y1 - 2014/01/02/ PY - 2014 DA - 2014 Jan 02 SP - 117 EP - 127 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 806 SN - 0003-2670, 0003-2670 KW - Environment Abstracts KW - High-throughput screening KW - Under-sampling KW - Over-sampling KW - PubChem KW - Imbalanced classification KW - Sensitivity KW - Bioassays KW - Classification KW - Forests KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1524412397?accountid=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=Analytica+Chimica+Acta&rft.atitle=An+efficient+algorithm+coupled+with+synthetic+minority+over-sampling+technique+to+classify+imbalanced+PubChem+BioAssay+data&rft.au=Hao%2C+Ming%3BWang%2C+Yanli%3BBryant%2C+Stephen+H&rft.aulast=Hao&rft.aufirst=Ming&rft.date=2014-01-02&rft.volume=806&rft.issue=&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Analytica+Chimica+Acta&rft.issn=00032670&rft_id=info:doi/10.1016%2Fj.aca.2013.10.050 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Number of references - 55 N1 - Last updated - 2015-09-03 N1 - SubjectsTermNotLitGenreText - Sensitivity; Bioassays; Classification; Forests DO - http://dx.doi.org/10.1016/j.aca.2013.10.050 ER - TY - JOUR T1 - From burden-sharing to opportunity-sharing: unlocking the climate negotiations AN - 1492624428; 18929304 AB - In conventional thinking on climate negotiations, traditional fossil fuel-based economic growth is coupled with carbon emissions, thus mitigation has been regarded as a burden on economic growth. The scarcity within the global emission budget and the interpretation of climate change as 'global public goods' have led climate change negotiations into a burden-sharing deadlock. However, some recent economics studies suggest that mitigation could actually promote local economic growth opportunities; consequently increasing the incentives for unilateral mitigation actions. This article highlights the implications for the strategies of unlocking the climate negotiations deadlock. Following an explanation of how climate change negotiations have led to a burden-sharing game and have become a deadlock, some new ways of thinking (based on the emerging literature) are used to suggest how mitigation could promote local economic growth.Policy relevanceOne policy implication is the need to change the current mindset in global climate change negotiations. The current framing of burden-sharing can be abandoned in favour of opportunity-sharing. This more positive approach will stimulate progress on climate action. Therefore, green growth should be situated at the heart of post-2020 climate change regime. A new two-track architecture is proposed for achieving the transformation as a combined top-down and bottom-up approach. A lower legally binding target based on equity principles of common but differentiated responsibilities (CBDR) could form a more politically realistic and inclusive basis for participation. To complement this, a green growth club would promote a higher voluntary global ambition and accelerate mitigation. JF - Climate Policy AU - Zhang, Yongsheng AU - Shi, He-Ling AD - Development Research Centre of the State Council, No. 225, Chaoyangmen Nei Dajie, Dongcheng District, Beijing 100010, China Y1 - 2014/01/02/ PY - 2014 DA - 2014 Jan 02 SP - 63 EP - 81 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 14 IS - 1 SN - 1469-3062, 1469-3062 KW - Sustainability Science Abstracts; Environment Abstracts; Meteorological & Geoastrophysical Abstracts KW - Mitigation KW - Responsibility KW - Climate change KW - Public policy and climate KW - Architecture KW - Economic growth KW - Incentives KW - Environmental policy KW - Carbon emissions KW - Economics KW - Emissions KW - Scarcity KW - Budgets KW - ENA 03:Energy KW - M2 551.583:Variations (551.583) KW - M3 1010:Issues in Sustainable Development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492624428?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Climate+Policy&rft.atitle=From+burden-sharing+to+opportunity-sharing%3A+unlocking+the+climate+negotiations&rft.au=Zhang%2C+Yongsheng%3BShi%2C+He-Ling&rft.aulast=Zhang&rft.aufirst=Yongsheng&rft.date=2014-01-02&rft.volume=14&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Climate+Policy&rft.issn=14693062&rft_id=info:doi/10.1080%2F14693062.2014.857979 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-01-01 N1 - Last updated - 2016-11-09 N1 - SubjectsTermNotLitGenreText - Public policy and climate; Climate change; Architecture; Carbon emissions; Mitigation; Responsibility; Economics; Emissions; Scarcity; Budgets; Incentives; Economic growth; Environmental policy DO - http://dx.doi.org/10.1080/14693062.2014.857979 ER - TY - JOUR T1 - Un-sung Samaritans in the Lives of People with Mental Illness: An Indian Experience AN - 1752993119; 201600254 AB - Caring is a fundamental issue in the rehabilitation of a person with mental illness and more so for people with severe mental illness. The study examines the load of care giving with reference to the types of care during the symptomatic and recovery phases of mental illness and the various ways in which caregivers adapt their lives to meet the needs of people with mental illness (PWMI). The present research draws its data from the families of 200 persons with mental illness in Andhra Pradesh and Karnataka in India. The data presented in the study was collected from interviews using an interview schedule with open ended questions. The results reveal that people with mental illness require more social care during their recovery phase so as to facilitate their reintegration into mainstream society. Despite their own hardships, families by and large take on the care of their family members with mental illness as a matter of their responsibility. The study records the incredulous gratitude of caregivers at being acknowledged for the work they do. In that regard, the study itself provides a boost to the morale of tired, unacknowledged caregivers. Adapted from the source document. JF - The Indian Journal of Social Work AU - Janardhana, N AU - SHRAVYA, AU - Naidu, D M AU - SARASWATHI, AU - Seshan, Valli AD - Department of Psychiatric Social Work, National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore Y1 - 2014/01// PY - 2014 DA - January 2014 SP - 7 EP - 32 PB - Tata Institute of Social Sciences, Mumbai India VL - 75 IS - 1 SN - 0019-5634, 0019-5634 KW - Caregivers KW - Rehabilitation KW - Social Services KW - Mental Illness KW - India KW - article KW - 6142: mental & emotional health problems UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1752993119?accountid=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+Indian+Journal+of+Social+Work&rft.atitle=Un-sung+Samaritans+in+the+Lives+of+People+with+Mental+Illness%3A+An+Indian+Experience&rft.au=Janardhana%2C+N%3BSHRAVYA%2C%3BNaidu%2C+D+M%3BSARASWATHI%2C%3BSeshan%2C+Valli&rft.aulast=Janardhana&rft.aufirst=N&rft.date=2014-01-01&rft.volume=75&rft.issue=1&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=The+Indian+Journal+of+Social+Work&rft.issn=00195634&rft_id=info:doi/ LA - English DB - Social Services Abstracts N1 - Date revised - 2016-01-01 N1 - Number of references - 58 N1 - Last updated - 2016-09-28 N1 - CODEN - IJSWA3 N1 - SubjectsTermNotLitGenreText - Mental Illness; Caregivers; Rehabilitation; India; Social Services ER - TY - JOUR T1 - Guidance for Performing Criticality Analyses of Fuel Storage at Light-Water Reactor Power Plants AN - 1692315007; PQ0001263023 AB - The Nuclear Energy Institute, through the Spent Fuel Criticality Task Force has developed a guidance document that describes acceptable methods that may be used to perform criticality analyses for the storage of new and spent fuel at light-water reactor (LWR) power plants [1]. The guidance is applicable to new fuel assemblies stored in a new fuel vault, and to new and spent used fuel assemblies stored in spent fuel racks in a spent fuel pool. JF - Transactions of the American Nuclear Society AU - Cummings, K W AD - Nuclear Energy Institute, 1201 F Street, NW, Suite 1100, Washington, DC 20004 kwc@nei.org Y1 - 2014 PY - 2014 DA - 2014 SP - 342 EP - 345 PB - American Nuclear Society, Inc. VL - 111 SN - 0003-018X, 0003-018X KW - Mechanical & Transportation Engineering Abstracts (MT); Environmental Engineering Abstracts (EN); Electronics and Communications Abstracts (EA); CSA / ASCE Civil Engineering Abstracts (CE) KW - Nuclear power generation KW - Nuclear reactors KW - Fuels KW - Electric power generation KW - Spent nuclear fuels KW - Nuclear reactor components KW - Electric power plants KW - Nuclear engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1692315007?accountid=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=Transactions+of+the+American+Nuclear+Society&rft.atitle=Guidance+for+Performing+Criticality+Analyses+of+Fuel+Storage+at+Light-Water+Reactor+Power+Plants&rft.au=Cummings%2C+K+W&rft.aulast=Cummings&rft.aufirst=K&rft.date=2014-01-01&rft.volume=111&rft.issue=&rft.spage=342&rft.isbn=&rft.btitle=&rft.title=Transactions+of+the+American+Nuclear+Society&rft.issn=0003018X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-07-01 N1 - Last updated - 2015-07-01 ER - TY - JOUR T1 - Can Substance Use Disorders be Managed Using the Chronic Care Model? Review and Recommendations from a NIDA Consensus Group AN - 1665163740 AB - Brain imaging and genetic studies over the past two decades suggest that substance use disorders are best considered chronic illnesses. The passing of the Affordable Care Act in the United States has set the occasion for integrating treatment of substance use disorders into mainstream healthcare; and for using the proactive, team-oriented Chronic Care Model (CCM). This paper systematically examines and compares whether and how well the CCM could be applied to the treatment of substance use disorders, using type 2 diabetes as a comparator. The chronic illness management approach is still new in the field of addiction and research is limited. However comparative findings suggest that most proactive, team treatment-oriented clinical management practices now used in diabetes management are applicable to the substance use disorders; capable of being implemented by primary care teams; and should offer comparable potential benefits in the treatment of substance use disorders. Such care should also improve the quality of care for many illnesses now negatively affected by unaddressed substance abuse. JF - Public Health Reviews AU - McLellan, A Thomas AU - Starrels, Joanna L AU - Tai, Betty AU - Gordon, Adam J AU - Brown, Richard AU - Ghitza, Udi AU - Gourevitch, Marc AU - Stein, Jack AU - Oros, Marla AU - Horton, Terry AU - Lindblad, Robert AU - McNeely, Jennifer AD - Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA ; Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA ; National Institute of Health, National Institute on Drug Abuse, Bethesda, MD, USA ; University of Pittsburgh School of Medicine, Pittsburgh, PA, USA ; University of Wisconsin, School of Medicine and Public Health, Madison, WI, USA ; New York University School of Medicine, Department of Population Health, New York. NY USA ; The Mosaic Group, Baltimore MD, USA ; Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA, Christiana Care Health System, Division of Addiction Medicine, Wilmington DE, USA ; Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA, The EMMES Corporation, Rockville, MD, USA ; Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA, New York University School of Medicine, Department of Population Health, New York. NY USA ; Treatment Research Institute, 600 Public Ledger Building, 150 S. Independence Mall, Philadelphia, PA 19106, USA Y1 - 2014 PY - 2014 DA - 2014 SP - 1 EP - 24 CY - Dordrecht PB - Springer Science & Business Media VL - 35 IS - 2 SN - 0301-0422 KW - Medical Sciences--Oncology KW - Substance use disorders KW - chronic illness KW - chronic care model KW - type 2 diabetes management KW - electronic health records KW - healthcare reform KW - Addiction KW - Teams KW - Treatment KW - Type 2 diabetes mellitus KW - Brain KW - Brain imaging KW - Chronic sickness KW - Clinical guidelines KW - Clinical management KW - Diabetes KW - Disease management KW - Genetic factors KW - Health care KW - Primary health care KW - Quality of care KW - Sickness KW - Substance abuse disorders KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665163740?accountid=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=Public+Health+Reviews&rft.atitle=Can+Substance+Use+Disorders+be+Managed+Using+the+Chronic+Care+Model%3F+Review+and+Recommendations+from+a+NIDA+Consensus+Group&rft.au=McLellan%2C+A+Thomas%3BStarrels%2C+Joanna+L%3BTai%2C+Betty%3BGordon%2C+Adam+J%3BBrown%2C+Richard%3BGhitza%2C+Udi%3BGourevitch%2C+Marc%3BStein%2C+Jack%3BOros%2C+Marla%3BHorton%2C+Terry%3BLindblad%2C+Robert%3BMcNeely%2C+Jennifer&rft.aulast=McLellan&rft.aufirst=A&rft.date=2014-01-01&rft.volume=35&rft.issue=2&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Public+Health+Reviews&rft.issn=03010422&rft_id=info:doi/ LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-06-24 N1 - SubjectsTermNotLitGenreText - United States--US ER - TY - JOUR T1 - carboxypeptidase E-ΔN, a neuroprotein transiently expressed during development protects embryonic neurons against glutamate neurotoxicity. AN - 1628881739; 25426952 AB - Neuroprotective proteins expressed in the fetus play a critical role during early embryonic neurodevelopment, especially during maternal exposure to alcohol and drugs that cause stress, glutamate neuroexcitotoxicity, and damage to the fetal brain, if prolonged. We have identified a novel protein, carboxypeptidase E-ΔN (CPE-ΔN), which is a splice variant of CPE that has neuroprotective effects on embryonic neurons. CPE-ΔN is transiently expressed in mouse embryos from embryonic day 5.5 to postnatal day 1. It is expressed in embryonic neurons, but not in 3 week or older mouse brains, suggesting a function primarily in utero. CPE-ΔN expression was up-regulated in embryonic hippocampal neurons in response to dexamethasone treatment. CPE-ΔN transduced into rat embryonic cortical and hippocampal neurons protected them from glutamate- and H2O2-induced cell death. When transduced into embryonic cortical neurons, CPE-ΔN was found in the nucleus and enhanced the transcription of FGF2 mRNA. Embryonic cortical neurons challenged with glutamate resulted in attenuated FGF2 levels and cell death, but CPE-ΔN transduced neurons treated in the same manner showed increased FGF2 expression and normal viability. This neuroprotective effect of CPE-ΔN was mediated by secreted FGF2. Through receptor signaling, FGF2 activated the AKT and ERK signaling pathways, which in turn increased BCL-2 expression. This led to inhibition of caspase-3 activity and cell survival. JF - PloS one AU - Qin, Xiao-Yan AU - Cheng, Yong AU - Murthy, Saravana R K AU - Selvaraj, Prabhuanand AU - Loh, Y Peng AD - Section on Cellular Neurobiology, Program on Developmental Neuroscience, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, United States of America; College of Life and Environmental Sciences, Minzu University of China, Beijing 100081, China. ; Section on Cellular Neurobiology, Program on Developmental Neuroscience, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 11 KW - Nerve Tissue Proteins KW - 0 KW - Neuroprotective Agents KW - Proto-Oncogene Proteins c-bcl-2 KW - RNA, Messenger KW - Fibroblast Growth Factor 2 KW - 103107-01-3 KW - Bcl2 protein, mouse KW - 114100-40-2 KW - Glutamic Acid KW - 3KX376GY7L KW - Hydrogen Peroxide KW - BBX060AN9V KW - Proto-Oncogene Proteins c-akt KW - EC 2.7.11.1 KW - Extracellular Signal-Regulated MAP Kinases KW - EC 2.7.11.24 KW - Carboxypeptidase H KW - EC 3.4.17.10 KW - Caspase 3 KW - EC 3.4.22.- KW - Index Medicus KW - Proto-Oncogene Proteins c-akt -- genetics KW - Cerebral Cortex -- cytology KW - Animals KW - Cerebral Cortex -- drug effects KW - Cell Nucleus -- metabolism KW - Transduction, Genetic KW - Hydrogen Peroxide -- pharmacology KW - Primary Cell Culture KW - Cell Nucleus -- drug effects KW - RNA, Messenger -- genetics KW - Hippocampus -- drug effects KW - Rats KW - Caspase 3 -- genetics KW - Cell Survival -- drug effects KW - Hippocampus -- enzymology KW - Embryo, Mammalian KW - Signal Transduction KW - Extracellular Signal-Regulated MAP Kinases -- genetics KW - Caspase 3 -- metabolism KW - Proto-Oncogene Proteins c-bcl-2 -- agonists KW - Proto-Oncogene Proteins c-akt -- metabolism KW - Cerebral Cortex -- enzymology KW - Mice KW - Extracellular Signal-Regulated MAP Kinases -- metabolism KW - Cell Death -- drug effects KW - RNA, Messenger -- metabolism KW - Proto-Oncogene Proteins c-bcl-2 -- metabolism KW - Hippocampus -- cytology KW - Proto-Oncogene Proteins c-akt -- agonists KW - Proto-Oncogene Proteins c-bcl-2 -- genetics KW - Gene Expression Regulation, Developmental KW - Carboxypeptidase H -- metabolism KW - Carboxypeptidase H -- genetics KW - Fibroblast Growth Factor 2 -- secretion KW - Neurons -- drug effects KW - Neurons -- cytology KW - Fibroblast Growth Factor 2 -- genetics KW - Neuroprotective Agents -- metabolism KW - Fibroblast Growth Factor 2 -- agonists KW - Neurons -- enzymology KW - Nerve Tissue Proteins -- metabolism KW - Nerve Tissue Proteins -- genetics KW - Glutamic Acid -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1628881739?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=carboxypeptidase+E-%CE%94N%2C+a+neuroprotein+transiently+expressed+during+development+protects+embryonic+neurons+against+glutamate+neurotoxicity.&rft.au=Qin%2C+Xiao-Yan%3BCheng%2C+Yong%3BMurthy%2C+Saravana+R+K%3BSelvaraj%2C+Prabhuanand%3BLoh%2C+Y+Peng&rft.aulast=Qin&rft.aufirst=Xiao-Yan&rft.date=2014-01-01&rft.volume=9&rft.issue=11&rft.spage=e112996&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0112996 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-13 N1 - Date created - 2014-11-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2000 Apr 14;275(15):10761-6 [10753867] Mol Psychiatry. 2015 Jun;20(6):744-54 [25330741] Methods. 2001 Dec;25(4):402-8 [11846609] Proc Natl Acad Sci U S A. 2003 Jul 8;100(14):8543-8 [12808140] Brain Res Dev Brain Res. 2003 Aug 12;144(1):83-90 [12888219] J Mol Neurosci. 2004;24(2):189-99 [15456932] Dev Dyn. 2004 Nov;231(3):564-75 [15376324] Exp Neurol. 1983 Nov;82(2):432-46 [6628629] Annu Rev Physiol. 1988;50:309-21 [2897826] Neuron. 1990 Oct;5(4):501-9 [1688327] Biochem Biophys Res Commun. 1992 Jun 30;185(3):1155-61 [1378265] Eur J Neurosci. 1993 Nov 1;5(11):1455-64 [7904521] J Neurochem. 1994 Aug;63(2):596-602 [7913489] J Neurosci. 1994 Aug;14(8):4656-73 [8046441] Anesthesiology. 1995 Feb;82(2):521-30 [7856910] Alcohol Clin Exp Res. 1995 Dec;19(6):1447-53 [8749809] Clin Endocrinol (Oxf). 1997 Feb;46(2):161-6 [9135697] J Clin Invest. 1997 Jul 15;100(2):390-7 [9218516] Ann N Y Acad Sci. 1997 Jun 21;821:271-84 [9238211] Brain Res Dev Brain Res. 1998 Feb 10;105(2):287-93 [9541746] J Cell Biol. 1999 Jan 25;144(2):281-92 [9922454] Neurosci Res. 2005 Apr;51(4):331-6 [15740796] Nat Rev Mol Cell Biol. 2005 Oct;6(10):777-88 [16314867] CNS Drug Rev. 2005 Winter;11(4):353-68 [16614735] Brain Res. 2007 Jun 18;1154:40-9 [17498671] J Neurosci. 2007 Jul 11;27(28):7532-40 [17626214] Proteomics. 2008 Mar;8(6):1257-65 [18283662] J Mol Neurosci. 2009 Sep;39(1-2):1-8 [19165633] J Clin Invest. 2011 Mar;121(3):880-92 [21285511] Placenta. 2011 Oct;32(10):737-44 [21831423] Endocr Rev. 2012 Apr;33(2):216-53 [22402194] Acta Neuropathol. 2012 Jul;124(1):83-97 [22249620] Cell Signal. 2013 Jan;25(1):12-8 [22974840] J Mol Neurosci. 2013 Jan;49(1):150-6 [23229836] J Cell Sci. 2013 Jul 1;126(Pt 13):2890-902 [23606745] PLoS One. 2013;8(8):e71578 [23977080] Int J Mol Sci. 2013;14(11):21727-40 [24189220] Development. 2013 Nov;140(22):4574-82 [24154528] Tumour Biol. 2013 Dec;34(6):3691-9 [23852859] Oncogene. 2014 May 15;33(20):2655-64 [23770853] J Neurochem. 1999 Dec;73(6):2341-7 [10582592] Exp Neurol. 2000 Feb;161(2):442-52 [10686066] Neurosci Bull. 2014 Aug;30(4):692-6 [24691800] J Physiol. 2001 Feb 15;531(Pt 1):147-63 [11179399] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0112996 ER - TY - JOUR T1 - Identification of functionally important residues of the rat P2X4 receptor by alanine scanning mutagenesis of the dorsal fin and left flipper domains. AN - 1628878480; 25398027 AB - Crystallization of the zebrafish P2X4 receptor in both open and closed states revealed conformational differences in the ectodomain structures, including the dorsal fin and left flipper domains. Here, we focused on the role of these domains in receptor activation, responsiveness to orthosteric ATP analogue agonists, and desensitization. Alanine scanning mutagenesis of the R203-L214 (dorsal fin) and the D280-N293 (left flipper) sequences of the rat P2X4 receptor showed that ATP potency/efficacy was reduced in 15 out of 26 alanine mutants. The R203A, N204A, and N293A mutants were essentially non-functional, but receptor function was restored by ivermectin, an allosteric modulator. The I205A, T210A, L214A, P290A, G291A, and Y292A mutants exhibited significant changes in the responsiveness to orthosteric analog agonists 2-(methylthio)adenosine 5'-triphosphate, adenosine 5'-(γ-thio)triphosphate, 2'(3'-O-(4-benzoylbenzoyl)adenosine 5'-triphosphate, and α,β-methyleneadenosine 5'-triphosphate. In contrast, the responsiveness of L206A, N208A, D280A, T281A, R282A, and H286A mutants to analog agonists was comparable to that of the wild type receptor. Among these mutants, D280A, T281A, R282A, H286A, G291A, and Y292A also exhibited increased time-constant of the desensitizing current response. These experiments, together with homology modeling, indicate that residues located in the upper part of the dorsal fin and left flipper domains, relative to distance from the channel pore, contribute to the organization of the ATP binding pocket and to the initiation of signal transmission towards residues in the lower part of both domains. The R203 and N204 residues, deeply buried in the protein, may integrate the output signal from these two domains towards the gate. In addition, the left flipper residues predominantly account for the control of transition of channels from an open to a desensitized state. JF - PloS one AU - Tvrdonova, Vendula AU - Rokic, Milos B AU - Stojilkovic, Stanko S AU - Zemkova, Hana AD - Department of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, Prague, Czech Republic; Department of Physiology of Animals, Faculty of Science, Charles University, Prague, Czech Republic. ; Department of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, Prague, Czech Republic; Section on Cellular Signaling, Program in Developmental Neuroscience, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America. ; Section on Cellular Signaling, Program in Developmental Neuroscience, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Cellular and Molecular Neuroendocrinology, Institute of Physiology Academy of Sciences of the Czech Republic, Prague, Czech Republic. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 11 KW - Purinergic P2X Receptor Agonists KW - 0 KW - Receptors, Purinergic P2X4 KW - Ivermectin KW - 70288-86-7 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Alanine KW - OF5P57N2ZX KW - Index Medicus KW - Animals KW - Ivermectin -- pharmacology KW - HEK293 Cells KW - Humans KW - Amino Acid Sequence KW - Molecular Dynamics Simulation KW - Protein Binding KW - Purinergic P2X Receptor Agonists -- pharmacology KW - Mutagenesis KW - Binding Sites KW - Ion Channel Gating -- drug effects KW - Rats KW - Patch-Clamp Techniques KW - Sequence Alignment KW - Alanine -- metabolism KW - Adenosine Triphosphate -- metabolism KW - Molecular Sequence Data KW - Alanine -- genetics KW - Protein Structure, Tertiary KW - Receptors, Purinergic P2X4 -- genetics KW - Receptors, Purinergic P2X4 -- chemistry KW - Receptors, Purinergic P2X4 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1628878480?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Identification+of+functionally+important+residues+of+the+rat+P2X4+receptor+by+alanine+scanning+mutagenesis+of+the+dorsal+fin+and+left+flipper+domains.&rft.au=Tvrdonova%2C+Vendula%3BRokic%2C+Milos+B%3BStojilkovic%2C+Stanko+S%3BZemkova%2C+Hana&rft.aulast=Tvrdonova&rft.aufirst=Vendula&rft.date=2014-01-01&rft.volume=9&rft.issue=11&rft.spage=e112902&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0112902 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-18 N1 - Date created - 2014-11-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pharmacol Rev. 2011 Sep;63(3):641-83 [21737531] EMBO J. 1998 Jun 1;17(11):3016-28 [9606184] Proc Natl Acad Sci U S A. 2011 Aug 16;108(33):13800-5 [21808018] Biochemistry. 2011 Oct 4;50(39):8427-36 [21879712] Proc Natl Acad Sci U S A. 2012 Mar 13;109(11):4140-5 [22378652] Nature. 2012 May 10;485(7397):207-12 [22535247] Proc Natl Acad Sci U S A. 2012 Jul 10;109(28):11396-401 [22745172] PLoS One. 2013;8(3):e59411 [23555667] Biochemistry. 2014 May 13;53(18):3012-9 [24762105] PLoS One. 2014;9(5):e97528 [24878662] Nat Commun. 2014;5:4189 [24943126] J Gen Physiol. 2014 Jul;144(1):81-104 [24935743] Br J Pharmacol. 2014 Nov;171(22):5093-112 [24989924] Pflugers Arch. 2015 Apr;467(4):713-26 [24917516] J Neurosci. 2004 Aug 4;24(31):6968-78 [15295032] J Neurosci. 2004 Aug 18;24(33):7378-86 [15317863] J Neurosci. 1996 Apr 15;16(8):2495-507 [8786426] Protein Sci. 1997 Jun;6(6):1302-7 [9194190] J Biol Chem. 2000 Sep 22;275(38):29361-7 [10827197] Protein Eng. 1999 Dec;12(12):1021-4 [10611392] FASEB J. 2008 Mar;22(3):861-9 [17928361] J Biol Chem. 2000 Nov 3;275(44):34190-6 [10940304] J Biol Chem. 2001 May 4;276(18):14902-8 [11278888] J Neurosci. 2001 Aug 15;21(16):5885-92 [11487611] J Neurochem. 2008 May;105(4):1264-75 [18194442] Pflugers Arch. 2008 Aug;456(5):939-50 [18427835] J Biol Chem. 2008 Jul 18;283(29):20126-36 [18487206] Nature. 2009 Jul 30;460(7255):592-8 [19641588] J Biol Chem. 2011 Jan 28;286(4):2739-49 [21098022] Proc Natl Acad Sci U S A. 2011 May 31;108(22):9066-71 [21576497] Rev Neurosci. 2011;22(3):335-54 [21639805] J Neurosci. 1998 Sep 15;18(18):7152-9 [9736638] J Neurosci. 1999 Sep 1;19(17):7289-99 [10460235] J Biol Chem. 2004 Dec 17;279(51):53109-15 [15475563] J Biol Chem. 2005 Feb 18;280(7):6118-29 [15556949] Mol Pharmacol. 2005 Apr;67(4):1078-88 [15632318] J Gen Physiol. 2005 Apr;125(4):347-59 [15795310] J Neurosci. 2005 Aug 24;25(34):7734-42 [16120774] Neurosci Lett. 2006 Jan 23;393(1):78-83 [16226373] J Biol Chem. 2001 Aug 17;276(33):30934-41 [11402044] Physiol Rev. 2002 Oct;82(4):1013-67 [12270951] Nucleic Acids Res. 2003 Jul 1;31(13):3381-5 [12824332] J Biol Chem. 2003 Sep 19;278(38):36777-85 [12819199] J Biol Chem. 2004 Feb 20;279(8):6426-33 [14625300] J Gen Physiol. 2004 Mar;123(3):281-93 [14769846] Neurosci Lett. 2004 Jul 29;365(3):195-9 [15246547] J Neurochem. 2005 Dec;95(6):1746-54 [16236030] Mol Pharmacol. 2006 Feb;69(2):576-87 [16282518] J Neurochem. 2006 Feb;96(3):843-52 [16371009] Mol Pharmacol. 2006 May;69(5):1692-700 [16452399] Biochem Biophys Res Commun. 2006 Oct 20;349(2):619-25 [16949036] J Biol Chem. 2006 Oct 27;281(43):32649-59 [16954225] J Neurosci. 2007 Feb 7;27(6):1456-66 [17287520] J Neurosci. 2007 Apr 11;27(15):4072-82 [17428985] J Neurochem. 2007 Aug;102(4):1139-50 [17663752] J Biol Chem. 2008 Feb 22;283(8):5110-7 [18048351] Proteins. 2008 Apr;71(1):261-77 [17932912] EMBO J. 1997 Jun 16;16(12):3446-54 [9218787] J Neurosci. 1998 Apr 1;18(7):2350-9 [9502796] J Biol Chem. 2011 Aug 19;286(33):29207-17 [21690089] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0112902 ER - TY - JOUR T1 - Photoimmunotherapy of gastric cancer peritoneal carcinomatosis in a mouse model. AN - 1626162789; 25401794 AB - Photoimmunotherapy (PIT) is a new cancer treatment that combines the specificity of antibodies for targeting tumors with the toxicity induced by photosensitizers after exposure to near infrared (NIR) light. We performed PIT in a model of disseminated gastric cancer peritoneal carcinomatosis and monitored efficacy with in vivo GFP fluorescence imaging. In vitro and in vivo experiments were conducted with a HER2-expressing, GFP-expressing, gastric cancer cell line (N87-GFP). A conjugate comprised of a photosensitizer, IR-700, conjugated to trastuzumab (tra-IR700), followed by NIR light was used for PIT. In vitro PIT was evaluated by measuring cytotoxicity with dead staining and a decrease in GFP fluorescence. In vivo PIT was evaluated in a disseminated peritoneal carcinomatosis model and a flank xenograft using tumor volume measurements and GFP fluorescence intensity. In vivo anti-tumor effects of PIT were confirmed by significant reductions in tumor volume (at day 15, p<0.0001 vs. control) and GFP fluorescence intensity (flank model: at day 3, PIT treated vs. control p<0.01 and peritoneal disseminated model: at day 3 PIT treated vs. control, p<0.05). Cytotoxic effects in vitro were shown to be dependent on the light dose and caused necrotic cell rupture leading to GFP release and a decrease in fluorescence intensity in vitro. Thus, loss of GFP fluorescence served as a useful biomarker of cell necrosis after PIT. JF - PloS one AU - Sato, Kazuhide AU - Choyke, Peter L AU - Kobayashi, Hisataka AD - Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 11 KW - Antineoplastic Agents KW - 0 KW - Immunoconjugates KW - Photosensitizing Agents KW - Green Fluorescent Proteins KW - 147336-22-9 KW - Trastuzumab KW - P188ANX8CK KW - Index Medicus KW - Animals KW - Apoptosis KW - Combined Modality Therapy KW - Humans KW - Tumor Burden KW - Mice, Nude KW - Mice KW - Cell Proliferation KW - Microscopy, Fluorescence KW - Tumor Cells, Cultured KW - Xenograft Model Antitumor Assays KW - Flow Cytometry KW - Antineoplastic Agents -- therapeutic use KW - Fluorescent Antibody Technique KW - Green Fluorescent Proteins -- metabolism KW - Female KW - Immunoenzyme Techniques KW - Stomach Neoplasms -- pathology KW - Stomach Neoplasms -- immunology KW - Peritoneal Neoplasms -- secondary KW - Peritoneal Neoplasms -- immunology KW - Immunotherapy KW - Stomach Neoplasms -- therapy KW - Photosensitizing Agents -- therapeutic use KW - Trastuzumab -- therapeutic use KW - Phototherapy KW - Peritoneal Neoplasms -- therapy KW - Immunoconjugates -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1626162789?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Photoimmunotherapy+of+gastric+cancer+peritoneal+carcinomatosis+in+a+mouse+model.&rft.au=Sato%2C+Kazuhide%3BChoyke%2C+Peter+L%3BKobayashi%2C+Hisataka&rft.aulast=Sato&rft.aufirst=Kazuhide&rft.date=2014-01-01&rft.volume=9&rft.issue=11&rft.spage=e113276&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0113276 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-01 N1 - Date created - 2014-11-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Bioconjug Chem. 2012 Mar 21;23(3):604-9 [22369484] Int J Cancer. 2014 Dec 1;135(11):2697-710 [24740257] Proc Natl Acad Sci U S A. 2000 Feb 1;97(3):1206-11 [10655509] Oncology. 2000 Feb;58(2):96-107 [10705236] J Immunol Methods. 2000 Sep 21;243(1-2):167-90 [10986414] Lancet Oncol. 2002 Sep;3(9):546-56 [12217792] Cancer Res. 2003 Sep 1;63(17):5521-5 [14500389] Cancer Res. 2004 Mar 1;64(5):1828-33 [14996746] J Immunol. 1983 Mar;130(3):1473-7 [6185591] J Immunol Methods. 1998 Aug 1;217(1-2):153-63 [9776585] Nat Rev Cancer. 2005 Oct;5(10):796-806 [16195751] Mol Biol Cell. 2011 Sep;22(17):3103-19 [21775625] J Cell Biochem. 2010 Aug 15;110(6):1439-46 [20506255] Br J Surg. 2006 Dec;93(12):1530-5 [17051604] Nat Med. 2011 Dec;17(12):1685-91 [22057348] Cancer Res. 2012 Sep 15;72(18):4622-8 [22800710] PLoS One. 2012;7(10):e47927 [23112873] ACS Nano. 2013 Jan 22;7(1):717-24 [23214407] Gastroenterol Clin North Am. 2013 Jun;42(2):219-40 [23639638] Theranostics. 2013;3(6):357-65 [23781283] Int J Cancer. 2014 Feb 1;134(3):622-8 [23832847] Proc Natl Acad Sci U S A. 2014 Mar 11;111(10):E933-42 [24572574] Eur J Cancer. 2014 May;50(7):1330-44 [24650579] Mol Oncol. 2014 May;8(3):620-32 [24508062] Gastric Cancer. 2014 Oct;17(4):638-47 [24414131] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0113276 ER - TY - JOUR T1 - A murine inhalation model to characterize pulmonary exposure to dry Aspergillus fumigatus conidia. AN - 1618161981; 25340353 AB - Most murine models of fungal exposure are based on the delivery of uncharacterized extracts or liquid conidia suspensions using aspiration or intranasal approaches. Studies that model exposure to dry fungal aerosols using whole body inhalation have only recently been described. In this study, we aimed to characterize pulmonary immune responses following repeated inhalation of conidia utilizing an acoustical generator to deliver dry fungal aerosols to mice housed in a nose only exposure chamber. Immunocompetent female BALB/cJ mice were exposed to conidia derived from Aspergillus fumigatus wild-type (WT) or a melanin-deficient (Δalb1) strain. Conidia were aerosolized and delivered to mice at an estimated deposition dose of 1×105 twice a week for 4 weeks (8 total). Histopathological and immunological endpoints were assessed 4, 24, 48, and 72 hours after the final exposure. Histopathological analysis showed that conidia derived from both strains induced lung inflammation, especially at 24 and 48 hour time points. Immunological endpoints evaluated in bronchoalveolar lavage fluid (BALF) and the mediastinal lymph nodes showed that exposure to WT conidia led to elevated numbers of macrophages, granulocytes, and lymphocytes. Importantly, CD8+ IL17+ (Tc17) cells were significantly higher in BALF and positively correlated with germination of A. fumigatus WT spores. Germination was associated with specific IgG to intracellular proteins while Δalb1 spores elicited antibodies to cell wall hydrophobin. These data suggest that inhalation exposures may provide a more representative analysis of immune responses following exposures to environmentally and occupationally prevalent fungal contaminants. JF - PloS one AU - Buskirk, Amanda D AU - Green, Brett J AU - Lemons, Angela R AU - Nayak, Ajay P AU - Goldsmith, W Travis AU - Kashon, Michael L AU - Anderson, Stacey E AU - Hettick, Justin M AU - Templeton, Steven P AU - Germolec, Dori R AU - Beezhold, Donald H AD - Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia, United States of America. ; Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia, United States of America. ; Biostatistics and Epidemiology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia, United States of America. ; Toxicology Branch, National Toxicology Program Division, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 10 KW - Antibodies, Fungal KW - 0 KW - Cytokines KW - Immunoglobulin G KW - Index Medicus KW - Animals KW - Hyphae -- physiology KW - Cell Count KW - Acoustics KW - Lymph Nodes -- pathology KW - Disease Models, Animal KW - Antibodies, Fungal -- immunology KW - Cytokines -- metabolism KW - Mice, Inbred BALB C KW - Cell Proliferation KW - Proteomics KW - Antibody Formation -- immunology KW - Flow Cytometry KW - Immunoglobulin G -- metabolism KW - Administration, Inhalation KW - Species Specificity KW - Bronchoalveolar Lavage Fluid -- cytology KW - Female KW - Inhalation Exposure KW - Aspergillus fumigatus -- physiology KW - Spores, Fungal -- physiology KW - Lung -- pathology KW - Lung -- microbiology KW - Aspergillus fumigatus -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618161981?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+murine+inhalation+model+to+characterize+pulmonary+exposure+to+dry+Aspergillus+fumigatus+conidia.&rft.au=Buskirk%2C+Amanda+D%3BGreen%2C+Brett+J%3BLemons%2C+Angela+R%3BNayak%2C+Ajay+P%3BGoldsmith%2C+W+Travis%3BKashon%2C+Michael+L%3BAnderson%2C+Stacey+E%3BHettick%2C+Justin+M%3BTempleton%2C+Steven+P%3BGermolec%2C+Dori+R%3BBeezhold%2C+Donald+H&rft.aulast=Buskirk&rft.aufirst=Amanda&rft.date=2014-01-01&rft.volume=9&rft.issue=10&rft.spage=e109855&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0109855 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-25 N1 - Date created - 2014-10-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Med Mycol. 2010 Mar;48(2):217-28 [20055736] BMB Rep. 2009 Dec 31;42(12):776-87 [20044948] Med Mycol. 2010 Dec;48(8):1056-65 [20482452] Infect Immun. 2011 Jan;79(1):125-35 [21041495] Fungal Biol. 2011 Jan;115(1):21-9 [21215951] PLoS One. 2011;6(4):e18777 [21533200] Clin Exp Allergy. 2011 Jul;41(7):1022-30 [21545549] Infect Immun. 2012 Jan;80(1):388-97 [22064716] Blood. 2012 Jan 26;119(4):967-77 [22147891] PLoS Pathog. 2012;8(7):e1002771 [22829762] J Allergy Clin Immunol. 2012 Sep;130(3):803-805.e6 [22608571] J Proteome Res. 2013 Jun 7;12(6):2552-70 [23656496] J Immunol. 2014 Feb 15;192(4):1745-52 [24442441] J Immunotoxicol. 2014 Apr-Jun;11(2):180-9 [23919459] Allergy. 2000 May;55(5):501-4 [10843433] J Allergy Clin Immunol. 2001 Feb;107(2):388-90 [11174210] J Allergy Clin Immunol. 2003 Feb;111(2):285-9 [12589346] J Microbiol Methods. 2003 Sep;54(3):295-313 [12842477] Nat Rev Immunol. 2003 Dec;3(12):994-1003 [14647481] Int J Exp Pathol. 1991 Aug;72(4):387-95 [1883739] Appl Environ Microbiol. 1998 Oct;64(10):3620-5 [9758776] J Bacteriol. 1999 Oct;181(20):6469-77 [10515939] J Allergy Clin Immunol. 2005 May;115(5):1043-8 [15867864] J Exp Med. 2005 May 16;201(10):1555-65 [15897273] Chem Immunol Allergy. 2006;91:121-33 [16354954] Med Mycol. 2006 Sep;44 Suppl 1:S245-55 [17050446] Nat Rev Immunol. 2006 Nov;6(11):869-74 [17063187] Rapid Commun Mass Spectrom. 2007;21(5):730-44 [17279597] J Immunol Methods. 2007 Oct 31;327(1-2):63-74 [17716680] J Immunol. 2007 Dec 1;179(11):7791-9 [18025225] Int Arch Allergy Immunol. 2008;145(1):58-86 [17709917] Curr Protoc Immunol. 2007 Aug;Chapter 6:Unit 6.24 [18432993] Am J Physiol Lung Cell Mol Physiol. 2008 Oct;295(4):L552-65 [18658273] J Immunol. 2009 Mar 15;182(6):3469-81 [19265125] Nature. 2009 Aug 27;460(7259):1117-21 [19713928] Inhal Toxicol. 2009 Oct;21(12):1053-61 [19555230] Crit Rev Toxicol. 2009;39(10):799-864 [19863384] Immunobiology. 2010 Nov;215(11):915-20 [19939494] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0109855 ER - TY - JOUR T1 - Effect of antigen shedding on targeted delivery of immunotoxins in solid tumors from a mathematical model. AN - 1618151061; 25343405 AB - Most cancer-specific antigens used as targets of antibody-drug conjugates and immunotoxins are shed from the cell surface (Zhang & Pastan (2008) Clin. Cancer Res. 14: 7981-7986), although at widely varying rates and by different mechanisms (Dello Sbarba & Rovida (2002) Biol. Chem. 383: 69-83). Why many cancer-specific antigens are shed and how the shedding affects delivery efficiency of antibody-based protein drugs are poorly understood questions at present. Before a detailed numerical study, it was assumed that antigen shedding would reduce the efficacy of antibody-drug conjugates and immunotoxins. However, our previous study using a comprehensive mathematical model showed that antigen shedding can significantly improve the efficacy of the mesothelin-binding immunotoxin, SS1P (anti-mesothelin-Fv-PE38), and suggested that receptor shedding can be a general mechanism for enhancing the effect of inter-cellular signaling molecules. Here, we improved this model and applied it to both SS1P and another recombinant immunotoxin, LMB-2, which targets CD25. We show that the effect of antigen shedding is influenced by a number of factors including the number of antigen molecules on the cell surface and the endocytosis rate. The high shedding rate of mesothelin is beneficial for SS1P, for which the antigen is large in number and endocytosed rapidly. On the other hand, the slow shedding of CD25 is beneficial for LMB-2, for which the antigen is small in number and endocytosed slowly. JF - PloS one AU - Pak, Youngshang AU - Pastan, Ira AU - Kreitman, Robert J AU - Lee, Byungkook AD - Department of Chemistry and Institute of Functional Materials, Pusan National University, Busan, Republic of Korea; Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 10 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Neoplasm KW - B3(Fv)-PE38KDEL recombinant immunotoxin KW - Exotoxins KW - SS1(dsFv)PE38 KW - Index Medicus KW - Animals KW - Exotoxins -- pharmacology KW - Tumor Burden -- drug effects KW - Kinetics KW - Humans KW - Endocytosis -- drug effects KW - Exotoxins -- therapeutic use KW - Models, Biological KW - Neoplasms -- drug therapy KW - Drug Delivery Systems KW - Antibodies, Monoclonal -- pharmacology KW - Antigens, Neoplasm -- immunology KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1618151061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+antigen+shedding+on+targeted+delivery+of+immunotoxins+in+solid+tumors+from+a+mathematical+model.&rft.au=Pak%2C+Youngshang%3BPastan%2C+Ira%3BKreitman%2C+Robert+J%3BLee%2C+Byungkook&rft.aulast=Pak&rft.aufirst=Youngshang&rft.date=2014-01-01&rft.volume=9&rft.issue=10&rft.spage=e110716&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0110716 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-26 N1 - Date created - 2014-10-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Chem Rev. 2002 Dec;102(12):4627-38 [12475204] Biol Chem. 2002 Jan;383(1):69-83 [11928824] Microvasc Res. 1985 Sep;30(2):246-8 [4046874] Ann Intern Med. 1986 Oct;105(4):560-72 [3019203] Cancer Res. 1989 Aug 15;49(16):4557-61 [2743340] J Nucl Med. 1990 Jul;31(7):1191-8 [2362198] J Immunol. 1990 Dec 15;145(12):4131-5 [2258611] Blood. 1994 Jan 15;83(2):426-34 [8286741] J Exp Med. 1996 Apr 1;183(4):1587-602 [8666917] Cancer Res. 1998 Mar 1;58(5):968-75 [9500458] Nat Biotechnol. 1996 Oct;14(10):1239-45 [9631086] Br J Cancer. 1964 Sep;13:490-502 [14219541] Nat Biotechnol. 2005 Sep;23(9):1147-57 [16151408] J Natl Cancer Inst. 2006 Mar 1;98(5):335-44 [16507830] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638] Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):17099-104 [17940013] Eur J Cancer. 2008 Jan;44(1):46-53 [17945478] Ann Biomed Eng. 2008 Mar;36(3):486-512 [18183487] Adv Drug Deliv Rev. 2008 Sep15;60(12):1421-34 [18541331] Mol Cancer Ther. 2008 Jul;7(7):2233-40 [18645032] Nat Clin Pract Oncol. 2008 Oct;5(10):588-99 [18695711] Clin Cancer Res. 2008 Dec 15;14(24):7981-6 [19088013] Clin Cancer Res. 2009 Sep 1;15(17):5323-37 [19723653] Mol Cancer Ther. 2009 Oct;8(10):2861-71 [19825804] Cancer Res. 2010 Feb 1;70(3):1082-9 [20103626] Cancer Res. 2011 Sep 1;71(17):5915-22 [21775520] Clin Cancer Res. 2012 Jan 1;18(1):152-60 [22068660] Cancer Res. 2012 Jul 1;72(13):3143-52 [22562466] Recent Pat Anticancer Drug Discov. 2014 Jan;9(1):35-65 [23477784] J Nucl Med. 2000 Apr;41(4):755-62 [10768579] Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8548-53 [10890891] Adv Drug Deliv Rev. 2001 Mar 1;46(1-3):149-68 [11259838] Cancer Res. 2001 Jul 1;61(13):5070-7 [11431343] Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):3937-42 [15217923] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0110716 ER - TY - JOUR T1 - The association between selenium and other micronutrients and thyroid cancer incidence in the NIH-AARP Diet and Health Study. AN - 1615261721; 25329812 AB - Selenium is an essential trace element that is important for thyroid hormone metabolism and has antioxidant properties which protect the thyroid gland from oxidative stress. The association of selenium, as well as intake of other micronutrients, with thyroid cancer is unclear. We evaluated associations of dietary selenium, beta-carotene, calcium, vitamin D, vitamin C, vitamin E, folate, magnesium, and zinc intake with thyroid cancer risk in the National Institutes of Health - American Association of Retired Persons Diet and Health Study, a large prospective cohort of 566,398 men and women aged 50-71 years in 1995-1996. Multivariable-adjusted Cox proportional hazards regression was used to examine associations between dietary intake of micronutrients, assessed using a food frequency questionnaire, and thyroid cancer cases, ascertained by linkage to state cancer registries and the National Death Index. With the exception of vitamin C, which was associated with an increased risk of thyroid cancer (HR(Q5 vs Q1), 1.34; 95% CI, 1.02-1.76; P(trend), <0.01), we observed no evidence of an association between quintile of selenium (HR(Q5 vs Q1), 1.23; 95% CI, 0.92-1.65; P(trend), 0.26) or other micronutrient intake and thyroid cancer. Our study does not suggest strong evidence for an association between dietary intake of selenium or other micronutrients and thyroid cancer risk. More studies are needed to clarify the role of selenium and other micronutrients in thyroid carcinogenesis. JF - PloS one AU - O'Grady, Thomas J AU - Kitahara, Cari M AU - DiRienzo, A Gregory AU - Gates, Margaret A AD - University at Albany, School of Public Health, Rensselaer, New York, United States of America. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 10 KW - Trace Elements KW - 0 KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - Prospective Studies KW - Risk Factors KW - National Cancer Institute (U.S.) KW - Humans KW - Incidence KW - Aged KW - Middle Aged KW - United States -- epidemiology KW - Male KW - Female KW - Thyroid Neoplasms -- epidemiology KW - Selenium -- adverse effects KW - Trace Elements -- adverse effects KW - Surveys and Questionnaires KW - Selenium -- administration & dosage KW - Trace Elements -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1615261721?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+association+between+selenium+and+other+micronutrients+and+thyroid+cancer+incidence+in+the+NIH-AARP+Diet+and+Health+Study.&rft.au=O%27Grady%2C+Thomas+J%3BKitahara%2C+Cari+M%3BDiRienzo%2C+A+Gregory%3BGates%2C+Margaret+A&rft.aulast=O%27Grady&rft.aufirst=Thomas&rft.date=2014-01-01&rft.volume=9&rft.issue=10&rft.spage=e110886&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0110886 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-29 N1 - Date created - 2014-10-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Nutr. 2010 Feb;140(2):317-24 [20032488] Cancer Causes Control. 2009 Jul;20(5):525-31 [19016336] Int J Cancer. 2010 Jun 15;126(12):2947-56 [19795465] Eur J Endocrinol. 2010 Sep;163(3):427-34 [20566590] Surgery. 2010 Dec;148(6):1147-52; discussion 1152-3 [21134545] Future Oncol. 2010 Nov;6(11):1771-9 [21142662] Cancer Epidemiol Biomarkers Prev. 2011 Mar;20(3):464-72 [21266520] Int J Cancer. 2011 Jul 1;129(1):160-72 [20824705] J Environ Public Health. 2011;2011:850105 [22187575] Int J Cancer. 2012 Mar 15;130(6):1411-9 [21544808] Thyroid. 2012 Apr;22(4):422-9 [22280227] Nutr Cancer. 2012;64(7):929-36 [23061901] Nutrients. 2012 Nov;4(11):1740-6 [23201844] Br J Nutr. 2013 Jan 14;109(1):118-28 [22455656] Clin Endocrinol (Oxf). 2013 Feb;78(2):155-64 [23046013] Eur J Cancer Prev. 2013 Mar;22(2):158-68 [22926510] Cochrane Database Syst Rev. 2014;3:CD005195 [24683040] Cancer Epidemiol Biomarkers Prev. 2014 Jun;23(6):1102-8 [24686895] J Clin Endocrinol Metab. 2014 Jun;99(6):E1031-4 [24601693] Am J Clin Nutr. 1999 Nov;70(5):896-903 [10539752] Am J Epidemiol. 2000 Aug 1;152(3):279-86 [10933275] Ann Epidemiol. 2002 Aug;12(6):395-401 [12160598] Eur J Cancer. 2002 Sep;38(13):1762-8 [12175693] Cancer Causes Control. 2002 Oct;13(8):765-75 [12420956] Eur J Cancer. 2003 Sep;39(13):1912-9 [12932671] Public Health Nutr. 2004 Feb;7(1A):187-200 [14972060] Am J Epidemiol. 1986 Jul;124(1):17-27 [3521261] Ann Clin Res. 1986;18(1):48-54 [3717873] Stat Med. 1989 May;8(5):551-61 [2657958] J Natl Cancer Inst. 1993 Feb 3;85(3):224-9 [8423627] Br J Cancer. 1993 Feb;67(2):330-40 [8431362] Am J Clin Nutr. 1993 Mar;57(3):408-13 [8438776] Cancer Causes Control. 1997 Mar;8(2):205-14 [9134245] Eur J Clin Nutr. 1998 May;52(5):363-7 [9630388] Environ Health Perspect. 1998 Aug;106(8):427-36 [9681969] Biochimie. 1999 May;81(5):527-33 [10403185] J Endocrinol. 2005 Mar;184(3):455-65 [15749805] Eur J Cancer Prev. 2006 Apr;15(2):178-86 [16523016] Public Health Nutr. 2008 Feb;11(2):183-95 [17610761] Cancer Causes Control. 2008 Aug;19(6):585-93 [18240001] Am J Clin Nutr. 2009 Jan;89(1):347-53 [19056579] Cancer Causes Control. 2009 Feb;20(1):75-86 [18766448] Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):784-91 [19240234] Epidemiology. 2010 May;21(3):389-95 [20335813] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0110886 ER - TY - JOUR T1 - Cysteine transport through excitatory amino acid transporter 3 (EAAT3). AN - 1586101928; 25275463 AB - Excitatory amino acid transporters (EAATs) limit glutamatergic signaling and maintain extracellular glutamate concentrations below neurotoxic levels. Of the five known EAAT isoforms (EAATs 1-5), only the neuronal isoform, EAAT3 (EAAC1), can efficiently transport the uncharged amino acid L-cysteine. EAAT3-mediated cysteine transport has been proposed to be a primary mechanism used by neurons to obtain cysteine for the synthesis of glutathione, a key molecule in preventing oxidative stress and neuronal toxicity. The molecular mechanisms underlying the selective transport of cysteine by EAAT3 have not been elucidated. Here we propose that the transport of cysteine through EAAT3 requires formation of the thiolate form of cysteine in the binding site. Using Xenopus oocytes and HEK293 cells expressing EAAT2 and EAAT3, we assessed the transport kinetics of different substrates and measured transporter-associated currents electrophysiologically. Our results show that L-selenocysteine, a cysteine analog that forms a negatively-charged selenolate ion at physiological pH, is efficiently transported by EAATs 1-3 and has a much higher apparent affinity for transport when compared to cysteine. Using a membrane tethered GFP variant to monitor intracellular pH changes associated with transport activity, we observed that transport of either L-glutamate or L-selenocysteine by EAAT3 decreased intracellular pH, whereas transport of cysteine resulted in cytoplasmic alkalinization. No change in pH was observed when cysteine was applied to cells expressing EAAT2, which displays negligible transport of cysteine. Under conditions that favor release of intracellular substrates through EAAT3 we observed release of labeled intracellular glutamate but did not detect cysteine release. Our results support a model whereby cysteine transport through EAAT3 is facilitated through cysteine de-protonation and that once inside, the thiolate is rapidly re-protonated. Moreover, these findings suggest that cysteine transport is predominantly unidirectional and that reverse transport does not contribute to depletion of intracellular cysteine pools. JF - PloS one AU - Watts, Spencer D AU - Torres-Salazar, Delany AU - Divito, Christopher B AU - Amara, Susan G AD - Center for Neuroscience, Department of Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America. ; Laboratory of Cellular and Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States of America. ; Center for Neuroscience, Department of Neurobiology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America; Laboratory of Cellular and Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 10 KW - Excitatory Amino Acid Transporter 2 KW - 0 KW - Excitatory Amino Acid Transporter 3 KW - Selenocysteine KW - 0CH9049VIS KW - Glutamic Acid KW - 3KX376GY7L KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Excitatory Amino Acid Transporter 2 -- metabolism KW - Animals KW - Glutamic Acid -- metabolism KW - Oocytes -- metabolism KW - Selenocysteine -- metabolism KW - Hydrogen-Ion Concentration KW - Humans KW - HEK293 Cells KW - Xenopus KW - Cysteine -- metabolism KW - Excitatory Amino Acid Transporter 3 -- metabolism KW - Cysteine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1586101928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cysteine+transport+through+excitatory+amino+acid+transporter+3+%28EAAT3%29.&rft.au=Watts%2C+Spencer+D%3BTorres-Salazar%2C+Delany%3BDivito%2C+Christopher+B%3BAmara%2C+Susan+G&rft.aulast=Watts&rft.aufirst=Spencer&rft.date=2014-01-01&rft.volume=9&rft.issue=10&rft.spage=e109245&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0109245 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-22 N1 - Date created - 2014-10-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Neurosci. 2006 Jan;9(1):119-26 [16311588] Annu Rev Pharmacol Toxicol. 1999;39:431-56 [10331091] J Biol Chem. 2007 Nov 30;282(48):34719-26 [17908688] IUBMB Life. 2008 Sep;60(9):609-19 [18543277] Biochim Biophys Acta. 2009 Nov;1790(11):1424-8 [19477234] Biol Trace Elem Res. 2010 Jun;134(3):235-51 [20306235] J Biol Chem. 2011 Feb 4;286(5):3935-43 [21127051] Ann Neurol. 2011 Mar;69(3):509-20 [21446024] PLoS One. 2012;7(4):e35373 [22506078] J Biol Chem. 2013 Mar 22;288(12):8250-7 [23393130] Amino Acids. 2013 Jul;45(1):133-42 [23462929] Mol Pharmacol. 1999 Dec;56(6):1095-104 [10570036] J Gen Physiol. 2000 Nov;116(5):609-22 [11055990] J Biol Chem. 2000 Dec 1;275(48):37436-42 [10978338] Prog Neurobiol. 2001 Sep;65(1):1-105 [11369436] J Biol Chem. 2001 Jun 8;276(23):19723-8 [11262417] Biofactors. 2001;14(1-4):69-74 [11568442] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15324-9 [11752470] Neurochem Int. 2002 Nov;41(5):313-8 [12176072] J Neurochem. 2002 Aug;82(4):987-97 [12358804] Trends Neurosci. 1993 Oct;16(10):415-9 [7504357] J Neurosci. 1994 Sep;14(9):5559-69 [7521911] J Biol Chem. 1995 Jul 14;270(28):16561-8 [7622462] Neuron. 1995 Sep;15(3):721-8 [7546750] J Neurochem. 2003 Mar;84(6):1332-9 [12614333] Science. 2003 May 30;300(5624):1439-43 [12775843] FEBS Lett. 1986 Apr 7;199(1):95-9 [2869976] Nucleic Acids Res. 1987 Oct 26;15(20):8125-48 [3313277] Am J Physiol. 1989 Jan;256(1 Pt 1):G44-52 [2536240] J Cell Biol. 1989 Feb;108(2):613-24 [2918027] J Biol Chem. 1993 Jul 25;268(21):15329-32 [8101838] J Biol Chem. 1996 Jun 21;271(25):14883-90 [8662767] J Physiol. 1996 Jun 1;493 ( Pt 2):419-23 [8782106] Annu Rev Biochem. 1996;65:83-100 [8811175] J Neurosci. 1996 Nov 1;16(21):6722-31 [8824313] Nature. 1996 Oct 17;383(6601):634-7 [8857541] J Biol Chem. 1996 Nov 8;271(45):27991-4 [8910405] J Neurosci. 1998 Dec 1;18(23):9620-8 [9822723] Biochemistry. 1999 Apr 27;38(17):5296-301 [10220315] Proc Natl Acad Sci U S A. 2007 Nov 13;104(46):18025-30 [17991780] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0109245 ER - TY - JOUR T1 - Examination of the ligand-binding and enzymatic properties of a bilin-binding protein from the poisonous caterpillar Lonomia obliqua. AN - 1542004600; 24972000 AB - The bilin-binding proteins (BBP) from lepidopteran insects are members of the lipocalin family of proteins and play a special role in pigmentation through the binding of biliverdin IXγ. Lopap, a BBP-like protein from the venom of the toxic caterpillar Lonomia obliqua has been reported to act as a serine protease that activates the coagulation proenzyme prothrombin. Here we show that BBPLo, a variant of lopap from the same organism binds biliverdin IXγ, forming a complex that is spectrally identical with previously described BBP proteins. Although BBPLo is nearly identical in sequence to lopap, no prothrombinase activity was detected in our recombinant preparations using reconstituted systems containing coagulation factors Xa and Va, as well as anionic phospholipids. In addition to biliverdin, BBPLo was found to form a 1:1 complex with heme prompting us to examine whether the unusual biliverdin IXγ ligand of BBPs forms as a result of oxidation of bound heme in situ rather than by a conventional heme oxygenase. Using ascorbate or a NADPH(+)-ferredoxin reductase-ferredoxin system as a source of reducing equivalents, spectral changes are seen that suggest an initial reduction of heme to the Fe(II) state and formation of an oxyferrous complex. The complex then disappears and a product identified as a 5-coordinate carbonyl complex of verdoheme, an intermediate in the biosynthesis of biliverdin, is formed. However, further reaction to form biliverdin was not observed, making it unlikely that biliverdin IXγ is formed by this pathway. JF - PloS one AU - Veiga, Ana B G AU - Ribeiro, José M C AU - Francischetti, Ivo M B AU - Xu, Xueqing AU - Guimarães, Jorge A AU - Andersen, John F AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Rockville, Maryland, United States of America; Center of Biotechnology, Universidade Federal do Rio Grande do Sul, Porto Alegre RS, Brazil. ; Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Rockville, Maryland, United States of America. ; Center of Biotechnology, Universidade Federal do Rio Grande do Sul, Porto Alegre RS, Brazil. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 6 KW - Bile Pigments KW - 0 KW - Insect Proteins KW - Ligands KW - Heme KW - 42VZT0U6YR KW - Ferredoxin-NADP Reductase KW - EC 1.18.1.2 KW - Endopeptidases KW - EC 3.4.- KW - Index Medicus KW - Oxidation-Reduction KW - Animals KW - Heme -- chemistry KW - Molecular Sequence Data KW - Heme -- pharmacology KW - Ferredoxin-NADP Reductase -- chemistry KW - Heme -- analogs & derivatives KW - Amino Acid Sequence KW - Substrate Specificity KW - Protein Binding KW - Lepidoptera -- enzymology KW - Insect Proteins -- chemistry KW - Bile Pigments -- pharmacology KW - Endopeptidases -- metabolism KW - Bile Pigments -- chemistry KW - Endopeptidases -- chemistry KW - Insect Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1542004600?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Examination+of+the+ligand-binding+and+enzymatic+properties+of+a+bilin-binding+protein+from+the+poisonous+caterpillar+Lonomia+obliqua.&rft.au=Veiga%2C+Ana+B+G%3BRibeiro%2C+Jos%C3%A9+M+C%3BFrancischetti%2C+Ivo+M+B%3BXu%2C+Xueqing%3BGuimar%C3%A3es%2C+Jorge+A%3BAndersen%2C+John+F&rft.aulast=Veiga&rft.aufirst=Ana+B&rft.date=2014-01-01&rft.volume=9&rft.issue=6&rft.spage=e95424&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0095424 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-26 N1 - Date created - 2014-06-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochemistry. 1999 Dec 14;38(50):16678-85 [10600131] Gene. 2005 Aug 1;355:11-27 [16023793] J Biol Chem. 2000 Apr 21;275(16):11686-92 [10766788] Biochem J. 2006 Sep 1;398(2):295-302 [16734589] J Biol Chem. 2000 Sep 29;275(39):30496-503 [10884386] Toxicon. 2001 Sep;39(9):1343-51 [11384722] J Am Chem Soc. 2001 Jul 18;123(28):6945-6 [11448209] Biochemistry. 2001 Sep 25;40(38):11327-37 [11560480] J Am Chem Soc. 2002 Dec 18;124(50):14879-92 [12475329] J Biol Chem. 2003 Feb 14;278(7):4611-7 [12464610] J Am Chem Soc. 2003 Apr 9;125(14):4103-10 [12670231] Thromb Res. 2003;111(1-2):95-101 [14644086] J Biol Chem. 2004 Oct 29;279(44):45791-802 [15310749] J Biol Chem. 1984 Nov 10;259(21):13159-65 [6386809] Biochemistry. 1985 Feb 26;24(5):1168-75 [4096898] Anal Biochem. 1987 Feb 15;161(1):1-15 [3578775] EMBO J. 1987 Jun;6(6):1565-70 [3608987] J Mol Biol. 1987 Dec 5;198(3):499-513 [3430616] Biochemistry. 1996 Jan 23;35(3):930-6 [8547275] Biochemistry. 1997 Dec 23;36(51):16141-6 [9405047] J Biol Chem. 1998 Jan 9;273(2):837-41 [9422739] Structure. 1998 Oct 15;6(10):1315-27 [9782054] Biochem J. 2005 May 1;387(Pt 3):871-7 [15617517] J Biol Chem. 2005 Jul 1;280(26):25022-8 [15866866] Curr Opin Chem Biol. 2000 Apr;4(2):221-7 [10742194] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0095424 ER - TY - JOUR T1 - Profiling animal toxicants by automatically mining public bioassay data: a big data approach for computational toxicology. AN - 1539713293; 24950175 AB - In vitro bioassays have been developed and are currently being evaluated as potential alternatives to traditional animal toxicity models. Already, the progress of high throughput screening techniques has resulted in an enormous amount of publicly available bioassay data having been generated for a large collection of compounds. When a compound is tested using a collection of various bioassays, all the testing results can be considered as providing a unique bio-profile for this compound, which records the responses induced when the compound interacts with different cellular systems or biological targets. Profiling compounds of environmental or pharmaceutical interest using useful toxicity bioassay data is a promising method to study complex animal toxicity. In this study, we developed an automatic virtual profiling tool to evaluate potential animal toxicants. First, we automatically acquired all PubChem bioassay data for a set of 4,841 compounds with publicly available rat acute toxicity results. Next, we developed a scoring system to evaluate the relevance between these extracted bioassays and animal acute toxicity. Finally, the top ranked bioassays were selected to profile the compounds of interest. The resulting response profiles proved to be useful to prioritize untested compounds for their animal toxicity potentials and form a potential in vitro toxicity testing panel. The protocol developed in this study could be combined with structure-activity approaches and used to explore additional publicly available bioassay datasets for modeling a broader range of animal toxicities. JF - PloS one AU - Zhang, Jun AU - Hsieh, Jui-Hua AU - Zhu, Hao AD - Department of Chemistry, Rutgers University, Camden, New Jersey, United States of America; The Rutgers Center for Computational and Integrative Biology, Camden, New Jersey, United States of America. ; Biomolecular Screening Branch, Division of National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 6 KW - Anti-Bacterial Agents KW - 0 KW - Hazardous Substances KW - Index Medicus KW - Rats KW - Animals KW - Data Mining KW - Humans KW - Toxicity Tests KW - Anti-Bacterial Agents -- toxicity KW - Drug Evaluation, Preclinical KW - Structure-Activity Relationship KW - Computational Biology -- methods KW - High-Throughput Screening Assays -- methods KW - Toxicology -- methods KW - Hazardous Substances -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1539713293?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Profiling+animal+toxicants+by+automatically+mining+public+bioassay+data%3A+a+big+data+approach+for+computational+toxicology.&rft.au=Zhang%2C+Jun%3BHsieh%2C+Jui-Hua%3BZhu%2C+Hao&rft.aulast=Zhang&rft.aufirst=Jun&rft.date=2014-01-01&rft.volume=9&rft.issue=6&rft.spage=e99863&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0099863 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-13 N1 - Date created - 2014-06-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: JAMA. 1993 Mar 24-31;269(12):1532-6 [8445816] Environ Health Perspect. 2013 Jul;121(7):A228 [23816934] Nat Rev Cancer. 2006 Oct;6(10):813-23 [16990858] Nat Protoc. 2006;1(3):1112-6 [17406391] Environ Health Perspect. 2008 Mar;116(3):284-91 [18335092] BMC Bioinformatics. 2008;9:401 [18817552] J Mol Graph Model. 2008 Nov;27(4):466-75 [18829357] Altern Lab Anim. 2008 Nov;36(5):503-19 [19025321] Toxicol In Vitro. 2009 Apr;23(3):476-85 [19159672] J Chem Inf Model. 2009 Feb;49(2):169-84 [19434821] Toxicol Sci. 2009 Jul;110(1):181-90 [19363143] Nucleic Acids Res. 2009 Jul;37(Web Server issue):W623-33 [19498078] Environ Health Perspect. 2009 Aug;117(8):1257-64 [19672406] J Chem Inf Model. 2009 Dec;49(12):2718-25 [19961205] J Mol Graph Model. 2010 Jan;28(5):420-6 [19897391] Environ Health Perspect. 2010 Apr;118(4):485-92 [20368123] Nat Rev Genet. 2010 Sep;11(9):647-57 [20717155] Nat Rev Genet. 2011 Mar;12(3):224 [21301474] Environ Health Perspect. 2011 Mar;119(3):364-70 [20980217] Nucleic Acids Res. 2012 Jan;40(Database issue):D1100-7 [21948594] Nucleic Acids Res. 2012 Jan;40(Database issue):D400-12 [22140110] Chem Res Toxicol. 2012 Jul 16;25(7):1287-302 [22519603] Molecules. 2013;18(1):735-56 [23299552] Chem Res Toxicol. 2013 Jun 17;26(6):878-95 [23611293] Environ Health Perspect. 1998 Apr;106 Suppl 2:497-503 [9599698] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0099863 ER - TY - JOUR T1 - Genome-wide binding of MBD2 reveals strong preference for highly methylated loci. AN - 1536682141; 24927503 AB - MBD2 is a subunit of the NuRD complex that is postulated to mediate gene repression via recruitment of the complex to methylated DNA. In this study we adopted an MBD2 tagging-approach to study its genome wide binding characteristics. We show that in vivo MBD2 is mainly recruited to CpG island promoters that are highly methylated. Interestingly, MBD2 binds around 1 kb downstream of the transcription start site of a subset of ∼ 400 CpG island promoters that are characterized by the presence of active histone marks, RNA polymerase II (Pol2) and low to medium gene expression levels and H3K36me3 deposition. These tagged-MBD2 binding sites in MCF-7 show increased methylation in a cohort of primary breast cancers but not in normal breast samples, suggesting a putative role for MBD2 in breast cancer. JF - PloS one AU - Menafra, Roberta AU - Brinkman, Arie B AU - Matarese, Filomena AU - Franci, Gianluigi AU - Bartels, Stefanie J J AU - Nguyen, Luan AU - Shimbo, Takashi AU - Wade, Paul A AU - Hubner, Nina C AU - Stunnenberg, Hendrik G AD - Department of Molecular Biology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen, Nijmegen, The Netherlands. ; Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 6 KW - DNA-Binding Proteins KW - 0 KW - MBD2 protein, human KW - RNA Polymerase II KW - EC 2.7.7.- KW - Index Medicus KW - Gene Expression Regulation, Neoplastic KW - Promoter Regions, Genetic KW - Humans KW - CpG Islands KW - Molecular Sequence Data KW - MCF-7 Cells KW - Sequence Analysis, RNA KW - Female KW - Binding Sites KW - Breast Neoplasms -- genetics KW - RNA Polymerase II -- metabolism KW - DNA-Binding Proteins -- chemistry KW - DNA Methylation KW - Breast Neoplasms -- metabolism KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1536682141?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genome-wide+binding+of+MBD2+reveals+strong+preference+for+highly+methylated+loci.&rft.au=Menafra%2C+Roberta%3BBrinkman%2C+Arie+B%3BMatarese%2C+Filomena%3BFranci%2C+Gianluigi%3BBartels%2C+Stefanie+J+J%3BNguyen%2C+Luan%3BShimbo%2C+Takashi%3BWade%2C+Paul+A%3BHubner%2C+Nina+C%3BStunnenberg%2C+Hendrik+G&rft.aulast=Menafra&rft.aufirst=Roberta&rft.date=2014-01-01&rft.volume=9&rft.issue=6&rft.spage=e99603&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0099603 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-26 N1 - Date created - 2014-06-14 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE54693; GEO N1 - SuppNotes - Cited By: Carcinogenesis. 2000 Mar;21(3):461-7 [10688866] PLoS Genet. 2013;9(12):e1004028 [24385926] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769] Science. 1975 Jan 24;187(4173):226-32 [1111098] Nature. 1983 Jan 6;301(5895):89-92 [6185846] Proc Natl Acad Sci U S A. 1984 May;81(9):2806-10 [6585829] Nature. 1986 May 15-21;321(6067):209-13 [2423876] Nat Genet. 1995 Mar;9(3):312-5 [7773295] Nature. 1997 Oct 16;389(6652):745-9 [9338788] Mol Cell Biol. 1998 Nov;18(11):6538-47 [9774669] Genes Dev. 1999 Aug 1;13(15):1924-35 [10444591] Mol Cell. 2005 Aug 5;19(3):381-91 [16061184] Mol Cell Biol. 2006 Feb;26(3):843-51 [16428440] Trends Biochem Sci. 2006 Feb;31(2):89-97 [16403636] EMBO Rep. 2006 Jun;7(6):628-34 [16648823] Science. 2007 Feb 23;315(5815):1141-3 [17322062] Mol Cell Biol. 2007 May;27(10):3750-7 [17353271] Mol Cell. 2008 Jun 20;30(6):755-66 [18514006] Pathobiology. 2008;75(5):281-7 [18931530] Nat Biotechnol. 2008 Dec;26(12):1367-72 [19029910] Elife. 2014;3:e02407 [24843027] Genome Res. 2014 Jun;24(6):896-905 [24714810] Nat Biotechnol. 2009 Apr;27(4):361-8 [19329998] BMC Genomics. 2010;11:137 [20181289] J Cell Biol. 2010 May 17;189(4):739-54 [20479470] PLoS One. 2010;5(8):e11982 [20700456] Methods. 2011 Apr;53(4):453-9 [21184827] Genes Dev. 2011 May 15;25(10):1010-22 [21576262] Cancer Res. 2011 Sep 1;71(17):5859-70 [21724586] EMBO J. 2011 Sep 14;30(18):3786-98 [21822215] Methods Mol Biol. 2012;809:105-20 [22113271] Genome Res. 2012 Feb;22(2):246-58 [22156296] Brief Funct Genomics. 2012 May;11(3):251-64 [22184333] PLoS One. 2012;7(8):e42822 [22912744] Nat Protoc. 2012 Sep;7(9):1728-40 [22936215] Nucleic Acids Res. 2013 Jan 7;41(1):e28 [23066101] Nucleic Acids Res. 2013 Mar 1;41(5):3010-21 [23361464] Cell. 2013 Apr 11;153(2):480-92 [23582333] PLoS Comput Biol. 2013;9(6):e1003100 [23818839] Cell Stem Cell. 2013 Sep 5;13(3):360-9 [23850244] Carcinogenesis. 2013 Dec;34(12):2738-49 [23955541] Genes Dev. 2000 Oct 1;14(19):2452-60 [11018013] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0099603 ER - TY - JOUR T1 - Coordinated regulation of nuclear receptor CAR by CCRP/DNAJC7, HSP70 and the ubiquitin-proteasome system. AN - 1521327612; 24789201 AB - The constitutive active/androstane receptor (CAR) plays an important role as a coordinate transcription factor in the regulation of various hepatic metabolic pathways for chemicals such as drugs, glucose, fatty acids, bilirubin, and bile acids. Currently, it is known that in its inactive state, CAR is retained in the cytoplasm in a protein complex with HSP90 and the tetratricopeptide repeat protein cytosoplasmic CAR retention protein (CCRP). Upon activation by phenobarbital (PB) or the PB-like inducer 1,4-bis[2-(3,5-dichloropyridyloxy)]-benzene (TCPOBOP), CAR translocates into the nucleus. We have identified two new components to the cytoplasmic regulation of CAR: ubiquitin-dependent degradation of CCRP and protein-protein interaction with HSP70. Treatment with the proteasome inhibitor MG132 (5 µM) causes CAR to accumulate in the cytoplasm of transfected HepG2 cells. In the presence of MG132, TCPOBOP increases CCRP ubiquitination in HepG2 cells co-expressing CAR, while CAR ubiquitination was not detected. MG132 treatment of HepG2 also attenuated of TCPOBOP-induced CAR transcriptional activation on reporter constructs which contain CAR-binding DNA elements derived from the human CYP2B6 gene. The elevation of cytoplasmic CAR protein with MG132 correlated with an increase of HSP70, and to a lesser extent HSP60. Both CCRP and CAR were found to interact with endogenous HSP70 in HepG2 cells by immunoprecipitation analysis. Induction of HSP70 levels by heat shock also increased cytoplasmic CAR levels, similar to the effect of MG132. Lastly, heat shock attenuated TCPOBOP-induced CAR transcriptional activation, also similar to the effect of MG132. Collectively, these data suggest that ubiquitin-proteasomal regulation of CCRP and HSP70 are important contributors to the regulation of cytoplasmic CAR levels, and hence the ability of CAR to respond to PB or PB-like inducers. JF - PloS one AU - Timsit, Yoav E AU - Negishi, Masahiko AD - The Pharmacogenetics Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 5 KW - Dnajc7 protein, mouse KW - 0 KW - HSP70 Heat-Shock Proteins KW - Leupeptins KW - Ligands KW - Proteasome Inhibitors KW - Pyridines KW - Receptors, Cytoplasmic and Nuclear KW - Ubiquitin KW - constitutive androstane receptor KW - 1,4-bis(2-(3,5-dichloropyridyloxy))benzene KW - 76150-91-9 KW - Proteasome Endopeptidase Complex KW - EC 3.4.25.1 KW - benzyloxycarbonylleucyl-leucyl-leucine aldehyde KW - RF1P63GW3K KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Animals KW - Proteasome Inhibitors -- pharmacology KW - Dose-Response Relationship, Drug KW - Humans KW - Transcriptional Activation -- drug effects KW - Mice KW - Cytoplasm -- drug effects KW - Leupeptins -- pharmacology KW - Phenobarbital -- pharmacology KW - Hep G2 Cells KW - Ubiquitination -- drug effects KW - Cytoplasm -- metabolism KW - Heat-Shock Response -- drug effects KW - Pyridines -- pharmacology KW - HSP70 Heat-Shock Proteins -- metabolism KW - Ubiquitin -- metabolism KW - Proteasome Endopeptidase Complex -- metabolism KW - Receptors, Cytoplasmic and Nuclear -- metabolism KW - Receptors, Cytoplasmic and Nuclear -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1521327612?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Coordinated+regulation+of+nuclear+receptor+CAR+by+CCRP%2FDNAJC7%2C+HSP70+and+the+ubiquitin-proteasome+system.&rft.au=Timsit%2C+Yoav+E%3BNegishi%2C+Masahiko&rft.aulast=Timsit&rft.aufirst=Yoav&rft.date=2014-01-01&rft.volume=9&rft.issue=5&rft.spage=e96092&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0096092 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-22 N1 - Date created - 2014-05-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2001 Nov 16;276(46):42938-44 [11557750] Anticancer Res. 2001 Jan-Feb;21(1A):295-300 [11299751] Arch Biochem Biophys. 2003 Feb 1;410(1):134-40 [12559985] J Biol Chem. 2003 May 9;278(19):17277-83 [12611900] EMBO J. 2003 Jul 15;22(14):3613-23 [12853476] FEBS Lett. 2003 Jul 31;548(1-3):17-20 [12885400] J Steroid Biochem Mol Biol. 2003 Jun;85(2-5):133-8 [12943697] Mol Pharmacol. 2003 Nov;64(5):1069-75 [14573755] Oncogene. 2004 Mar 15;23(11):2057-70 [15021893] Genes Cells. 2004 Jun;9(6):533-48 [15189447] J Biol Chem. 2004 Jul 16;279(29):30643-53 [15107424] Cancer Res. 2004 Oct 15;64(20):7197-200 [15492232] Anal Biochem. 1976 May 7;72:248-54 [942051] J Biol Chem. 1991 Nov 5;266(31):21150-7 [1718971] Mol Cell Biol. 1994 Mar;14(3):1544-52 [8114692] Gene. 1995 Jun 9;158(2):263-8 [7607552] J Biol Chem. 1996 Apr 19;271(16):9746-53 [8621653] J Biol Chem. 1996 Oct 4;271(40):24769-75 [8798747] Toxicol Appl Pharmacol. 1996 Nov;141(1):117-23 [8917683] J Biol Chem. 1997 Sep 19;272(38):23565-71 [9295294] J Biochem Mol Toxicol. 1998;12(1):3-9 [9414482] Trends Biochem Sci. 1998 Jun;23(6):222-7 [9644977] J Steroid Biochem Mol Biol. 1998 Apr;65(1-6):51-8 [9699857] Nature. 1998 Oct 8;395(6702):612-5 [9783588] J Biol Chem. 1999 Mar 5;274(10):6043-6 [10037683] Mol Cell Biol. 1999 Jun;19(6):4535-45 [10330192] Mol Cell Biol. 1999 Sep;19(9):6318-22 [10454578] EMBO J. 2004 Dec 8;23(24):4813-23 [15538384] Mol Cell. 2004 Dec 22;16(6):893-905 [15610733] J Biol Chem. 2005 Feb 4;280(5):3458-66 [15563456] Mol Endocrinol. 2005 Jun;19(6):1646-53 [15831521] Hepatology. 2005 Nov;42(5):1118-26 [16231353] FEBS Lett. 2005 Dec 19;579(30):6733-6 [16310787] Methods Enzymol. 2005;399:243-8 [16338360] Mol Pharmacol. 2006 Apr;69(4):1095-102 [16377764] Handb Exp Pharmacol. 2006;(172):111-38 [16610357] Annu Rev Biomed Eng. 2006;8:403-24 [16834562] Biochem J. 2006 Aug 15;398(1):125-33 [16623664] J Cell Biochem. 2006 Nov 1;99(4):1085-95 [16767695] J Pharmacol Exp Ther. 2007 Jan;320(1):307-13 [17050775] Steroids. 2007 Mar;72(3):231-46 [17284330] Mol Pharmacol. 2007 May;71(5):1217-21 [17314319] FEBS Lett. 2007 Oct 16;581(25):4937-42 [17904126] Mol Pharmacol. 2008 Apr;73(4):1113-21 [18202305] J Biol Chem. 2008 Apr 18;283(16):10425-32 [18303024] Drug Metab Dispos. 2008 Jul;36(7):1189-93 [18362160] Biochemistry. 2008 Aug 5;47(31):8203-13 [18620420] Annu Rev Biochem. 2012;81:231-59 [22404628] Sci Signal. 2013 May 7;6(274):ra31 [23652203] Biochem J. 2014 Feb 15;458(1):95-107 [24224465] Cell Mol Life Sci. 2002 May;59(5):821-31 [12088282] Mol Cell Biol. 2000 May;20(9):2951-8 [10757780] Nature. 2000 Oct 19;407(6806):920-3 [11057673] Nat Cell Biol. 2001 Jan;3(1):93-6 [11146632] Mol Pharmacol. 2002 Jan;61(1):1-6 [11752199] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0096092 ER - TY - JOUR T1 - Effects of calorie restriction and diet-induced obesity on murine colon carcinogenesis, growth and inflammatory factors, and microRNA expression. AN - 1516722074; 24732966 AB - Obesity is an established colon cancer risk factor, while preventing or reversing obesity via a calorie restriction (CR) diet regimen decreases colon cancer risk. Unfortunately, the biological mechanisms underlying these associations are poorly understood, hampering development of mechanism-based approaches for preventing obesity-related colon cancer. We tested the hypotheses that diet-induced obesity (DIO) would increase (and CR would decrease) colon tumorigenesis in the mouse azoxymethane (AOM) model. In addition, we established that changes in inflammatory cytokines, growth factors, and microRNAs are associated with these energy balance-colon cancer links, and thus represent mechanism-based targets for colon cancer prevention. Mice were injected with AOM once a week for 5 weeks and randomized to: 1) control diet; 2) 30% CR diet; or 3) DIO diet. Mice were euthanized at week 5 (n = 12/group), 10 (n = 12/group), and 20 (n = 20/group) after the last AOM injection. Colon tumors were counted, and cytokines, insulin-like growth factor 1 (IGF-1), IGF binding protein 3 (IGFBP-3), adipokines, proliferation, apoptosis, and expression of microRNAs (miRs) were measured. The DIO diet regimen induced an obese phenotype (∼36% body fat), while CR induced a lean phenotype (∼14% body fat); controls were intermediate (∼26% body fat). Relative to controls, DIO increased (and CR decreased) the number of colon tumors (p = 0.01), cytokines (p<0.001), IGF-1 (p = 0.01), and proliferation (p<0.001). DIO decreased (and CR increased) IGFBP-3 and apoptosis (p<0.001). miRs including mir-425, mir-196, mir-155, mir-150, mir-351, mir-16, let-7, mir34, and mir-138 were differentially expressed between the dietary groups. We conclude that the enhancing effects of DIO and suppressive effects of CR on colon carcinogenesis are associated with alterations in several biological pathways, including inflammation, IGF-1, and microRNAs. JF - PloS one AU - Olivo-Marston, Susan E AU - Hursting, Stephen D AU - Perkins, Susan N AU - Schetter, Aaron AU - Khan, Mohammed AU - Croce, Carlo AU - Harris, Curtis C AU - Lavigne, Jackie AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland, United States of America; Division of Epidemioogy, The Ohio State University College of Public Health, Columbus, Ohio, United States of America. ; Department of Nutritional Sciences, University of Texas-Austin, Austin, Texas, United States of America; Department of Molecular Carcinogenesis, University of Texas-MD Anderson Cancer Center, Smithville, Texas, United States of America. ; Center for Cancer Training, The National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Laboratory of Human Carcinogenesis, National Cancer Institute, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University College of Medicine, Columbus, Ohio, United States of America. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 4 KW - Adipokines KW - 0 KW - Cytokines KW - Insulin-Like Growth Factor Binding Protein 3 KW - MicroRNAs KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Index Medicus KW - Animals KW - Glucose Tolerance Test KW - Apoptosis KW - Random Allocation KW - Insulin-Like Growth Factor I -- metabolism KW - Mice KW - Body Composition KW - Cytokines -- metabolism KW - Cell Proliferation KW - Body Weight KW - Risk Factors KW - Carcinogenesis KW - Inflammation -- metabolism KW - Adipokines -- metabolism KW - Insulin-Like Growth Factor Binding Protein 3 -- metabolism KW - Male KW - Gene Expression Regulation, Neoplastic KW - MicroRNAs -- metabolism KW - Colonic Neoplasms -- complications KW - Caloric Restriction KW - Diet KW - Colonic Neoplasms -- pathology KW - Obesity -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1516722074?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+calorie+restriction+and+diet-induced+obesity+on+murine+colon+carcinogenesis%2C+growth+and+inflammatory+factors%2C+and+microRNA+expression.&rft.au=Olivo-Marston%2C+Susan+E%3BHursting%2C+Stephen+D%3BPerkins%2C+Susan+N%3BSchetter%2C+Aaron%3BKhan%2C+Mohammed%3BCroce%2C+Carlo%3BHarris%2C+Curtis+C%3BLavigne%2C+Jackie&rft.aulast=Olivo-Marston&rft.aufirst=Susan&rft.date=2014-01-01&rft.volume=9&rft.issue=4&rft.spage=e94765&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0094765 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-19 N1 - Date created - 2014-04-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Epidemiol Biomarkers Prev. 2000 Apr;9(4):345-9 [10794477] Dig Dis Sci. 2000 May;45(5):890-5 [10795750] Growth Horm IGF Res. 2000 Apr;10 Suppl A:S30-1 [10984283] Gastroenterology. 2001 Jul;121(1):79-90 [11438496] J Nutr. 2001 Nov;131(11 Suppl):3109S-20S [11694656] Gut. 2002 May;50(5):642-6 [11950809] Annu Rev Med. 2003;54:131-52 [12525670] Cancer Res. 2003 Apr 15;63(8):1752-5 [12702556] Cancer Res. 2003 Oct 15;63(20):6595-601 [14583451] Proc Natl Acad Sci U S A. 2004 Jun 29;101(26):9740-4 [15210942] J Natl Cancer Inst. 1982 Feb;68(2):249-57 [6278189] Cancer Res. 1987 Mar 1;47(5):1226-8 [3815332] Cancer Res. 1987 Jun 1;47(11):2759-62 [3567901] Nutr Cancer. 1987;9(4):199-217 [3299283] Jpn J Cancer Res. 1989 Jan;80(1):51-8 [2540132] Cancer Res. 1990 Sep 15;50(18):5761-6 [2393850] Prev Med. 1993 Sep;22(5):750-66 [8234215] Ann Intern Med. 1995 Mar 1;122(5):327-34 [7847643] Cancer Causes Control. 1996 Mar;7(2):253-63 [8740738] Cancer Res. 1997 Jan 1;57(1):75-80 [8988044] Clin Cancer Res. 2005 May 15;11(10):3642-6 [15897559] Cancer Epidemiol Biomarkers Prev. 2005 Jul;14(7):1646-52 [16030096] Carcinogenesis. 2005 Sep;26(9):1563-72 [15888492] Nat Rev Immunol. 2005 Oct;5(10):749-59 [16175180] J Natl Cancer Inst. 2005 Nov 16;97(22):1688-94 [16288122] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460] Cancer Cell. 2006 Mar;9(3):189-98 [16530703] Expert Opin Investig Drugs. 2006 Aug;15(8):917-31 [16859394] Endocrinology. 2006 Dec;147(12):5826-34 [16959846] Am J Clin Nutr. 2007 Apr;85(4):1121-6 [17413114] Curr Cancer Drug Targets. 2007 Aug;7(5):484-91 [17691908] JAMA. 2008 Jan 30;299(4):425-36 [18230780] Nutr Cancer. 2008;60(1):61-8 [18444137] Nutr Cancer. 2008;60(3):373-81 [18444172] Cancer Res. 2008 Jun 1;68(11):4123-32 [18519671] Mol Carcinog. 2008 Sep;47(9):667-77 [18240295] Cancer Res. 2008 Nov 15;68(22):9423-32 [19010917] Cancer Prev Res (Phila). 2008 Jun;1(1):65-76 [19138937] Cancer Prev Res (Phila). 2009 Jan;2(1):60-9 [19139019] Diabetes Obes Metab. 2009 Apr;11(4):343-54 [19267713] World J Gastroenterol. 2009 May 7;15(17):2089-96 [19418581] Gut. 2009 Aug;58(8):1169; author reply 1169-70 [19592697] Mol Carcinog. 2009 Dec;48(12):1071-6 [19760669] World J Gastroenterol. 2010 Mar 14;16(10):1252-7 [20222170] J Gastroenterol Hepatol. 2010 May;25 Suppl 1:S129-33 [20586854] Mol Carcinog. 2011 May;50(5):370-82 [21480390] J Cell Physiol. 2011 Aug;226(8):2123-30 [21520064] Cancer Prev Res (Phila). 2011 Jul;4(7):1041-51 [21593197] Leukemia. 2011 Aug;25(8):1324-34 [21502955] Clin Exp Pharmacol Physiol. 2012 Feb;39(2):161-7 [21418088] Mol Biol Rep. 2012 May;39(5):5727-36 [22193626] J Nutr Biochem. 2012 Oct;23(10):1207-13 [22209007] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0094765 ER - TY - JOUR T1 - Cytocidal activities of topoisomerase 1 inhibitors and 5-azacytidine against pheochromocytoma/paraganglioma cells in primary human tumor cultures and mouse cell lines. AN - 1499137534; 24516563 AB - There is currently no effective treatment for metastatic pheochromocytomas and paragangliomas. A deficiency in current chemotherapy regimens is that the metastases usually grow very slowly. Drugs that target dividing tumor cells have therefore had limited success. To improve treatment, new strategies and valid experimental models are required for pre-clinical testing. However, development of models has itself been hampered by the absence of human pheochromocytoma/paraganglioma cell lines for cultures or xenografts. Topoisomerase 1 (TOP1) inhibitors are drugs that interfere with mechanisms that maintain DNA integrity during transcription in both quiescent and dividing cells. We used primary cultures of representative human tumors to establish the cytotoxicity of camptothecin, a prototypical TOP1 inhibitor, against non-dividing pheochromocytoma/paraganglioma cells, and then employed a mouse pheochromocytoma model (MPC) to show that efficacy of low concentrations of camptothecin and other TOP1 inhibitors is increased by intermittent coadministration of sub-toxic concentrations of 5-azacytidine, a DNA methylation inhibitor that modulates transcription. We then tested the same drugs against a clonal MPC derivative that expresses CMV reporter-driven luciferase and GFP, intended for in vivo drug testing. Unexpectedly, luciferase expression, bioluminescence and GFP expression were paradoxically increased by both camptothecin and SN38, the active metabolite of irinotecan, thereby masking cell death. Expression of chromogranin A, a marker for neuroendocrine secretory granules, was not increased, indicating that the drug effects on levels of luciferase and GFP are specific to the GFP-luciferase construct rather than generalized cellular responses. Our findings provide proof of principle for use of TOP1 inhibitors against pheochromocytoma/paraganglioma and suggest novel strategies for enhancing efficacy and reducing toxicity by optimizing the combination and timing of their use in conjunction with other drugs. The paradoxical effects of TOP1 inhibitors on luciferase and GFP dictate a need for caution in the use of CMV promoter-regulated constructs for cancer-related imaging studies. JF - PloS one AU - Powers, James F AU - Korgaonkar, Parimal G AU - Fliedner, Stephanie AU - Giubellino, Alessio AU - Pacak, Karel AU - Sahagian, G Gary AU - Tischler, Arthur S AD - Department of Pathology, Tufts Medical Center, Boston, Massachusetts, United States of America. ; Small Animal Imaging/Preclinical Testing Facility, Tufts University School of Medicine, Boston, Massachusetts, United States of America. ; Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America ; 1st Department of Medicine, University Medical Center Schleswig-Holstein Lübeck, Lübeck, Germany. ; Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 2 KW - Topoisomerase I Inhibitors KW - 0 KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Animals KW - Humans KW - Mice KW - Cell Line, Tumor KW - Topoisomerase I Inhibitors -- pharmacology KW - Azacitidine -- therapeutic use KW - Azacitidine -- pharmacology KW - Paraganglioma -- pathology KW - Topoisomerase I Inhibitors -- therapeutic use KW - Paraganglioma -- drug therapy KW - Pheochromocytoma -- drug therapy KW - Adrenal Gland Neoplasms -- pathology KW - Pheochromocytoma -- pathology KW - Cell Death -- drug effects KW - Adrenal Gland Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1499137534?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytocidal+activities+of+topoisomerase+1+inhibitors+and+5-azacytidine+against+pheochromocytoma%2Fparaganglioma+cells+in+primary+human+tumor+cultures+and+mouse+cell+lines.&rft.au=Powers%2C+James+F%3BKorgaonkar%2C+Parimal+G%3BFliedner%2C+Stephanie%3BGiubellino%2C+Alessio%3BPacak%2C+Karel%3BSahagian%2C+G+Gary%3BTischler%2C+Arthur+S&rft.aulast=Powers&rft.aufirst=James&rft.date=2014-01-01&rft.volume=9&rft.issue=2&rft.spage=e87807&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0087807 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-22 N1 - Date created - 2014-02-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Lett. 2012 Mar;316(1):46-52 [22154086] J Histochem Cytochem. 1992 Jul;40(7):1043-5 [1351491] Int J Pharm. 2012 Feb 28;423(2):509-15 [22178618] Epigenetics. 2012 Feb;7(2):141-5 [22395463] Endocr Pathol. 2012 Mar;23(1):43-54 [22323007] Endocr Pathol. 2012 Mar;23(1):21-33 [22391976] Anticancer Res. 2012 Apr;32(4):1453-6 [22493385] Horm Metab Res. 2012 May;44(5):328-33 [22328163] Endocr Relat Cancer. 2013 Feb;20(1):65-78 [23154831] Cancer Discov. 2013 Jun;3(6):648-57 [23550148] PLoS One. 2013;8(6):e65624 [23785438] Nat Commun. 2013;4:2326 [23933660] Cancer Res. 1993 Sep 1;53(17):3976-85 [8358726] J Biol Chem. 1994 Mar 18;269(11):7893-900 [8132507] J Neurosci. 1997 Feb 15;17(4):1256-70 [9006970] Br J Cancer. 1997;76(2):211-9 [9231921] Nat Genet. 1998 Jun;19(2):187-91 [9620779] Nat Clin Pract Endocrinol Metab. 2007 Feb;3(2):92-102 [17237836] Ann Surg Oncol. 2007 May;14(5):1752-62 [17195906] Exp Cell Res. 2007 Oct 1;313(16):3635-44 [17643424] Epigenetics. 2006 Jul-Sep;1(3):127-30 [17965610] Surgery. 2008 Jun;143(6):759-68 [18549892] Arch Pathol Lab Med. 2008 Aug;132(8):1272-84 [18684026] Nucl Med Biol. 2008 Aug;35 Suppl 1:S9-20 [18707637] BMC Cancer. 2008;8:228 [18691423] Clin Exp Metastasis. 2009;26(3):239-50 [19169894] Nat Rev Cancer. 2009 May;9(5):327-37 [19377505] Expert Opin Ther Pat. 2009 May;19(5):555-74 [19441934] Horm Metab Res. 2009 Sep;41(9):710-4 [19551609] Neuroreport. 2010 Mar 10;21(4):282-6 [20145501] J Alzheimers Dis. 2010;22(4):1209-21 [20930312] Endocr Relat Cancer. 2011 Feb;18(1):143-57 [21098082] Mol Imaging Biol. 2011 Feb;13(1):43-52 [20396957] Biomaterials. 2012 Feb;33(4):1162-9 [22074663] Cell Tissue Res. 2000 Dec;302(3):309-20 [11151443] Ann N Y Acad Sci. 2000;922:1-10 [11193884] Mol Ther. 2002 Jun;5(6):731-8 [12027557] Carcinogenesis. 2003 Oct;24(10):1625-35 [12869421] J Gene Med. 2004 Apr;6(4):395-404 [15079814] Histol Histopathol. 2004 Jul;19(3):883-95 [15168351] J Biol Chem. 1988 Oct 5;263(28):13983-6 [2844750] J Biol Chem. 1991 Oct 25;266(30):20152-8 [1657914] Cancer Res. 1992 Mar 1;52(5):1245-51 [1737386] Erratum In: PLoS One. 2014;9(3):e92492 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0087807 ER - TY - JOUR T1 - Overview of Exocrine Pancreatic Pathobiology AN - 1496897455; 19022983 AB - Exocrine pancreas is a source of several enzymes that are essential for the digestive process. The exocrine pancreatic secretion is tightly regulated by the neuroendocrine system. The endocrine pancreas is tightly integrated anatomically and physiologically with the exocrine pancreas and modulates its function. Compound-induced pancreatitis is not a common event in toxicology or drug development, but it becomes a significant liability when encountered. Understanding the species-specific differences in physiology is essential to understand the underlying pathobiology of pancreatic disease in animal models and its relevance to human disease. This review will mainly focus on understanding the morphology and physiology of the pancreas, unique islet-exocrine interactions, and pancreatitis. JF - Toxicologic Pathology AU - Pandiri, Arun R AD - Experimental Pathology Laboratories, Inc., Research Triangle Park, North Carolina, USA, pandiriak@niehs.nih.govapandiri@epl-inc.com Y1 - 2014/01// PY - 2014 DA - January 2014 SP - 207 EP - 216 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 42 IS - 1 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - animal models KW - digestive system KW - endocrine system. KW - Pancreatic diseases KW - Pancreas KW - Reviews KW - Secretion KW - Animal models KW - Enzymes KW - Drug development KW - Neuroendocrine system KW - Pancreatitis KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496897455?accountid=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=Overview+of+Exocrine+Pancreatic+Pathobiology&rft.au=Pandiri%2C+Arun+R&rft.aulast=Pandiri&rft.aufirst=Arun&rft.date=2014-01-01&rft.volume=42&rft.issue=1&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313509907 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Number of references - 96 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Pancreatic diseases; Secretion; Reviews; Pancreas; Animal models; Enzymes; Drug development; Neuroendocrine system; Pancreatitis DO - http://dx.doi.org/10.1177/0192623313509907 ER - TY - JOUR T1 - Overview of the Pancreatic Toxicity and Carcinogenesis Session AN - 1496880899; 19022962 AB - The theme of the Society of Toxicologic Pathology Annual Symposium 2013 was "Toxicologic Pathology of the Digestive Tract and Pancreas." The last session focused on pancreatic toxicity and carcinogenesis. This overview highlights the various presentations in this session, focusing on pancreatic Toxicologic Pathology, responses of the pancreas to xenobiotics, and current understanding on pancreatic carcinogenesis. The objective of this symposium overview and the subsequent articles from this session is to enable the audience to develop a better appreciation for the pancreas as a target organ in toxicological studies. JF - Toxicologic Pathology AU - Pandiri, Arun R AU - Schultze, AEric AD - Experimental Pathology Laboratories, Inc., Research Triangle Park, North Carolina, USA, pandiriak@niehs.nih.govapandiri@epl-inc.com Y1 - 2014/01// PY - 2014 DA - January 2014 SP - 204 EP - 206 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 42 IS - 1 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - exocrine pancreas KW - islet-acinar axis KW - pancreatitis KW - cholecystokinin KW - CCK agonist KW - pancreatic cancer. KW - Digestive tract KW - Pancreas KW - Reviews KW - Carcinogenesis KW - Toxicity KW - Xenobiotics KW - Toxicity testing KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496880899?accountid=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=Overview+of+the+Pancreatic+Toxicity+and+Carcinogenesis+Session&rft.au=Pandiri%2C+Arun+R%3BSchultze%2C+AEric&rft.aulast=Pandiri&rft.aufirst=Arun&rft.date=2014-01-01&rft.volume=42&rft.issue=1&rft.spage=204&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623313505931 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Number of references - 17 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Digestive tract; Reviews; Pancreas; Carcinogenesis; Xenobiotics; Toxicity; Toxicity testing DO - http://dx.doi.org/10.1177/0192623313505931 ER - TY - JOUR T1 - Histone deacetylase inhibitors selectively target homology dependent DNA repair defective cells and elevate non-homologous endjoining activity. AN - 1492707586; 24466340 AB - We have previously used the ATAD5-luciferase high-throughput screening assay to identify genotoxic compounds with potential chemotherapeutic capabilities. The successful identification of known genotoxic agents, including the histone deacetylase inhibitor (HDACi) trichostatin A (TSA), confirmed the specificity of the screen since TSA has been widely studied for its ability to cause apoptosis in cancer cells. Because many cancers have acquired mutations in DNA damage checkpoints or repair pathways, we hypothesized that these cancers may be susceptible to treatments that target compensatory pathways. Here, we used a panel of isogenic chicken DT40 B lymphocyte mutant and human cell lines to investigate the ability of TSA to define selective pathways that promote HDACi toxicity. HDACi induced a DNA damage response and reduced viability in all repair deficient DT40 mutants although ATM-nulls were least affected. The most dramatic sensitivity was observed in mutants lacking the homology dependent repair (HDR) factor BLM or the non-homologous end-joining (NHEJ) and HDR factors, KU/RAD54, suggesting an involvement of either HDR or NHEJ in HDACi-induced cell death. To extend these findings, we measured the frequencies of HDR and NHEJ after HDACi treatment and monitored viability in human cell lines comparably deficient in HDR or NHEJ. Although no difference in HDR frequency was observed between HDACi treated and untreated cells, HDR-defective human cell lines were clearly more sensitive than wild type. Unexpectedly, cells treated with HDACis showed a significantly elevated NHEJ frequency. HDACi targeting drugs induced significant increases in NHEJ activity in human cell lines but did not alter HDR frequency. Moreover, HDR is required for cellular resistance to HDACi therapy; therefore, NHEJ does not appear to be a critical axis for HDACi resistance. Rather, HDACi compounds induced DNA damage, most likely double strand breaks (DSBs), and HDR proficiency is correlated with cell survival. JF - PloS one AU - Smith, Stephanie AU - Fox, Jennifer AU - Mejia, Marco AU - Ruangpradit, Wanvipa AU - Saberi, Alihossein AU - Kim, Sunmi AU - Choi, Yongjun AU - Oh, Sehyun AU - Wang, Yucai AU - Choi, Kyungho AU - Li, Lei AU - Hendrickson, Eric A AU - Takeda, Shunichi AU - Muller, Mark AU - Myung, Kyungjae AD - Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Molecular Biology and Microbiology, College of Medicine, University of Central Florida, Orlando, Florida, United States of America. ; Department of Radiation Genetics Kyoto University, Medical School, Kyoto, 606-8501 Japan. ; Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America ; Department of Radiation Genetics Kyoto University, Medical School, Kyoto, 606-8501 Japan ; Department of Environmental Health School of Public Hearth, Seoul National University, Seoul, Korea. ; Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America. ; Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America ; The University of Texas Graduate School of Biomedical Sciences at Houston, Houston Texas, United States of America. ; Department of Environmental Health School of Public Hearth, Seoul National University, Seoul, Korea. ; Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America ; Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 1 KW - Antigens, Nuclear KW - 0 KW - DNA-Binding Proteins KW - Histone Deacetylase Inhibitors KW - Hydroxamic Acids KW - RNA, Small Interfering KW - trichostatin A KW - 3X2S926L3Z KW - vorinostat KW - 58IFB293JI KW - Luciferases KW - EC 1.13.12.- KW - RAD51 protein, human KW - EC 2.7.7.- KW - Rad51 Recombinase KW - Bloom syndrome protein KW - EC 3.6.1.- KW - RecQ Helicases KW - EC 3.6.4.12 KW - Xrcc6 protein, human KW - Ku Autoantigen KW - EC 4.2.99.- KW - Index Medicus KW - Rad51 Recombinase -- antagonists & inhibitors KW - Animals KW - Humans KW - RecQ Helicases -- metabolism KW - Luciferases -- metabolism KW - DNA-Binding Proteins -- genetics KW - RNA, Small Interfering -- genetics KW - Antigens, Nuclear -- genetics KW - DNA Damage -- genetics KW - DNA Damage -- drug effects KW - Rad51 Recombinase -- metabolism KW - Blotting, Western KW - Chickens KW - Antigens, Nuclear -- metabolism KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Electrophoresis, Gel, Pulsed-Field KW - RecQ Helicases -- genetics KW - DNA-Binding Proteins -- antagonists & inhibitors KW - Rad51 Recombinase -- genetics KW - Hydroxamic Acids -- pharmacology KW - Fluorescent Antibody Technique KW - DNA-Binding Proteins -- metabolism KW - DNA Repair -- genetics KW - Neoplasms -- drug therapy KW - B-Lymphocytes -- drug effects KW - Neoplasms -- pathology KW - Histone Deacetylase Inhibitors -- pharmacology KW - B-Lymphocytes -- cytology KW - Mutation -- genetics KW - DNA End-Joining Repair -- genetics KW - B-Lymphocytes -- metabolism KW - Neoplasms -- genetics KW - DNA Repair -- drug effects KW - DNA End-Joining Repair -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492707586?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Histone+deacetylase+inhibitors+selectively+target+homology+dependent+DNA+repair+defective+cells+and+elevate+non-homologous+endjoining+activity.&rft.au=Smith%2C+Stephanie%3BFox%2C+Jennifer%3BMejia%2C+Marco%3BRuangpradit%2C+Wanvipa%3BSaberi%2C+Alihossein%3BKim%2C+Sunmi%3BChoi%2C+Yongjun%3BOh%2C+Sehyun%3BWang%2C+Yucai%3BChoi%2C+Kyungho%3BLi%2C+Lei%3BHendrickson%2C+Eric+A%3BTakeda%2C+Shunichi%3BMuller%2C+Mark%3BMyung%2C+Kyungjae&rft.aulast=Smith&rft.aufirst=Stephanie&rft.date=2014-01-01&rft.volume=9&rft.issue=1&rft.spage=e87203&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0087203 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-29 N1 - Date created - 2014-01-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: DNA Repair (Amst). 2003 Nov 21;2(11):1239-52 [14599745] J Biol Chem. 2009 Mar 20;284(12):7505-17 [19150983] Cell Cycle. 2009 Oct 1;8(19):3199-207 [19755857] PLoS Genet. 2010 Feb;6(2):e1000855 [20195511] J Biol Chem. 2010 Apr 2;285(14):10362-9 [20147293] Cell. 2010 Apr 16;141(2):243-54 [20362325] Annu Rev Biochem. 2010;79:181-211 [20192759] Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14639-44 [20679231] J Biol Chem. 2010 Nov 26;285(48):37630-40 [20864525] DNA Repair (Amst). 2010 Dec 10;9(12):1292-8 [21030320] J Biol Chem. 2011 Mar 11;286(10):7722-6 [21247901] DNA Repair (Amst). 2011 Apr 3;10(4):438-44 [21269891] Cell Death Differ. 2011 Dec;18(12):1904-13 [21637290] Semin Cell Dev Biol. 2011 Oct;22(8):886-97 [22027614] Nat Rev Cancer. 2012 Jan;12(1):68-78 [22193408] Epigenomics. 2011 Apr;3(2):145-55 [21743813] Mol Cell. 2012 Jan 13;45(1):75-86 [22153967] Curr Med Chem. 2012;19(4):475-87 [22204328] Protein J. 2012 Mar;31(3):195-205 [22354665] Nucleic Acids Res. 2012 Mar;40(6):2481-93 [22135303] Proc Natl Acad Sci U S A. 2012 Apr 3;109(14):5423-8 [22431602] PLoS One. 2012;7(5):e36177 [22655027] Anticancer Res. 2012 Jul;32(7):2791-9 [22753739] Nucleic Acids Res. 2012 Jul;40(13):5795-818 [22467216] Mol Cell. 2012 Aug 24;47(4):497-510 [22920291] Methods Mol Biol. 2012;920:379-91 [22941618] Nucleic Acids Res. 2013 Feb 1;41(3):1734-49 [23275564] Mol Cell. 2013 Mar 7;49(5):997-1009 [23333308] Proc Natl Acad Sci U S A. 2013 Apr 2;110(14):5564-9 [23509290] J Mol Cell Biol. 2013 Jun;5(3):157-65 [23329852] Genes Dev. 1999 Oct 15;13(20):2633-8 [10541549] J Biol Chem. 2004 Sep 3;279(36):37282-90 [15194694] Science. 1995 Feb 24;267(5201):1178-83 [7855601] Cell. 1995 Mar 10;80(5):813-23 [7889575] Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3171-4 [7724535] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10792-5 [7479885] Blood. 1997 Nov 15;90(10):3996-4003 [9354668] Proc Natl Acad Sci U S A. 2005 Jan 25;102(4):1110-5 [15650050] DNA Repair (Amst). 2005 Aug 15;4(9):1006-18 [15941674] Nat Cell Biol. 2006 Jan;8(1):91-9 [16341205] Mol Cell. 2006 Jun 23;22(6):719-29 [16793542] Genes Dev. 2006 Jul 1;20(13):1721-6 [16818604] EMBO J. 2006 Aug 23;25(16):3880-9 [16874298] Toxicol Sci. 2006 Oct;93(2):341-7 [16857700] Oncogene. 2006 Sep 25;25(43):5875-84 [16998502] Genes Dev. 2007 Dec 1;21(23):3073-84 [18003859] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19482-7 [18042714] PLoS Genet. 2007 Jul;3(7):e110 [17616978] DNA Repair (Amst). 2008 Oct 1;7(10):1765-71 [18675941] Cell. 2008 Oct 17;135(2):261-71 [18957201] Nat Rev Cancer. 2009 Sep;9(9):644-54 [19657341] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0087203 ER - TY - JOUR T1 - Bisphenol A exposure alters developmental gene expression in the fetal rhesus macaque uterus. AN - 1492705012; 24465770 AB - Bisphenol A (BPA) exposure results in numerous developmental and functional abnormalities in reproductive organs in rodent models, but limited data are available regarding BPA effects in the primate uterus. To determine if maternal oral BPA exposure affects fetal uterine development in a non-human primate model, pregnant rhesus macaques carrying female fetuses were exposed orally to 400 µg/kg BPA or vehicle control daily from gestation day (GD) 50-100 or GD100-165. Fetal uteri were collected at the completion of treatment (GD100 or GD165); tissue histology, cell proliferation, and expression of estrogen receptor alpha (ERα) and progesterone receptor (PR) were compared to that of controls. Gene expression analysis was conducted using rhesus macaque microarrays. There were no significant differences in histology or in the percentage of cells expressing the proliferation marker Ki-67, ERα, or PR in BPA-exposed uteri compared to controls at GD100 or GD165. Minimal differences in gene expression were observed between BPA-exposed and control GD100 uteri. However, at GD165, BPA-exposed uteri had significant differences in gene expression compared to controls. Several of the altered genes, including HOXA13, WNT4, and WNT5A, are critical for reproductive organ development and/or adult function. We conclude that second or third trimester BPA exposure does not significantly affect fetal uterus development based on morphological, proliferation, and steroid hormone receptor assessments. However, differences in expression of key developmental genes after third trimester exposure suggest that BPA could alter transcriptional signals influencing uterine function later in life. JF - PloS one AU - Calhoun, Kathryn C AU - Padilla-Banks, Elizabeth AU - Jefferson, Wendy N AU - Liu, Liwen AU - Gerrish, Kevin E AU - Young, Steven L AU - Wood, Charles E AU - Hunt, Patricia A AU - Vandevoort, Catherine A AU - Williams, Carmen J AD - Reproductive Medicine Group, Laboratory of Reproductive & Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America ; Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States of America. ; Reproductive Medicine Group, Laboratory of Reproductive & Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America. ; Microarray Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America. ; Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, United States of America. ; National Health and Environmental Effects Research Laboratory, Office of Research and Development, US Environmental Protection Agency, Research Triangle Park, North Carolina, United States of America. ; School of Molecular Biosciences, Washington State University, Pullman, Washington, United States of America. ; Department of Obstetrics and Gynecology and California National Primate Research Center, University of California Davis, Davis, California, United States of America. Y1 - 2014 PY - 2014 DA - 2014 SP - 1 VL - 9 IS - 1 KW - Benzhydryl Compounds KW - 0 KW - Endocrine Disruptors KW - Estrogen Receptor alpha KW - Phenols KW - Receptors, Progesterone KW - beta Catenin KW - bisphenol A KW - MLT3645I99 KW - Index Medicus KW - Animals KW - Oligonucleotide Array Sequence Analysis KW - Gene Regulatory Networks KW - Fetal Development -- drug effects KW - Estrogen Receptor alpha -- metabolism KW - Maternal Exposure KW - Pregnancy KW - Receptors, Progesterone -- genetics KW - Maternal-Fetal Exchange KW - Receptors, Progesterone -- metabolism KW - Estrogen Receptor alpha -- genetics KW - beta Catenin -- metabolism KW - Environmental Exposure KW - Macaca mulatta KW - Female KW - Transcriptome -- drug effects KW - Uterus -- metabolism KW - Endocrine Disruptors -- toxicity KW - Benzhydryl Compounds -- toxicity KW - Phenols -- toxicity KW - Uterus -- pathology KW - Uterus -- embryology KW - Uterus -- drug effects KW - Gene Expression Regulation, Developmental -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492705012?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Bisphenol+A+exposure+alters+developmental+gene+expression+in+the+fetal+rhesus+macaque+uterus.&rft.au=Calhoun%2C+Kathryn+C%3BPadilla-Banks%2C+Elizabeth%3BJefferson%2C+Wendy+N%3BLiu%2C+Liwen%3BGerrish%2C+Kevin+E%3BYoung%2C+Steven+L%3BWood%2C+Charles+E%3BHunt%2C+Patricia+A%3BVandevoort%2C+Catherine+A%3BWilliams%2C+Carmen+J&rft.aulast=Calhoun&rft.aufirst=Kathryn&rft.date=2014-01-01&rft.volume=9&rft.issue=1&rft.spage=e85894&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0085894 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-11-11 N1 - Date created - 2014-01-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Development. 2004 May;131(9):2061-72 [15073149] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886] Biol Reprod. 1975 Apr;12(3):335-45 [1222158] Am J Obstet Gynecol. 1982 Apr 1;142(7):905-21 [6121486] Toxicol Lett. 1982 Apr;11(1-2):43-7 [6953621] Am J Med Genet. 1992 Nov 1;44(4):482-4 [1442892] Nat Genet. 1997 Feb;15(2):179-80 [9020844] Biol Reprod. 1997 Dec;57(6):1338-45 [9408238] J Clin Invest. 1998 Apr 1;101(7):1379-84 [9525980] Ann N Y Acad Sci. 2004 Dec;1034:1-18 [15731295] Biol Reprod. 2005 Jun;72(6):1344-51 [15689538] J Biochem. 2005 Jun;137(6):677-83 [16002989] Mol Cell Endocrinol. 2006 Jul 25;254-255:179-86 [16781053] FASEB J. 2007 Jan;21(1):239-46 [17093138] Reprod Toxicol. 2007 Aug-Sep;24(2):199-224 [17683900] Am J Hum Genet. 2008 Jan;82(1):39-47 [18179883] Biol Reprod. 2009 May;80(5):989-1000 [19164167] Curr Top Dev Biol. 2009;88:235-55 [19651307] Dev Dyn. 2010 Jan;239(1):327-37 [19918918] Mol Cell Endocrinol. 2010 Apr 12;317(1-2):106-11 [19962424] J Endocrinol. 2010 Mar;204(3):223-31 [19833720] Cold Spring Harb Perspect Biol. 2010 Feb;2(2):a000869 [20182616] Hum Mol Genet. 2010 Apr 15;19(8):1539-50 [20106871] FASEB J. 2010 Jul;24(7):2273-80 [20181937] Environ Health Perspect. 2010 Aug;118(8):1055-70 [20338858] Curr Opin Pharmacol. 2010 Dec;10(6):643-9 [20810315] Curr Opin Pediatr. 2011 Apr;23(2):233-9 [21293273] FASEB J. 2011 Apr;25(4):1176-87 [21163860] Environ Health Perspect. 2011 Apr;119(4):422-30 [20855240] Toxicol Appl Pharmacol. 2011 Sep 15;255(3):261-70 [21820460] J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):27-34 [21605673] Environ Health Perspect. 2011 Nov;119(11):1575-82 [21810550] Proc Natl Acad Sci U S A. 2012 May 22;109(21):8190-5 [22566636] Proc Natl Acad Sci U S A. 2012 Oct 23;109(43):17525-30 [23012422] Dev Dyn. 2013 Jan;242(1):53-66 [23073994] Neurotoxicology. 2013 Mar;35:113-20 [23337607] Trends Cell Biol. 2013 Aug;23(8):380-9 [23607968] Methods Mol Biol. 2000;132:365-86 [10547847] Genes Dev. 2000 Mar 15;14(6):650-4 [10733525] N Engl J Med. 2004 Aug 19;351(8):792-8 [15317892] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0085894 ER - TY - JOUR T1 - Genetic polymorphisms in NQO1 and SOD2: interactions with smoking, schistosoma infection, and bladder cancer risk in Egypt. AN - 1490762841; 24035474 AB - Bladder cancer is the most prevalent form of cancer in men among Egyptians, for whom tobacco smoke exposure and Schistosoma haematobium (SH) infection are the major risk factors. We hypothesized that functional polymorphisms in quinone oxidoreductase 1 (NQO1) and superoxide dismutase 2 (SOD2), modulators of the effects of reactive oxidative species, can influence an individual's susceptibility to these carcinogenic exposures and hence the risk of bladder cancer. We assessed the effects of potential interactions between functional polymorphisms in the NQO1 and SOD2 genes and exposure to smoking and SH infection on bladder cancer risk among 902 cases and 804 population-based controls in Egypt. We used unconditional logistic regression to estimate the odds ratios (OR) and confidence intervals (CI) 95%. Water pipe and cigarette smoking were more strongly associated with cancer risk among individuals with the TT genotype for SOD2 (OR [CI 95%] = 4.41 [1.86-10.42]) as compared with those with the CC genotype (OR [CI 95%] = 2.26 [0.97-6.74]). Conversely, the risk associated with SH infection was higher among the latter (OR [CI 95%] = 3.59 [2.21-5.84]) than among the former (OR [CI 95%] = 1.86 [1.33-2.60]). Polymorphisms in NQO1 genotype showed a similar pattern, but to a much lesser extent. The highest odds for having bladder cancer following SH infection were observed among individuals with the CC genotypes for both NQO1 and SOD2 (OR [CI 95%] = 4.41 [2.32-8.38]). Our findings suggest that genetic polymorphisms in NQO1 and SOD2 play important roles in the etiology of bladder cancer by modulating the effects of known contributing factors such as smoking and SH infection. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Urologic oncology AU - Goerlitz, David AU - Amr, Sania AU - Dash, Chiranjeev AU - Saleh, Doa'a A AU - El Daly, Mai AU - Abdel-Hamid, Mohamed AU - El Kafrawy, Sherif AU - Hifnawy, Tamer AU - Ezzat, Sameera AU - Abdel-Aziz, Mohamed A AU - Khaled, Hussein AU - Zheng, Yun-Ling AU - Mikhail, Nabiel AU - Loffredo, Christopher A AD - Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC. ; Department of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, MD. ; Department of Public Health, Cairo University, Cairo, Egypt. ; Department of Microbiology, National Hepatology and Tropical Medicine Research Institute, Cairo, Egypt; National Liver Institute, Menoufiya University, Shibin El Kom, Egypt. ; Department of Microbiology, National Hepatology and Tropical Medicine Research Institute, Cairo, Egypt; Department of Microbiology, Minia University, Minia, Egypt. ; Department of Microbiology, National Hepatology and Tropical Medicine Research Institute, Cairo, Egypt; National Liver Institute, Menoufiya University, Shibin El Kom, Egypt; King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia. ; Public Health Department, Beni Suif University, Beni Suif, Egypt. ; National Liver Institute, Menoufiya University, Shibin El Kom, Egypt. ; Department of Urology, Assiut University, Assiut, Egypt. ; Department of Medical Oncology, National Cancer Institute, Cairo, Egypt. ; Department of Microbiology, National Hepatology and Tropical Medicine Research Institute, Cairo, Egypt; Department of Urology, Assiut University, Assiut, Egypt. ; Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC. Electronic address: cal9@georgetown.edu. Y1 - 2014/01// PY - 2014 DA - January 2014 SP - 47.e15 EP - 20 VL - 32 IS - 1 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - superoxide dismutase 2 KW - NAD(P)H Dehydrogenase (Quinone) KW - EC 1.6.5.2 KW - NQO1 protein, human KW - Index Medicus KW - Bladder cancer KW - Smoking KW - Epidemiology KW - Schistosomiasis KW - NQO1 KW - SOD2 KW - Animals KW - Odds Ratio KW - Gene Frequency KW - Humans KW - Smoking -- adverse effects KW - Aged KW - Egypt KW - Genotype KW - Logistic Models KW - Risk Factors KW - Host-Parasite Interactions KW - Middle Aged KW - Schistosomiasis haematobia -- parasitology KW - Female KW - Male KW - Schistosoma haematobium -- physiology KW - NAD(P)H Dehydrogenase (Quinone) -- genetics KW - Polymorphism, Single Nucleotide KW - Urinary Bladder Neoplasms -- etiology KW - Genetic Predisposition to Disease -- genetics KW - Urinary Bladder Neoplasms -- genetics KW - Superoxide Dismutase -- genetics KW - Urinary Bladder Neoplasms -- parasitology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490762841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Urologic+oncology&rft.atitle=Genetic+polymorphisms+in+NQO1+and+SOD2%3A+interactions+with+smoking%2C+schistosoma+infection%2C+and+bladder+cancer+risk+in+Egypt.&rft.au=Goerlitz%2C+David%3BAmr%2C+Sania%3BDash%2C+Chiranjeev%3BSaleh%2C+Doa%27a+A%3BEl+Daly%2C+Mai%3BAbdel-Hamid%2C+Mohamed%3BEl+Kafrawy%2C+Sherif%3BHifnawy%2C+Tamer%3BEzzat%2C+Sameera%3BAbdel-Aziz%2C+Mohamed+A%3BKhaled%2C+Hussein%3BZheng%2C+Yun-Ling%3BMikhail%2C+Nabiel%3BLoffredo%2C+Christopher+A&rft.aulast=Goerlitz&rft.aufirst=David&rft.date=2014-01-01&rft.volume=32&rft.issue=1&rft.spage=47.e15&rft.isbn=&rft.btitle=&rft.title=Urologic+oncology&rft.issn=1873-2496&rft_id=info:doi/10.1016%2Fj.urolonc.2013.06.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-09-26 N1 - Date created - 2013-12-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1188-93 [11158615] Arch Environ Occup Health. 2014;69(1):3-10 [23930791] Mutat Res. 2003 Apr 20;536(1-2):131-7 [12694753] Pharmacogenetics. 2003 Jun;13(6):349-55 [12777965] Mol Pharmacol. 2004 May;65(5):1238-47 [15102952] Int J Cancer. 2004 Jul 1;110(4):598-604 [15122594] Science. 1983 Apr 22;220(4595):425-7 [6301009] Methods Enzymol. 1990;186:287-301 [2233301] Cancer Res. 1994 Apr 1;54(7 Suppl):1929s-1933s [8137314] Proc Natl Acad Sci U S A. 1994 Aug 30;91(18):8413-7 [8078896] Mol Pharmacol. 1995 May;47(5):934-9 [7746280] Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4471-3 [8633092] Biochem Biophys Res Commun. 1996 Sep 13;226(2):561-5 [8806673] Br J Cancer. 1997;75(1):69-75 [9000600] Cancer Causes Control. 1997 May;8(3):444-72 [9498904] Pharmacogenet Genomics. 2005 May;15(5):311-9 [15864132] Pharmacogenet Genomics. 2006 Apr;16(4):279-86 [16538174] Nicotine Tob Res. 2007 May;9(5):591-6 [17454715] Ann Oncol. 2007 Jul;18(7):1230-42 [17496311] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1595-600 [17684133] J Cancer Res Clin Oncol. 2008 Feb;134(2):203-9 [17619904] Cancer Causes Control. 2008 May;19(4):421-9 [18188671] Maturitas. 2010 Dec;67(4):353-7 [20813471] Oncol Rep. 2012 Feb;27(2):356-62 [22089035] Cancer Epidemiol Biomarkers Prev. 2012 Mar;21(3):537-46 [22147365] Jpn J Cancer Res. 2002 Jul;93(7):736-43 [12149138] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.urolonc.2013.06.016 ER - TY - JOUR T1 - Cytotoxicity of synthetic cannabinoids on primary neuronal cells of the forebrain: the involvement of cannabinoid CB1 receptors and apoptotic cell death. AN - 1490743906; 24211273 AB - The abuse of herbal products containing synthetic cannabinoids has become an issue of public concern. The purpose of this paper was to evaluate the acute cytotoxicity of synthetic cannabinoids on mouse brain neuronal cells. Cytotoxicity induced by synthetic cannabinoid (CP-55,940, CP-47,497, CP-47,497-C8, HU-210, JWH-018, JWH-210, AM-2201, and MAM-2201) was examined using forebrain neuronal cultures. These synthetic cannabinoids induced cytotoxicity in the forebrain cultures in a concentration-dependent manner. The cytotoxicity was suppressed by preincubation with the selective CB1 receptor antagonist AM251, but not with the selective CB2 receptor antagonist AM630. Furthermore, annexin-V-positive cells were found among the treated forebrain cells. Synthetic cannabinoid treatment induced the activation of caspase-3, and preincubation with a caspase-3 inhibitor significantly suppressed the cytotoxicity. These synthetic cannabinoids induced apoptosis through a caspase-3-dependent mechanism in the forebrain cultures. Our results indicate that the cytotoxicity of synthetic cannabinoids towards primary neuronal cells is mediated by the CB1 receptor, but not by the CB2 receptor, and further suggest that caspase cascades may play an important role in the apoptosis induced by these synthetic cannabinoids. In conclusion, excessive synthetic cannabinoid abuse may present a serious acute health concern due to neuronal damage or deficits in the brain. Copyright © 2013 Elsevier Inc. All rights reserved. JF - Toxicology and applied pharmacology AU - Tomiyama, Ken-ichi AU - Funada, Masahiko AD - Department of Drug Dependence Research, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. ; Department of Drug Dependence Research, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. Electronic address: mfunada@ncnp.go.jp. Y1 - 2014/01/01/ PY - 2014 DA - 2014 Jan 01 SP - 17 EP - 23 VL - 274 IS - 1 KW - Cannabinoids KW - 0 KW - Cytotoxins KW - Receptor, Cannabinoid, CB1 KW - Index Medicus KW - Apoptosis KW - ∆(9)-tetrahydrocannabinol KW - Δ(9)-THC KW - Z-DEVD-FMK KW - CB KW - phosphate-buffered saline KW - Designer drug KW - PBS KW - Cannabinoid receptor KW - Z-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-fluoromethylketone KW - cannabinoid KW - DMEM KW - DMSO KW - fetal bovine serum KW - Dulbecco's modified Eagle's medium KW - FBS KW - room temperature KW - MAP-2 KW - RT KW - Cytotoxicity KW - microtubule-associated protein-2 KW - Primary neuronal cells KW - dimethyl sulfoxide KW - Synthetic cannabinoid KW - Animals KW - Mice, Inbred ICR KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Mice KW - Female KW - Pregnancy KW - Neurons -- metabolism KW - Prosencephalon -- metabolism KW - Cytotoxins -- toxicity KW - Cannabinoids -- toxicity KW - Neurons -- drug effects KW - Apoptosis -- physiology KW - Apoptosis -- drug effects KW - Prosencephalon -- drug effects KW - Receptor, Cannabinoid, CB1 -- biosynthesis KW - Cannabinoids -- chemical synthesis KW - Cytotoxins -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490743906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytotoxicity+of+synthetic+cannabinoids+on+primary+neuronal+cells+of+the+forebrain%3A+the+involvement+of+cannabinoid+CB1+receptors+and+apoptotic+cell+death.&rft.au=Tomiyama%2C+Ken-ichi%3BFunada%2C+Masahiko&rft.aulast=Tomiyama&rft.aufirst=Ken-ichi&rft.date=2014-01-01&rft.volume=274&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2013.10.028 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-02-24 N1 - Date created - 2013-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2013.10.028 ER - TY - JOUR T1 - Phase II trial of bevacizumab and satraplatin in docetaxel-pretreated metastatic castrate-resistant prostate cancer. AN - 1490735993; 23433892 AB - Satraplatin is an oral platinum compound that has demonstrated efficacy and tolerability in prostate cancer. Preclinical synergy between bevacizumab and platinum has been noted. Docetaxel-pretreated metastatic castrate-resistant prostate cancer patients with disease progression were eligible. Satraplatin 80 mg/m(2) orally on days 1 to 5, prednisone 5mg twice daily, and bevacizumab 10mg/kg on day 1, and 15 mg/kg on day 15 were administered in 35-day cycles. Thirty one patients were enrolled. Grade 3 or 4 toxicities were pulmonary embolism in 2 patients and thrombocytopenia in 1 patient. 31% of the patients had a ≥ 30% decline in prostate-specific antigen. Median time to progression was 7.0 months (90% confidence interval [CI] 4.7-8.5mo) and median overall survival was 11.2 months (90% CI 9.1-16.4 mo). Polymorphism in the excision repair cross-complementation-1 (ERCC-1) gene was associated with time to progression (hazard ratio = 1.91). A circulating tumor cell count ≥ 5 was moderately prognostic of overall survival (hazard ratio = 1.49) as compared with CTC <5. The combination was tolerable, and revealed promising efficacy in metastatic castrate-resistant prostate cancer. ERCC1 genotype maybe predictive of clinical benefit with platinum-based therapy in metastatic prostate cancer. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Urologic oncology AU - Vaishampayan, Ulka N AU - Fontana, Joseph AU - Heilbrun, Lance K AU - Smith, Daryn AU - Heath, Elisabeth AU - Dickow, Brenda AU - Figg, William D AD - Department of Oncology, Department of Medicine, Barbara Ann Karmanos Cancer Institute, Wayne State University, Detroit, MI. Electronic address: vaishamu@karmanos.org. ; Department of Oncology, Department of Medicine, Barbara Ann Karmanos Cancer Institute, Wayne State University, Detroit, MI. ; Biostatistics Core, Barbara Ann Karmanos Cancer Institute, Detroit, MI. ; Clinical Trials Office, Barbara Ann Karmanos Cancer Institute, Detroit, MI. ; Medical Oncology Branch, National Cancer Institute, Bethesda, MD. Y1 - 2014/01// PY - 2014 DA - January 2014 SP - 31.e25 EP - 33 VL - 32 IS - 1 KW - Antibodies, Monoclonal, Humanized KW - 0 KW - DNA-Binding Proteins KW - Organoplatinum Compounds KW - Bevacizumab KW - 2S9ZZM9Q9V KW - satraplatin KW - 8D7B37T28G KW - ERCC1 protein, human KW - EC 3.1.- KW - Endonucleases KW - Prostate-Specific Antigen KW - EC 3.4.21.77 KW - Index Medicus KW - Prostate cancer KW - Excision repair polymorphism KW - Phase II clinical trial KW - Chemotherapy KW - Humans KW - DNA-Binding Proteins -- genetics KW - Disease Progression KW - Aged KW - Endonucleases -- genetics KW - Genotype KW - Aged, 80 and over KW - Prostate-Specific Antigen -- blood KW - Treatment Outcome KW - Neoplasm Metastasis KW - Middle Aged KW - Male KW - Neoplastic Cells, Circulating KW - Proportional Hazards Models KW - Organoplatinum Compounds -- administration & dosage KW - Antibodies, Monoclonal, Humanized -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Prostatic Neoplasms, Castration-Resistant -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490735993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Urologic+oncology&rft.atitle=Phase+II+trial+of+bevacizumab+and+satraplatin+in+docetaxel-pretreated+metastatic+castrate-resistant+prostate+cancer.&rft.au=Vaishampayan%2C+Ulka+N%3BFontana%2C+Joseph%3BHeilbrun%2C+Lance+K%3BSmith%2C+Daryn%3BHeath%2C+Elisabeth%3BDickow%2C+Brenda%3BFigg%2C+William+D&rft.aulast=Vaishampayan&rft.aufirst=Ulka&rft.date=2014-01-01&rft.volume=32&rft.issue=1&rft.spage=31.e25&rft.isbn=&rft.btitle=&rft.title=Urologic+oncology&rft.issn=1873-2496&rft_id=info:doi/10.1016%2Fj.urolonc.2012.11.017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-12-29 N1 - Date created - 2013-12-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: BJU Int. 2005 Nov;96(7):990-4 [16225514] Oncology. 2005;68(1):2-9 [15741753] N Engl J Med. 2006 Dec 14;355(24):2542-50 [17167137] J Clin Oncol. 2007 Apr 20;25(12):1539-44 [17442997] Curr Treat Options Oncol. 2007 Feb;8(1):89-95 [17634836] Oncology. 2007;72(5-6):364-70 [18204222] Clin Cancer Res. 2008 Oct 1;14(19):6302-9 [18829513] Pharmacogenet Genomics. 2009 Aug;19(8):613-25 [19620936] Expert Opin Investig Drugs. 2009 Nov;18(11):1787-97 [19888874] J Clin Oncol. 2009 Nov 10;27(32):5431-8 [19805692] N Engl J Med. 2011 May 26;364(21):1995-2005 [21612468] Urol Oncol. 2011 Nov-Dec;29(6):676-81 [20451413] J Clin Oncol. 2012 May 1;30(13):1534-40 [22454414] N Engl J Med. 2012 Sep 27;367(13):1187-97 [22894553] J Clin Oncol. 1999 Nov;17(11):3461-7 [10550143] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] Cancer Res. 2001 Mar 15;61(6):2533-6 [11289126] Clin Cancer Res. 2001 Jul;7(7):1932-6 [11448906] Lung Cancer. 2004 Jun;44(3):311-6 [15140544] Ann Oncol. 2004 Aug;15(8):1194-203 [15277258] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214] Science. 2005 Jan 7;307(5706):58-62 [15637262] Urology. 2006 Jun;67(6):1235-40 [16765185] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.urolonc.2012.11.017 ER - TY - JOUR T1 - CYP2E1-dependent and leptin-mediated hepatic CD57 expression on CD8+ T cells aid progression of environment-linked nonalcoholic steatohepatitis. AN - 1490730983; 24211274 AB - Environmental toxins induce a novel CYP2E1/leptin signaling axis in liver. This in turn activates a poorly characterized innate immune response that contributes to nonalcoholic steatohepatitis (NASH) progression. To identify the relevant subsets of T-lymphocytes in CYP2E1-dependent, environment-linked NASH, we utilized a model of diet induced obese (DIO) mice that are chronically exposed to bromodichloromethane. Mice deficient in CYP2E1, leptin (ob/ob mice), or both T and B cells (Pfp/Rag2 double knockout (KO) mice) were used to delineate the role of each of these factors in metabolic oxidative stress-induced T cell activation. Results revealed that elevated levels of lipid peroxidation, tyrosyl radical formation, mitochondrial tyrosine nitration and hepatic leptin as a consequence of metabolic oxidative stress caused increased levels of hepatic CD57, a marker of peripheral blood lymphocytes including NKT cells. CD8+CD57+ cytotoxic T cells but not CD4+CD57+ cells were significantly decreased in mice lacking CYP2E1 and leptin. There was a significant increase in the levels of T cell cytokines IL-2, IL-1β, and IFN-γ in bromodichloromethane exposed DIO mice but not in mice that lacked CYP2E1, leptin or T and B cells. Apoptosis as evidenced by TUNEL assay and levels of cleaved caspase-3 was significantly lower in leptin and Pfp/Rag2 KO mice and highly correlated with protection from NASH. The results described above suggest that higher levels of oxidative stress-induced leptin mediated CD8+CD57+ T cells play an important role in the development of NASH. It also provides a novel insight of immune dysregulation and may be a key biomarker in NASH. © 2013. JF - Toxicology and applied pharmacology AU - Seth, Ratanesh Kumar AU - Das, Suvarthi AU - Kumar, Ashutosh AU - Chanda, Anindya AU - Kadiiska, Maria B AU - Michelotti, Gregory AU - Manautou, Jose AU - Diehl, Anna Mae AU - Chatterjee, Saurabh AD - Environmental Health and Disease Laboratory, Department of Environmental Health Sciences, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA. ; Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; Division of Gastroenterology, Duke University, Durham, NC 27707, USA. ; Dept. of Pharmaceutical Sciences, University of Connecticut, Storrs, CT 06269-3092, USA. ; Environmental Health and Disease Laboratory, Department of Environmental Health Sciences, Arnold School of Public Health, University of South Carolina, Columbia, SC 29208, USA. Electronic address: schatt@mailbox.sc.edu. Y1 - 2014/01/01/ PY - 2014 DA - 2014 Jan 01 SP - 42 EP - 54 VL - 274 IS - 1 KW - Antigens, CD57 KW - 0 KW - Cytokines KW - Inflammation Mediators KW - Leptin KW - Trihalomethanes KW - bromodichloromethane KW - 7LN464CH2O KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - Index Medicus KW - Apoptosis KW - CD3 KW - IL-2 KW - Bromodichloromethane KW - Lipid peroxidation KW - Animals KW - Cytokines -- biosynthesis KW - Mice KW - Non-alcoholic Fatty Liver Disease KW - Inflammation Mediators -- metabolism KW - Mice, Knockout KW - Mice, 129 Strain KW - Oxidative Stress -- physiology KW - Obesity -- metabolism KW - Oxidative Stress -- drug effects KW - Mice, Inbred C57BL KW - Trihalomethanes -- toxicity KW - Gene Expression Regulation KW - Obesity -- chemically induced KW - Male KW - CD8-Positive T-Lymphocytes -- drug effects KW - Fatty Liver -- chemically induced KW - Fatty Liver -- metabolism KW - CD8-Positive T-Lymphocytes -- metabolism KW - Cytochrome P-450 CYP2E1 -- deficiency KW - Antigens, CD57 -- biosynthesis KW - Leptin -- deficiency KW - Environmental Exposure -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490730983?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=CYP2E1-dependent+and+leptin-mediated+hepatic+CD57+expression+on+CD8%2B+T+cells+aid+progression+of+environment-linked+nonalcoholic+steatohepatitis.&rft.au=Seth%2C+Ratanesh+Kumar%3BDas%2C+Suvarthi%3BKumar%2C+Ashutosh%3BChanda%2C+Anindya%3BKadiiska%2C+Maria+B%3BMichelotti%2C+Gregory%3BManautou%2C+Jose%3BDiehl%2C+Anna+Mae%3BChatterjee%2C+Saurabh&rft.aulast=Seth&rft.aufirst=Ratanesh&rft.date=2014-01-01&rft.volume=274&rft.issue=1&rft.spage=42&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2013.10.029 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-02-24 N1 - Date created - 2013-12-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Gastroenterology. 2002 May;122(5):1399-410 [11984526] Hepatogastroenterology. 2003 Jan-Feb;50(49):178-82 [12630018] Blood. 2003 Apr 1;101(7):2711-20 [12433688] Apoptosis. 2003 Jun;8(3):237-49 [12766484] Gastroenterology. 2004 Sep;127(3):870-82 [15362042] FASEB J. 2004 Oct;18(13):1612-4 [15319373] Liver. 1985 Jun;5(3):134-41 [3876501] Hepatology. 1989 Nov;10(5):795-800 [2509321] Gut. 1994 Nov;35(11):1509-16 [7828963] Int J Clin Lab Res. 1995;25(3):153-6 [8562979] Hepatology. 1996 May;23(5):1189-99 [8621153] Autoimmunity. 1995;22(3):163-71 [8734570] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):12908-13 [8917518] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10663-8 [9380692] Br J Haematol. 1998 Mar;100(3):469-77 [9504628] Gastroenterology. 2005 Jan;128(1):138-46 [15633130] J Immunol. 2005 Mar 15;174(6):3137-42 [15749839] Immunol Rev. 2005 Jun;205:158-69 [15882352] Clin Immunol. 2006 Dec;121(3):314-23 [17035093] Am J Physiol Gastrointest Liver Physiol. 2007 Feb;292(2):G628-38 [17038628] Exp Gerontol. 2007 Sep;42(9):852-8 [17604927] Int Immunol. 2007 Aug;19(8):1021-9 [17698563] J Hepatol. 2007 Dec;47(6):826-33 [17923165] Hepatobiliary Pancreat Dis Int. 2007 Dec;6(6):572-8 [18086620] Free Radic Biol Med. 2008 Apr 1;44(7):1475-82 [18267128] FASEB J. 2008 Jun;22(6):2012-22 [18218920] Hepatology. 2008 Sep;48(3):963-77 [18726940] J Gastroenterol. 2008;43(11):811-22 [19012034] J Hepatol. 2009 Jan;50(1):204-10 [19014878] Front Biosci (Landmark Ed). 2009;14:3771-81 [19273309] Trends Immunol. 2009 Jul;30(7):306-12 [19540809] Gastroenterology. 2009 Aug;137(2):713-23 [19375424] Semin Immunopathol. 2009 Sep;31(3):345-58 [19533130] Proc Am Thorac Soc. 2009 Dec 1;6(7):573-80 [19934352] Antioxid Redox Signal. 2011 Jul 15;15(2):485-504 [21128703] Hepatology. 2011 Jul;54(1):133-44 [21488066] Immunology. 2011 Sep;134(1):17-32 [21711350] Free Radic Biol Med. 2012 May 1;52(9):1666-79 [22343416] J Hepatol. 2012 Oct;57(4):860-6 [22668639] Toxicol Pathol. 2013 Feb;41(2):343-60 [23262638] Toxicol Appl Pharmacol. 2013 Jun 15;269(3):297-306 [23438451] J Hepatol. 2013 Apr;58(4):778-84 [23207144] Toxicol Sci. 2013 Aug;134(2):291-303 [23640861] J Gastroenterol Hepatol. 2013 Aug;28 Suppl 1:11-7 [23855290] J Hepatol. 2013 Oct;59(4):859-71 [23751754] Int Immunol. 2000 Jul;12(7):1005-13 [10882412] Clin Immunol. 2000 Sep;96(3):230-5 [10964541] Alcohol. 2001 Jul;24(3):155-67 [11557301] Immunol Cell Biol. 2002 Feb;80(1):1-13 [11869357] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2013.10.029 ER - TY - CONF T1 - Cumulative risk: toxicity and interactions of physical and chemical stressors. AN - 1490725836; 24154487 AB - Recent efforts to update cumulative risk assessment procedures to incorporate nonchemical stressors ranging from physical to psychosocial reflect increased interest in consideration of the totality of variables affecting human health and the growing desire to develop community-based risk assessment methods. A key roadblock is the uncertainty as to how nonchemical stressors behave in relationship to chemical stressors. Physical stressors offer a reasonable starting place for measuring the effects of nonchemical stressors and their modulation of chemical effects (and vice versa), as they clearly differ from chemical stressors; and "doses" of many physical stressors are more easily quantifiable than those of psychosocial stressors. There is a commonly held belief that virtually nothing is known about the impact of nonchemical stressors on chemically mediated toxicity or the joint impact of coexposure to chemical and nonchemical stressors. Although this is generally true, there are several instances where a substantial body of evidence exists. A workshop titled "Cumulative Risk: Toxicity and Interactions of Physical and Chemical Stressors" held at the 2013 Society of Toxicology Annual Meeting provided a forum for discussion of research addressing the toxicity of physical stressors and what is known about their interactions with chemical stressors, both in terms of exposure and effects. Physical stressors including sunlight, heat, radiation, infectious disease, and noise were discussed in reference to identifying pathways of interaction with chemical stressors, data gaps, and suggestions for future incorporation into cumulative risk assessments. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Rider, Cynthia V AU - Boekelheide, Kim AU - Catlin, Natasha AU - Gordon, Christopher J AU - Morata, Thais AU - Selgrade, Maryjane K AU - Sexton, Kenneth AU - Simmons, Jane Ellen Y1 - 2014/01// PY - 2014 DA - January 2014 SP - 3 EP - 11 VL - 137 IS - 1 KW - Environmental Pollutants KW - 0 KW - Index Medicus KW - radiation KW - infectious disease KW - cumulative risk KW - joint action KW - noise. KW - sunlight KW - nonchemical stressors KW - temperature KW - Animals KW - Sunlight -- adverse effects KW - Risk Factors KW - Humans KW - Hot Temperature -- adverse effects KW - X-Rays -- adverse effects KW - Communicable Diseases -- complications KW - Noise -- adverse effects KW - Risk Assessment KW - Toxicology -- methods KW - Environmental Exposure -- adverse effects KW - Environmental Pollutants -- adverse effects KW - Stress, Physiological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490725836?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Cumulative+risk%3A+toxicity+and+interactions+of+physical+and+chemical+stressors.&rft.au=Rider%2C+Cynthia+V%3BBoekelheide%2C+Kim%3BCatlin%2C+Natasha%3BGordon%2C+Christopher+J%3BMorata%2C+Thais%3BSelgrade%2C+Maryjane+K%3BSexton%2C+Kenneth%3BSimmons%2C+Jane+Ellen&rft.aulast=Rider&rft.aufirst=Cynthia&rft.date=2014-01-01&rft.volume=137&rft.issue=1&rft.spage=3&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%2Fkft228 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-28 N1 - Date created - 2013-12-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Hear Res. 2000 Dec;150(1-2):206-14 [11077204] Sci Total Environ. 2013 May 1;452-453:50-7 [23500398] Toxicol Sci. 2002 May;67(1):88-97 [11961220] J Toxicol Environ Health A. 2003 Feb 14;66(3):291-304 [12521673] Occup Environ Med. 2003 Oct;60(10):739-45 [14504361] Schriftenr Ver Wasser Boden Lufthyg. 2003;(112):81-99 [14753026] Inhal Toxicol. 2004;16 Suppl 1:107-14 [15204799] Noise Health. 2004 Apr-Jun;6(23):21-8 [15273021] Toxicol Appl Pharmacol. 1984 Nov;76(2):356-64 [6093289] Toxicol Appl Pharmacol. 1986 Dec;86(3):372-9 [3787631] Psychopharmacology (Berl). 1987;91(1):34-9 [3103157] Fundam Appl Toxicol. 1988 Jul;11(1):169-80 [3209012] J Biochem Toxicol. 1989 Winter;4(4):221-9 [2483849] Neurotoxicol Teratol. 1994 Sep-Oct;16(5):427-53 [7845326] Occup Med. 1995 Jul-Aug;10(3):609-21 [8578422] Radiat Res. 1997 Apr;147(4):457-67 [9092926] Toxicology. 1997 Mar 28;118(2-3):149-58 [9129169] Hear Res. 1999 Jun;132(1-2):149-59 [10392557] Ann N Y Acad Sci. 1952 Nov 20;55(4):548-73 [13139144] J Natl Cancer Inst Monogr. 2005;(34):6-8 [15784812] Chem Biol Interact. 2007 Mar 20;166(1-3):163-9 [16860297] Toxicol Sci. 2007 Dec;100(2):328-32 [17878151] Drug Metab Dispos. 2008 Feb;36(2):205-16 [18218849] Nat Rev Immunol. 2008 Apr;8(4):279-89 [18340345] Biochem Pharmacol. 2009 Feb 15;77(4):642-53 [19027719] Sci Total Environ. 2010 Aug 15;408(18):3719-24 [20580411] J Air Waste Manag Assoc. 2010 Jul;60(7):838-48 [20681431] Toxicol Sci. 2010 Oct;117(2):466-74 [20616204] Toxicol Sci. 2010 Oct;117(2):457-65 [20616210] Sci Total Environ. 2010 Nov 1;408(23):5784-93 [20828789] Toxicol Sci. 2011 Mar;120 Suppl 1:S28-48 [20881231] Environ Health Perspect. 2011 May;119(5):701-6 [21193384] Environ Health Perspect. 2011 Nov;119(11):1583-9 [21757418] Int J Environ Res Public Health. 2012 Feb;9(2):370-90 [22470298] Environ Health. 2012;11 Suppl 1:S18 [22759500] Toxicol Lett. 2012 Aug 3;212(3):241-51 [22705057] Environ Sci Technol. 2012 Aug 21;46(16):9062-70 [22834915] Toxicol Sci. 2000 Dec;58(2):315-23 [11099644] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kft228 ER - TY - JOUR T1 - Purification of a serine protease and evidence for a protein C activator from the saliva of the tick, Ixodes scapularis. AN - 1490712270; 24184517 AB - The saliva of ticks is critical to their survival as parasites and hematophagous animals. In this study, we have purified an enzyme with trypsin-like activity from the saliva of the tick vector of Lyme Disease, Ixodes scapularis. This enzyme, named as IXOSP (I. scapularis salivary serine protease), is a 29.9 kDa molecule with N-terminus FPxMVxLRIKxR. A BLAST search identified IXOSP as a secreted serine protease (AAY66740) with a conserved catalytic triad His, Asp, and Ser. In vitro studies demonstrated that IXOSP cleaves chromogenic substrates with arginine in the P1 position, by a mechanism inhibited by PMSF or aprotinin. Gene expression studies revealed that IXOSP is expressed at different tick developmental stages, including eggs, and unfed or fed adult tick salivary glands, but not in nymphs or in the midgut. While the physiological substrate for IXOSP remains to be identified, we demonstrated that I. scapularis saliva activate protein C (PC) resulting in the production of activated PC, a potent anticoagulant that also regulates a myriad of inflammatory responses through protease activated receptors. In contrast, the salivary glands of Anopheles gambiae, Anopheles stephensi, Anopheles albimanus, Aedes aegypti, Lutzomyia longipalpis, and Phlebotomus ariasi did not activate protein C. These discoveries are discussed in the context of blood coagulation, inflammation and vector-host interactions. Published by Elsevier Ltd. JF - Toxicon : official journal of the International Society on Toxinology AU - Pichu, Sivakamasundari AU - Ribeiro, José M C AU - Mather, Thomas N AU - Francischetti, Ivo M B AD - Center for Vector-Borne Disease, University of Rhode Island, Kingston, RI 02881, USA. Electronic address: au_sudha@yahoo.com. ; Section of Vector Biology, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. ; Center for Vector-Borne Disease, University of Rhode Island, Kingston, RI 02881, USA. ; Section of Vector Biology, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: ifrancischetti@niaid.nih.gov. Y1 - 2014/01// PY - 2014 DA - January 2014 SP - 32 EP - 39 VL - 77 KW - DNA Primers KW - 0 KW - Oligopeptides KW - protein C activator peptide KW - Serine Proteases KW - EC 3.4.- KW - Index Medicus KW - Serine protease KW - Activated protein C (APC) KW - Saliva KW - Ixodes scapularis KW - Protease activated receptors (PAR) KW - Sequence Analysis, Protein KW - Mass Spectrometry KW - Gene Expression Regulation, Developmental -- physiology KW - Animals KW - Rhode Island KW - DNA Primers -- genetics KW - Gene Expression Regulation, Enzymologic -- physiology KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Computational Biology KW - Species Specificity KW - Serine Proteases -- toxicity KW - Serine Proteases -- isolation & purification KW - Serine Proteases -- genetics KW - Hemostasis -- drug effects KW - Oligopeptides -- genetics KW - Oligopeptides -- isolation & purification KW - Saliva -- enzymology KW - Ixodes -- enzymology KW - Oligopeptides -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1490712270?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.atitle=Purification+of+a+serine+protease+and+evidence+for+a+protein+C+activator+from+the+saliva+of+the+tick%2C+Ixodes+scapularis.&rft.au=Pichu%2C+Sivakamasundari%3BRibeiro%2C+Jos%C3%A9+M+C%3BMather%2C+Thomas+N%3BFrancischetti%2C+Ivo+M+B&rft.aulast=Pichu&rft.aufirst=Sivakamasundari&rft.date=2014-01-01&rft.volume=77&rft.issue=&rft.spage=32&rft.isbn=&rft.btitle=&rft.title=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.issn=1879-3150&rft_id=info:doi/10.1016%2Fj.toxicon.2013.10.025 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-08-19 N1 - Date created - 2013-12-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Insect Biochem Mol Biol. 2000 Feb;30(2):95-105 [10696585] Front Cell Infect Microbiol. 2013;3:43 [23971008] J Biol Chem. 2001 Apr 6;276(14):11199-203 [11278252] Clin Microbiol Infect. 2001 Feb;7(2):80-3 [11298147] Insect Biochem Mol Biol. 2001 Jun 22;31(8):817-25 [11378417] Prep Biochem Biotechnol. 2001 May;31(2):201-7 [11426706] J Exp Biol. 2002 Sep;205(Pt 18):2843-64 [12177149] J Exp Med. 2002 Sep 2;196(5):561-4 [12208872] Annu Rev Entomol. 2003;48:73-88 [12194906] Insect Biochem Mol Biol. 2003 Apr;33(4):407-15 [12650689] Biochem Biophys Res Commun. 2003 Jun 13;305(4):869-75 [12767911] Insect Biochem Mol Biol. 2004 Jan;34(1):1-17 [14723893] Insect Mol Biol. 2004 Feb;13(1):9-18 [14728662] Med Vet Entomol. 2004 Mar;18(1):20-4 [15009442] Infect Immun. 2004 May;72(5):2989-94 [15102811] J Mol Biol. 2004 Jul 16;340(4):783-95 [15223320] Anal Biochem. 1983 Jul 15;132(2):288-93 [6353999] Int J Parasitol. 1983 Oct;13(5):447-54 [6642860] Eur J Biochem. 1990 Mar 30;188(3):507-15 [2110057] J Med Entomol. 1990 Jul;27(4):646-50 [2388239] Nucleic Acids Res. 1997 Sep 1;25(17):3389-402 [9254694] Nucleic Acids Res. 1997 Dec 15;25(24):4876-82 [9396791] Thromb Haemost. 2005 Jul;94(1):167-74 [16113800] Toxicon. 2006 Jan;47(1):1-20 [16364387] Insect Biochem Mol Biol. 2006 Feb;36(2):111-29 [16431279] Trends Parasitol. 2007 Sep;23(9):397-407 [17656153] Exp Appl Acarol. 2007;42(4):291-300 [17710557] Eukaryot Cell. 2007 Oct;6(10):1745-57 [17715367] Annu Rev Entomol. 2008;53:323-43 [17877457] Parasitol Int. 2008 Dec;57(4):499-505 [18775510] Front Biosci (Landmark Ed). 2009;14:2051-88 [19273185] Thromb Haemost. 2009 Sep;102(3):437-53 [19718463] J Biol Chem. 2011 Apr 1;286(13):10960-9 [21270122] BMC Biochem. 2011;12:32 [21708020] Ticks Tick Borne Dis. 2012 Feb;3(1):18-26 [22309855] Arterioscler Thromb Vasc Biol. 2012 Sep;32(9):2185-98 [22796577] Ticks Tick Borne Dis. 2013 Feb;4(1-2):160-3 [23141105] Insect Biochem Mol Biol. 2001 Mar 15;31(4-5):465-72 [11222956] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.toxicon.2013.10.025 ER - TY - JOUR T1 - Serum- and glucocorticoid-regulated kinase 2 determines drug-activated pregnane X receptor to induce gluconeogenesis in human liver cells. AN - 1469217474; 24204015 AB - Drug activation of the human nuclear pregnane X receptor (PXR) induced gluconeogenic genes and increased glucose production. In this study, we have determined that serum- and glucocorticoid-regulated kinase 2 (SGK2) is an essential factor that mediates this PXR-regulated glucose 6-phosphatase (G6Pase) induction and glucose production. Both SGK2 and G6Pase mRNAs were increased in rifampicin-treated HepG2 cells stably expressing human PXR. Reporter and chromatin immunoprecipitation assays delineated PXR activation of the SGK2 gene to a distal and proximal DNA sequence within its promoter: distal PXR response element (-2587/-2209) and proximal PXR response element (-115/-75), respectively. Small interfering RNA (siRNA) knockdown of SGK2 severely attenuated PXR-regulated induction of G6Pase as well as glucose production. SGK2 constitutes an insulin-independent signal pathway to regulate gluconeogenesis because siRNA knockdown of the insulin-responsive transcription factor forkhead box protein O1 did not affect rifampicin induction of G6Pase. Rifampicin treatment of two different samples of human primary hepatocytes revealed that PXR induces G6Pase in the presence of high levels of SGK2, whereas PXR represses G6Pase in its absence. Mediating PXR activation of the G6Pase gene is the first biological role found for hepatic SGK2 and might have therapeutic implications for side effects, such as diabetes, caused by drugs that activate PXR. JF - The Journal of pharmacology and experimental therapeutics AU - Gotoh, Saki AU - Negishi, Masahiko AD - Pharmacogenetics Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina. Y1 - 2014/01// PY - 2014 DA - January 2014 SP - 131 EP - 140 VL - 348 IS - 1 KW - Enzyme Inhibitors KW - 0 KW - Immediate-Early Proteins KW - Receptors, Steroid KW - pregnane X receptor KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - serum-glucocorticoid regulated kinase KW - Rifampin KW - VJT6J7R4TR KW - Index Medicus KW - Animals KW - Hep G2 Cells KW - Liver -- drug effects KW - Cells, Cultured KW - Humans KW - Mice, Inbred C3H KW - Liver -- metabolism KW - Enzyme Inhibitors -- pharmacology KW - Mice KW - Rifampin -- pharmacology KW - Male KW - Gluconeogenesis -- drug effects KW - Hepatocytes -- drug effects KW - Protein-Serine-Threonine Kinases -- metabolism KW - Gluconeogenesis -- physiology KW - Immediate-Early Proteins -- metabolism KW - Receptors, Steroid -- metabolism KW - Immediate-Early Proteins -- antagonists & inhibitors KW - Protein-Serine-Threonine Kinases -- antagonists & inhibitors KW - Receptors, Steroid -- agonists KW - Hepatocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1469217474?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Serum-+and+glucocorticoid-regulated+kinase+2+determines+drug-activated+pregnane+X+receptor+to+induce+gluconeogenesis+in+human+liver+cells.&rft.au=Gotoh%2C+Saki%3BNegishi%2C+Masahiko&rft.aulast=Gotoh&rft.aufirst=Saki&rft.date=2014-01-01&rft.volume=348&rft.issue=1&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.113.209379 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-02-10 N1 - Date created - 2013-12-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem J. 1999 Nov 15;344 Pt 1:189-97 [10548550] Annu Rev Physiol. 2006;68:461-90 [16460280] Clin Pharmacol Ther. 2001 Jun;69(6):400-6 [11406737] J Clin Invest. 2002 Nov;110(9):1263-8 [12417564] Clin Pharmacol Ther. 2003 Oct;74(4):334-40 [14534520] Obes Res. 2004 May;12(5):862-70 [15166308] Mol Cell Biol. 2004 Sep;24(18):7931-40 [15340055] Am Rev Respir Dis. 1982 Jan;125(1):23-7 [7039435] Natl Med J India. 1997 Jan-Feb;10(1):11-2 [9069698] Biochem J. 1999 Apr 15;339 ( Pt 2):319-28 [10191262] Biochem Biophys Res Commun. 2005 Apr 1;329(1):275-80 [15721303] Clin Pharmacol Ther. 2013 Jun;93(6):556-63 [23588309] Pflugers Arch. 2007 Mar;453(6):863-70 [17051390] J Biol Chem. 2007 Mar 30;282(13):9768-76 [17267396] Biochem J. 2007 Nov 1;407(3):373-81 [17635106] Drug Metab Pharmacokinet. 2008;23(1):8-13 [18305370] J Clin Invest. 2008 Sep;118(9):3228-39 [18677425] J Investig Med. 2009 Mar;57(3):495-9 [19188844] J Biol Chem. 2011 Feb 4;286(5):3570-8 [21127053] Environ Health Perspect. 2012 Jun;120(6):779-89 [22296744] Atheroscler Suppl. 2012 Aug;13(1):1-10 [22818818] Clin Pharmacol Ther. 2000 Nov;68(5):495-500 [11103752] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/jpet.113.209379 ER - TY - JOUR T1 - Chemopreventive effects of an HDAC2-selective inhibitor on rat colon carcinogenesis and APCmin/+ mouse intestinal tumorigenesis. AN - 1467635900; 24218540 AB - Epigenetic modulators, particularly histone deacetylases (HDACs), are valid targets for cancer prevention and therapy. Recent studies report that HDAC2 overexpression is associated with colon tumor progression and is a potential target for colon cancer prevention. This study tested chemopreventive and dose-response effects of Ohio State University HDAC42 (OSU-HDAC42), a selective HDAC2 inhibitor, using a rat colon carcinogenesis model to assess aberrant crypt foci inhibition and a familial adenomatous polyposis model to assess intestinal tumor inhibition. Colonic aberrant crypt foci were induced by azoxymethane (AOM) (15 mg/kg body weight, once-weekly subcutaneous injections at 8 and 9 weeks age). One week after AOM treatment, groups of rats were fed an AIN-76A diet containing 0, 75, 150, and 300 ppm OSU-HDAC42 for 8 weeks, and colonic aberrant crypt foci were evaluated. To assess the inhibitory effect of OSU-HDAC42 on small-intestinal polyps and colon tumor growth, 6-week-old male C57Bl/6J-APC(min/+)mice were fed an AIN-76A diet containing 150 ppm OSU-HADC42 or 300 ppm pan-HDAC inhibitor suberoylanilide hydroxyamic acid (SAHA) for 80 days. Our results demonstrate that dietary OSU-HDAC42 produced dose-dependent inhibition of AOM-induced colonic aberrant crypt foci formation (13-50%; P 46%; P 1 mm (P 26%) in APC(min/+)mice, whereas 300 ppm SAHA showed nonsignificant inhibition. Mice fed 150 ppm OSU-HDAC42 had significantly decreased HDAC2, proliferating cell nuclear antigen, B cell lymphoma 2, cyclin-dependent kinase 2, and cell division cycle homolog 25C expression levels and increased p53 expression levels. These observations demonstrate the chemopreventive efficacy of OSU-HDAC42 against chemically induced and polyposis models of intestinal tumorigenesis. JF - The Journal of pharmacology and experimental therapeutics AU - Ravillah, Durgadevi AU - Mohammed, Altaf AU - Qian, Li AU - Brewer, Misty AU - Zhang, Yuting AU - Biddick, Laura AU - Steele, Vernon E AU - Rao, Chinthalapally V AD - Hematology-Oncology Section, Department of Medicine, Center for Cancer Prevention and Drug Development, PCS Oklahoma Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma (D.R., A.M., L.Q., M.B., Y.Z., L.B., C.V.R.); and Division of Cancer Prevention, Chemoprevention Agent Development Research Group, National Institutes of Health National Cancer Institute, Bethesda, Maryland (V.E.S.). Y1 - 2014/01// PY - 2014 DA - January 2014 SP - 59 EP - 68 VL - 348 IS - 1 KW - APC protein, human KW - 0 KW - Adenomatous Polyposis Coli Protein KW - Histone Deacetylase Inhibitors KW - OSU-HDAC42 compound KW - Phenylbutyrates KW - Hdac2 protein, mouse KW - EC 3.5.1.98 KW - Histone Deacetylase 2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Humans KW - Mice, Inbred C57BL KW - Mice KW - HCT116 Cells KW - Mice, Transgenic KW - Male KW - Female KW - Histone Deacetylase 2 -- antagonists & inhibitors KW - Phenylbutyrates -- therapeutic use KW - Colonic Neoplasms -- genetics KW - Adenomatous Polyposis Coli Protein -- biosynthesis KW - Phenylbutyrates -- pharmacology KW - Disease Models, Animal KW - Carcinogenesis -- pathology KW - Intestinal Neoplasms -- prevention & control KW - Histone Deacetylase 2 -- metabolism KW - Carcinogenesis -- genetics KW - Carcinogenesis -- drug effects KW - Histone Deacetylase Inhibitors -- therapeutic use KW - Intestinal Neoplasms -- genetics KW - Intestinal Neoplasms -- enzymology KW - Colonic Neoplasms -- pathology KW - Colonic Neoplasms -- prevention & control KW - Adenomatous Polyposis Coli Protein -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1467635900?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chemopreventive+effects+of+an+HDAC2-selective+inhibitor+on+rat+colon+carcinogenesis+and+APCmin%2F%2B+mouse+intestinal+tumorigenesis.&rft.au=Ravillah%2C+Durgadevi%3BMohammed%2C+Altaf%3BQian%2C+Li%3BBrewer%2C+Misty%3BZhang%2C+Yuting%3BBiddick%2C+Laura%3BSteele%2C+Vernon+E%3BRao%2C+Chinthalapally+V&rft.aulast=Ravillah&rft.aufirst=Durgadevi&rft.date=2014-01-01&rft.volume=348&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.113.208645 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2014-02-10 N1 - Date created - 2013-12-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell Death Differ. 2005 Apr;12(4):395-404 [15665816] J Biol Chem. 1998 Oct 30;273(44):28921-30 [9786895] J Clin Oncol. 2005 Jun 10;23(17):3923-31 [15897550] J Clin Oncol. 2006 Jan 1;24(1):166-73 [16330674] Nat Rev Cancer. 2006 Jan;6(1):38-51 [16397526] Science. 2006 Feb 10;311(5762):844-7 [16469925] Cancer Res. 2007 Apr 1;67(7):3145-52 [17409421] Gut. 2007 Oct;56(10):1453-9 [17566021] Blood. 2008 Feb 1;111(3):1060-6 [17962510] Br J Cancer. 2008 Feb 12;98(3):604-10 [18212746] N Engl J Med. 2008 Mar 13;358(11):1148-59 [18337604] Cancer Lett. 2009 May 8;277(1):8-21 [18824292] N Engl J Med. 2009 Dec 17;361(25):2449-60 [20018966] Carcinogenesis. 2010 Jan;31(1):27-36 [19752007] PLoS One. 2011;6(11):e28103 [22132221] J Cell Biochem. 2012 Jun;113(6):2167-77 [22492270] PLoS One. 2013;8(1):e54001 [23342059] Cell. 1999 Oct 29;99(3):335-45 [10555149] Oncogene. 1999 Nov 1;18(45):6145-57 [10557106] J Biol Chem. 1999 Dec 17;274(51):36031-4 [10593882] Nature. 2000 Jan 6;403(6765):41-5 [10638745] Cell. 2000 Jan 7;100(1):57-70 [10647931] EMBO J. 2000 Mar 15;19(6):1176-9 [10716917] J Biol Chem. 2000 Jul 7;275(27):20436-43 [10777477] Trends Endocrinol Metab. 2001 Sep;12(7):294-300 [11504668] Oncogene. 2001 Sep 27;20(43):6152-63 [11593423] EMBO J. 2001 Dec 17;20(24):6969-78 [11742974] Annu Rev Biochem. 2001;70:81-120 [11395403] Nat Rev Cancer. 2001 Dec;1(3):194-202 [11902574] Nat Rev Drug Discov. 2002 Feb;1(2):111-21 [12120092] Cancer Res. 2003 Mar 1;63(5):1114-21 [12615730] Genes Dev. 2003 Apr 1;17(7):832-7 [12670866] EMBO J. 2003 Jul 1;22(13):3411-20 [12840003] Clin Cancer Res. 2003 Sep 1;9(10 Pt 1):3578-88 [14506144] Cancer Cell. 2004 May;5(5):455-63 [15144953] EMBO J. 1992 Mar;11(3):961-71 [1312467] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2824-8 [1532660] Science. 1992 May 1;256(5057):668-70 [1350108] J Cell Biol. 1993 Apr;121(1):101-11 [8458862] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):8969-73 [8090754] Cell. 1996 Oct 18;87(2):159-70 [8861899] Biochim Biophys Acta. 1997 Apr 18;1332(2):F25-48 [9141462] Nature. 1997 Sep 25;389(6649):349-52 [9311776] Nature. 1998 Feb 5;391(6667):597-601 [9468139] Science. 1998 Sep 4;281(5382):1509-12 [9727977] Cell Death Differ. 2005 Apr;12(4):377-83 [15706352] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/jpet.113.208645 ER -