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 - 1815699833; PQ0003312906 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/1815699833?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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 - 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 - Synthesis and characterisation of ultrasound imageable heat-sensitive liposomes for HIFU therapy. AN - 1713529735; 26185910 AB - Novel approaches allowing efficient, readily translatable image-guided drug delivery (IGDD) against solid tumours is needed. The objectives of this study were to: 1) develop echogenic low temperature sensitive liposomes (E-LTSLs) loaded with an ultrasound (US) contrast agent (perfluoropentane, PFP), 2) determine the in vitro and in vivo stability of contrast agent encapsulation, 3) co-encapsulate and characterise doxorubicin (Dox) E-LTSL, and cellular uptake and cytotoxicity in combination with high intensity focused ultrasound (HIFU). E-LTSLs were loaded passively with PFP and actively with Dox. PFP encapsulation in E-LTSL was determined by transmission electron microscopy (TEM), and US imageability was determined in tissue-mimicking phantoms and mouse tumour model. Dox release from E-LTSL in physiological buffer was quantified by fluorescence spectroscopy. Cellular uptake and cytotoxicity of E-LTSL in the presence of HIFU-induced mild hyperthermia (∼40-42 °C) was determined in a 3D tumour spheroid model. TEM and US confirmed that the PFP emulsion was contained within LTSLs. Phantom and animal studies showed that the E-LTSLs were echogenic. Temperature versus size increase and Dox release kinetics of E-LTSLs demonstrated no difference compared to LTSL alone. Dox release was 99% under hyperthermia. E-LTSL plus HIFU achieved significantly greater Dox uptake in spheroids and cytotoxicity compared to body temperature. A stable US-imageable liposome co-loaded with Dox and PFP for in vivo IGDD was developed. Data suggest that HIFU can induce cellular uptake and toxicity with E-LTSLs. JF - International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group AU - Maples, Danny AU - McLean, Kevin AU - Sahoo, Kaustuv AU - Newhardt, Ryan AU - Venkatesan, Perumal AU - Wood, Bradford AU - Ranjan, Ashish AD - a Center for Veterinary Health Sciences, Oklahoma State University , Stillwater , Oklahoma and. ; b Center for Interventional Oncology, National Institutes of Health , Bethesda , Maryland , USA. Y1 - 2015 PY - 2015 DA - 2015 SP - 674 EP - 685 VL - 31 IS - 6 KW - Antibiotics, Antineoplastic KW - 0 KW - Contrast Media KW - Fluorocarbons KW - Liposomes KW - perfluoropentane KW - 678-26-2 KW - Doxorubicin KW - 80168379AG KW - Index Medicus KW - Echogenic heat-sensitive liposome KW - Tumor KW - HIFU KW - Spheroid KW - Perfluoropentane KW - Image Guided Drug Delivery KW - Hot Temperature KW - Animals KW - Humans KW - Mice, Nude KW - Cell Line, Tumor KW - Mice, Inbred BALB C KW - Male KW - Doxorubicin -- pharmacokinetics KW - Fluorocarbons -- pharmacokinetics KW - Neoplasms -- drug therapy KW - Antibiotics, Antineoplastic -- administration & dosage KW - Contrast Media -- pharmacokinetics KW - High-Intensity Focused Ultrasound Ablation KW - Doxorubicin -- administration & dosage KW - Neoplasms -- therapy KW - Antibiotics, Antineoplastic -- pharmacokinetics KW - Antibiotics, Antineoplastic -- therapeutic use KW - Fluorocarbons -- administration & dosage KW - Contrast Media -- administration & dosage KW - Doxorubicin -- therapeutic use KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1713529735?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+hyperthermia+%3A+the+official+journal+of+European+Society+for+Hyperthermic+Oncology%2C+North+American+Hyperthermia+Group&rft.atitle=Synthesis+and+characterisation+of+ultrasound+imageable+heat-sensitive+liposomes+for+HIFU+therapy.&rft.au=Maples%2C+Danny%3BMcLean%2C+Kevin%3BSahoo%2C+Kaustuv%3BNewhardt%2C+Ryan%3BVenkatesan%2C+Perumal%3BWood%2C+Bradford%3BRanjan%2C+Ashish&rft.aulast=Maples&rft.aufirst=Danny&rft.date=2015-01-01&rft.volume=31&rft.issue=6&rft.spage=674&rft.isbn=&rft.btitle=&rft.title=International+journal+of+hyperthermia+%3A+the+official+journal+of+European+Society+for+Hyperthermic+Oncology%2C+North+American+Hyperthermia+Group&rft.issn=1464-5157&rft_id=info:doi/10.3109%2F02656736.2015.1057622 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-01 N1 - Date created - 2015-09-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Langmuir. 2012 Oct 16;28(41):14720-9 [22989347] Invest Radiol. 2013 Jun;48(6):395-405 [23399809] Int J Hyperthermia. 2013 Sep;29(6):569-81 [23957326] Theranostics. 2013;3(9):687-91 [24019853] BioDrugs. 2013 Oct;27(5):533-40 [24018470] J Control Release. 2013 Nov 28;172(1):391 [24113486] Contrast Media Mol Imaging. 2014 Jul-Aug;9(4):283-90 [24706612] Cancer Res. 2000 Mar 1;60(5):1197-201 [10728674] Cancer Res. 2000 Dec 15;60(24):6950-7 [11156395] Biochim Biophys Acta. 2003 Aug 7;1614(2):135-8 [12896806] Ann Oncol. 2004 Mar;15(3):440-9 [14998846] Science. 2004 Mar 19;303(5665):1818-22 [15031496] Magn Reson Med. 2004 Jun;51(6):1153-62 [15170835] Eur J Cancer. 2004 Dec;40(18):2851-8 [15571970] Inhal Toxicol. 2005 Aug;17(9):487-93 [16020043] Biochem Biophys Res Commun. 2005 Sep 16;335(1):124-31 [16055092] Magn Reson Med. 2006 Nov;56(5):1011-8 [17029236] J Natl Cancer Inst. 2007 Jan 3;99(1):53-63 [17202113] J Natl Cancer Inst. 2007 Jul 18;99(14):1095-106 [17623798] Biochim Biophys Acta. 2007 Oct;1768(10):2491-9 [17618599] Int J Hyperthermia. 2008 Feb;24(1):79-90 [18214771] Adv Drug Deliv Rev. 2008 Jun 30;60(10):1153-66 [18486268] Langmuir. 2010 Apr 6;26(7):4655-60 [20218695] Int J Hyperthermia. 2011;27(2):140-55 [21314334] J Control Release. 2011 Feb 28;150(1):102-10 [21059375] Biomaterials. 2011 Sep;32(27):6579-87 [21683439] J Control Release. 2011 Jul 15;153(1):4-15 [21277919] J Control Release. 2011 Aug 10;153(3):198-205 [21663778] J Control Release. 2011 Nov 7;155(3):358-66 [21745505] J Control Release. 2012 Mar 28;158(3):487-94 [22210162] Radiology. 2012 Jun;263(3):633-43 [22623690] Radiology. 2012 Aug;264(2):349-68 [22821695] Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2012 Sep-Oct;4(5):492-510 [22730185] J Control Release. 2012 Sep 10;162(2):400-6 [22759980] J Control Release. 2012 Oct 10;163(1):75-81 [22580225] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/02656736.2015.1057622 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 - Patterns of non-suicidal self-injurious behaviours among college students in India AN - 1673612534 AB - Background: Non-suicidal self-injurious behaviour (NSSI) is a growing concern among youth and rarely reaches the attention of mental health and medical services. Aims: The study explored the occurrence, methods, characteristics and reported reasons for NSSI among a sample of college students in India. Methods: A total of 470 participants from undergraduate and postgraduate colleges completed the Functional Assessment of Self Mutilation (FASM) questionnaire. Results: Results indicated that 31.2% of the participants reported NSSI in the past year, with the mean age of onset being 15.9 years. Moderate/severe forms of NSSI were reported by 19.8% of the sample. The most common method was self-hitting (15.2%) followed by cutting or carving skin (13.2%). A majority of self-injurers endorsed multiple methods of NSSI, and there were no significant gender differences in NSSI rates. The NSSI was performed both to regulate internal emotional states (automatic reinforcement) and to influence others in the environment (social reinforcement).The most commonly endorsed reasons for NSSI were ‘to feel relaxed’ and ‘to get control of the situation’, while the least frequently endorsed reasons were ‘to make others angry’ and ‘to avoid college, work, or other activities’. Conclusion: The findings underscore the need to increase the awareness and understanding of NSSIs and to plan targeted interventions among college youth. JF - The International Journal of Social Psychiatry AU - Kharsati, Naphisabet AU - Bhola, Poornima AD - SAN-KER Hospital, Department of Clinical Psychology, Shillong, India ; Department of Clinical Psychology, National Institute of Mental Health and Neuro Sciences, Bangalore, India ; SAN-KER Hospital, Department of Clinical Psychology, Shillong, India Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 39 EP - 49 CY - London PB - SAGE PUBLICATIONS, INC. VL - 61 IS - 1 SN - 0020-7640 KW - Medical Sciences--Psychiatry And Neurology KW - Non-suicidal self-injurious behaviours KW - self-harm KW - cutting KW - youth KW - college KW - community KW - Suicidal behaviour KW - Undergraduate students KW - India UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673612534?accountid=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=Patterns+of+non-suicidal+self-injurious+behaviours+among+college+students+in+India&rft.au=Kharsati%2C+Naphisabet%3BBhola%2C+Poornima&rft.aulast=Kharsati&rft.aufirst=Naphisabet&rft.date=2015-01-01&rft.volume=61&rft.issue=1&rft.spage=39&rft.isbn=&rft.btitle=&rft.title=The+International+Journal+of+Social+Psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764014535755 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-03-24 N1 - Last updated - 2016-09-07 N1 - SubjectsTermNotLitGenreText - India DO - http://dx.doi.org/10.1177/0020764014535755 ER - TY - JOUR T1 - The Design of Covalent Allosteric Drugs AN - 1668254088; PQ0001286074 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; Sackler Institute of Molecular Medicine, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel, NussinoR@helix.nih.gov Y1 - 2015///0, PY - 2015 DA - 0, 2015 SP - 249 EP - 267 PB - Annual Reviews, Inc., 4139 El Camino Way Palo Alto CA 94303-0139 United States VL - 55 SN - 0362-1642, 0362-1642 KW - Toxicology Abstracts KW - allosteric modulator KW - agonist KW - antagonist KW - pharmacology KW - toxicity KW - allosteric drug discovery KW - K-Ras protein KW - Drug discovery KW - Allosteric properties KW - Reviews KW - Drug development KW - Toxicity KW - Drugs KW - Side effects KW - X 24310:Pharmaceuticals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668254088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+Review+of+Pharmacology+and+Toxicology&rft.atitle=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=03621642&rft_id=info:doi/10.1146%2Fannurev-pharmtox-010814-124401 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Drug discovery; K-Ras protein; Reviews; Allosteric properties; Drug development; Toxicity; Drugs; Side effects DO - http://dx.doi.org/10.1146/annurev-pharmtox-010814-124401 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 Biol Chem. 2007 Sep 21;282(38):28004-13 [17650498] Nature. 2007 Nov 22;450(7169):509-14 [17965729] DNA Repair (Amst). 2008 Feb 1;7(2):292-302 [18077224] Chem Res Toxicol. 2008 Jan;21(1):206-19 [18052112] DNA Repair (Amst). 2008 Mar 1;7(3):452-63 [18206427] Chem Res Toxicol. 2008 Apr;21(4):936-43 [18293940] Curr Opin Genet Dev. 2008 Feb;18(1):80-6 [18343102] PLoS Genet. 2008 Jun;4(6):e1000110 [18584027] Nat Rev Genet. 2008 Aug;9(8):619-31 [18626472] J Biol Chem. 2008 Jul 25;283(30):21074-83 [18515798] Cell. 2008 Sep 19;134(6):981-94 [18805091] J Mol Biol. 2004 Jan 9;335(2):573-82 [14672664] Cell. 2008 Oct 3;135(1):97-109 [18854158] J Biol Chem. 2008 Dec 5;283(49):33994-4001 [18836178] Mol Cell. 2009 Jan 16;33(1):117-23 [19150433] Mol Cell Biol. 2009 Mar;29(5):1354-62 [19103743] Nat Genet. 2010 Mar;42(3):245-9 [20118933] Nucleic Acids Res. 2010 Mar;38(5):1489-503 [20008512] Proc Natl Acad Sci U S A. 2010 Mar 16;107(11):4949-54 [20194773] Nucleic Acids Res. 2010 Apr;38(6):e85 [20008099] Proc Natl Acad Sci U S A. 2010 Apr 13;107(15):6805-10 [20351257] Chem Res Toxicol. 2010 Apr 19;23(4):766-70 [20232790] Nature. 2010 Apr 22;464(7292):1214-7 [20383123] DNA Repair (Amst). 2010 Jun 4;9(6):690-9 [20399152] DNA Repair (Amst). 2010 Jul 1;9(7):835-41 [20471329] Biochemistry. 2010 Jul 27;49(29):6165-76 [20518483] Nature. 2010 Sep 2;467(7311):108-11 [20811460] Nat Chem Biol. 2010 Oct;6(10):774-81 [20729855] Nat Struct Mol Biol. 2011 Jan;18(1):80-4 [21131978] Nat Struct Mol Biol. 2011 Jan;18(1):75-9 [21131982] DNA Repair (Amst). 2011 Mar 7;10(3):344-8 [21227759] Nucleic Acids Res. 2011 Mar;39(6):2144-52 [21087997] Nat Struct Mol Biol. 2011 Apr;18(4):423-31 [21441914] Cell. 2011 Apr 15;145(2):198-211 [21496641] Cell. 2011 Apr 15;145(2):212-23 [21496642] Proc Natl Acad Sci U S A. 2011 May 3;108(18):7437-42 [21502511] Trends Biochem Sci. 2011 May;36(5):262-71 [21353781] Genes Dev. 2011 May 15;25(10):1091-104 [21511873] Science. 2011 Jun 24;332(6037):1561-4 [21700875] Biochemistry. 2011 Jul 19;50(28):6273-9 [21696131] Proc Natl Acad Sci U S A. 2011 Aug 2;108(31):12663-8 [21768349] J Mol Biol. 2011 Sep 2;411(5):960-71 [21762700] J Biol Chem. 2011 Sep 9;286(36):31490-500 [21778232] J Biol Chem. 2011 Sep 16;286(37):32638-50 [21775435] Biochem Soc Trans. 2011 Oct;39(5):1387-92, suppl 2 p following 1392 [21936820] Nucleic Acids Res. 2011 Sep 1;39(17):7816-27 [21652643] J Biol Chem. 2011 Sep 30;286(39):33845-53 [21816818] PLoS Genet. 2011 Oct;7(10):e1002310 [21998596] Mol Cell. 2011 Nov 4;44(3):385-96 [22055185] Nat Struct Mol Biol. 2011 Nov;18(11):1189-95 [21984210] Nature. 2011 Nov 10;479(7372):241-4 [22002605] DNA Repair (Amst). 2011 Dec 10;10(12):1232-42 [21982441] Proc Natl Acad Sci U S A. 2011 Dec 27;108(52):21022-7 [22171004] Proc Natl Acad Sci U S A. 2011 Dec 27;108(52):20855-6 [22184240] Nucleic Acids Res. 2012 Jan;40(2):914-27 [21937514] Nucleic Acids Res. 2012 Feb;40(4):1868-78 [22287571] Trends Biochem Sci. 2012 Apr;37(4):162-72 [22285516] J Biol Chem. 2012 Apr 20;287(17):13686-93 [22362780] Nucleic Acids Res. 2012 May;40(10):4507-19 [22319208] Cell. 2012 May 25;149(5):1008-22 [22579044] Nat Struct Mol Biol. 2012 Jul;19(7):693-700 [22705791] PLoS Genet. 2013 Mar;9(3):e1003420 [23555316] Annu Rev Biochem. 2013;82:119-38 [23451868] Proc Natl Acad Sci U S A. 2013 Jun 25;110(26):10592-7 [23754435] Cell. 2013 Jul 3;154(1):157-68 [23827680] DNA Repair (Amst). 2013 Aug;12(8):558-67 [23712058] Mol Cell Biol. 2013 Oct;33(20):4008-16 [23938298] Environ Mol Mutagen. 2013 Dec;54(9):691-704 [24123395] Mech Ageing Dev. 2013 Oct;134(10):440-8 [23643943] Proc Natl Acad Sci U S A. 2013 Dec 17;110(51):20437-42 [24218597] Proc Natl Acad Sci U S A. 2013 Dec 17;110(51):20354-5 [24282304] Science. 2014 Jan 17;343(6168):260-1 [24436412] Antioxid Redox Signal. 2014 Feb 1;20(4):678-707 [23834463] Nature. 2008 Oct 9;455(7214):770-4 [18806779] Biochemistry. 2012 Mar 27;51(12):2407-16 [22390730] Nature. 2005 Sep 15;437(7057):440-3 [16163361] Mol Cell. 2005 Sep 16;19(6):724-6 [16168369] J Biol Chem. 2005 Oct 28;280(43):36518-28 [16141202] DNA Repair (Amst). 2005 Dec 8;4(12):1347-57 [16172026] DNA Repair (Amst). 2005 Dec 8;4(12):1442-9 [16199212] Chem Rev. 2006 Feb;106(2):687-99 [16464020] Chem Res Toxicol. 2006 Feb;19(2):300-9 [16485907] DNA Repair (Amst). 2006 Mar 7;5(3):362-8 [16388993] Nucleic Acids Res. 2006;34(9):2508-15 [16687656] DNA Repair (Amst). 2006 Jul 13;5(7):799-809 [16713756] Biochemistry. 2006 Aug 22;45(33):10140-52 [16906772] DNA Repair (Amst). 2006 Aug 13;5(8):986-96 [16955546] Nature. 2006 Oct 12;443(7112):713-6 [16964241] Ann Neurol. 2007 Feb;61(2):162-74 [17315206] Biochemistry. 2007 Mar 13;46(10):2856-64 [17298034] DNA Repair (Amst). 2007 Apr 1;6(4):443-53 [17118715] J Biol Chem. 2007 Mar 30;282(13):9469-74 [17276982] Nat Struct Biol. 2000 Mar;7(3):176-8 [10700268] J Biol Chem. 2000 Jul 21;275(29):22427-34 [10806210] EMBO J. 2000 Nov 15;19(22):5962-70 [11080143] Cell. 2001 Jan 12;104(1):107-17 [11163244] Mol Cell Biol. 2001 Mar;21(5):1656-61 [11238902] Cell. 2001 May 18;105(4):473-85 [11371344] Nature. 2001 Aug 9;412(6847):607-14 [11493912] Nat Struct Biol. 2001 Oct;8(10):838-42 [11573086] Mutat Res. 2001 May 10;485(4):283-307 [11585362] Nat Genet. 2001 Oct;29(2):184-8 [11586299] Nat Genet. 2001 Oct;29(2):189-93 [11586300] Nat Struct Biol. 2001 Dec;8(12):1015-9 [11702069] J Biol Chem. 2001 Dec 7;276(49):46290-6 [11591703] Nucleic Acids Res. 2002 Feb 1;30(3):823-9 [11809897] Nature. 2002 Feb 7;415(6872):655-9 [11832948] Structure. 2002 Feb;10(2):237-48 [11839309] J Mol Biol. 2002 Feb 22;316(3):853-66 [11866537] EMBO J. 2002 Jun 3;21(11):2827-32 [12032095] J Biol Chem. 2002 Jul 26;277(30):27162-8 [12023295] Nat Genet. 2002 Oct;32(2):267-72 [12244316] Cell. 2002 Nov 15;111(4):495-505 [12437923] Nat Immunol. 2003 Feb;4(2):145-53 [12524539] Cell. 2003 Feb 7;112(3):391-401 [12581528] Chem Biol. 2003 Feb;10(2):139-47 [12618186] Mol Cell Biol. 2003 Apr;23(7):2309-15 [12640116] J Mol Biol. 2003 Jul 25;330(5):1027-37 [12860125] DNA Repair (Amst). 2003 Oct 7;2(10):1087-100 [13679147] Cell. 2004 Jan 9;116(1):39-50 [14718165] J Med Chem. 2004 Feb 12;47(4):829-37 [14761185] Biochemistry. 2004 Mar 30;43(12):3731-9 [15035644] Cell. 2004 Apr 2;117(1):17-28 [15066279] J Mol Biol. 2004 May 14;338(5):895-906 [15111055] Nat Struct Mol Biol. 2004 Jun;11(6):519-25 [15133503] Nucleic Acids Res. 2009 Feb;37(3):738-48 [19042970] Nucleic Acids Res. 2009 Apr;37(5):1701-12 [19155274] Nat Rev Cancer. 2009 May;9(5):327-37 [19377505] Nat Rev Cancer. 2009 May;9(5):338-50 [19377506] Mol Cell Biol. 2009 Jun;29(11):3163-72 [19332554] Chem Rev. 2009 Jul;109(7):2894-902 [19476377] Nucleic Acids Res. 2009 Jul;37(12):3946-58 [19401441] Nature. 2009 Oct 1;461(7264):674-8 [19794497] Cell. 2009 Oct 2;139(1):87-99 [19804755] Hum Mol Genet. 2009 Nov 1;18(21):4102-17 [19643912] Nucleic Acids Res. 2009 Oct;37(18):6161-73 [19671525] PLoS Genet. 2009 Nov;5(11):e1000722 [19911044] PLoS One. 2009;4(12):e8104 [19956605] J Biol Chem. 2010 Jan 8;285(2):1414-23 [19893054] Cell. 1994 May 20;77(4):609-16 [8187179] Science. 1994 Jun 24;264(5167):1891-903 [7516580] J Biol Chem. 1994 Jul 8;269(27):18096-101 [8027071] J Biol Chem. 1994 Nov 11;269(45):27855-62 [7961715] Science. 1995 Aug 4;269(5224):699-702 [7624801] Nat Struct Biol. 1995 Jul;2(7):561-8 [7664124] Cell. 1995 Sep 8;82(5):849-56 [7671312] J Biol Chem. 1996 Jul 26;271(30):17811-5 [8663612] Biochemistry. 1996 Oct 1;35(39):12742-61 [8841118] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11534-9 [8876170] EMBO J. 1996 Dec 2;15(23):6662-70 [8978692] J Biol Chem. 1997 Mar 21;272(12):7792-6 [9065442] Mol Cell. 2010 Oct 22;40(2):179-204 [20965415] Structure. 2010 Nov 10;18(11):1431-42 [21070942] Nat Struct Mol Biol. 2010 Dec;17(12):1478-85 [21102445] J Biol Chem. 2010 Dec 24;285(52):40479-88 [20952393] J Biol Chem. 2011 Jan 7;286(1):403-9 [21030584] Science. 1997 Oct 10;278(5336):286-90 [9323207] J Biol Chem. 1997 Oct 17;272(42):26441-7 [9334220] J Biol Chem. 1998 May 1;273(18):11121-6 [9556598] Biochemistry. 1998 May 5;37(18):6456-64 [9572863] Cell. 1998 May 1;93(3):477-86 [9590181] J Biol Chem. 1998 Jun 12;273(24):15263-70 [9614142] Mol Cell. 1998 Jun;1(7):969-79 [9651580] Mol Cell. 1997 Dec;1(1):89-97 [9659906] Mol Cell. 1998 Apr;1(5):741-8 [9660957] J Biol Chem. 1998 Aug 21;273(34):21447-50 [9705271] Genes Dev. 1998 Oct 1;12(19):3137-43 [9765213] EMBO J. 1998 Nov 2;17(21):6404-11 [9799248] Eur J Cancer. 1998 Sep;34(10):1514-21 [9893622] J Biol Chem. 1999 Mar 26;274(13):8516-23 [10085084] Mol Cell. 2004 Jul 23;15(2):209-20 [15260972] Mol Cell Biol. 2004 Oct;24(19):8356-65 [15367657] DNA Repair (Amst). 2004 Nov 2;3(11):1493-502 [15380105] EMBO J. 2004 Oct 1;23(19):3874-85 [15385968] Biochemistry. 1972 Sep 12;11(19):3610-8 [4626532] Biochemistry. 1980 Oct 28;19(22):5087-92 [6779863] Biochem Biophys Res Commun. 1982 Dec 31;109(4):1297-302 [6301434] J Biol Chem. 1983 Dec 25;258(24):15365-70 [6317692] J Biol Chem. 1984 Jul 25;259(14):9177-81 [6086624] Biochem Biophys Res Commun. 1988 Nov 30;157(1):183-9 [2848517] Biochemistry. 1993 Mar 9;32(9):2186-93 [8443160] Biochemistry. 1993 Apr 6;32(13):3221-37 [7681688] Mol Cell Biol. 1994 Jan;14(1):68-76 [8264637] J Mol Biol. 1994 Feb 11;236(1):275-85 [7508984] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7166-9 [9207062] Nature. 1997 Jul 31;388(6641):492-5 [9242410] Structure. 1997 Jun 15;5(6):763-74 [9261067] Curr Biol. 1997 Aug 1;7(8):588-98 [9259561] J Biol Chem. 1997 Sep 26;272(39):24159-64 [9305865] J Exp Med. 2012 Jul 30;209(8):1419-26 [22802351] Nucleic Acids Res. 2012 Aug;40(14):6608-19 [22508754] Proc Natl Acad Sci U S A. 2012 Sep 4;109(36):14634-9 [22908287] Biochemistry. 2011 Jan 11;50(1):136-43 [21155533] Mol Cell. 2012 Sep 28;47(6):980-6 [22864116] Proc Natl Acad Sci U S A. 2012 Oct 16;109(42):16852-7 [23035246] Nat Rev Cancer. 2012 Dec;12(12):801-17 [23175119] Nat Struct Mol Biol. 2012 Dec;19(12):1363-71 [23104055] Nat Struct Mol Biol. 2012 Dec;19(12):1372-7 [23104058] ACS Chem Biol. 2013 Jan 18;8(1):82-95 [23259582] Biochem Cell Biol. 2013 Feb;91(1):31-41 [23442139] DNA Repair (Amst). 2013 Mar 1;12(3):205-11 [23305949] Mol Cell. 2013 Mar 7;49(5):1010-5 [23375499] PLoS Genet. 2013;9(3):e1003226 [23505375] EMBO J. 1999 Apr 1;18(7):2008-18 [10202163] Cancer Res. 1999 Jun 1;59(11):2522-6 [10363965] J Biol Chem. 1999 Aug 20;274(34):24176-86 [10446192] Nucleic Acids Res. 1999 Sep 1;27(17):3494-502 [10446239] Nature. 2004 Nov 25;432(7016):473-8 [15565146] Neurology. 2005 Feb 8;64(3):539-41 [15699391] Cell Mol Life Sci. 2005 Feb;62(4):485-91 [15719174] Nature. 2005 Mar 3;434(7029):108-13 [15744309] Mol Cell. 2005 Mar 4;17(5):657-70 [15749016] Science. 2005 Apr 22;308(5721):551-4 [15790808] EMBO J. 2005 Jun 15;24(12):2224-33 [15920477] Curr Med Chem Anticancer Agents. 2005 Jul;5(4):363-72 [16101488] Nature. 2014 Feb 6;506(7486):111-5 [24362567] EMBO J. 2014 Mar 3;33(5):482-500 [24493214] Nucleic Acids Res. 2014 Mar;42(5):3125-37 [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 - 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 - Profiling of the Tox21 chemical collection for mitochondrial function to identify compounds that acutely decrease mitochondrial membrane potential. AN - 1643406948; 25302578 AB - 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. We sought to identify individual chemicals and general structural features associated with changes in mitochondrial membrane potential (MMP). 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. 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 ≤ 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. 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. 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 - 2015/01// PY - 2015 DA - January 2015 SP - 49 EP - 56 VL - 123 IS - 1 KW - Environmental Pollutants KW - 0 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Index Medicus KW - Hep G2 Cells KW - Dose-Response Relationship, Drug KW - Humans KW - Toxicity Tests KW - Adenosine Triphosphate -- analysis KW - Cell Survival KW - High-Throughput Screening Assays KW - Membrane Potential, Mitochondrial -- drug effects KW - Environmental Pollutants -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1643406948?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=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=2015-01-01&rft.volume=123&rft.issue=1&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408642 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-22 N1 - Date created - 2015-01-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Risk Anal. 2009 Apr;29(4):485-7; discussion 492-7 [19076321] Exp Mol Pathol. 2007 Aug;83(1):84-92 [17239370] J Mol Cell Cardiol. 2010 Nov;49(5):728-36 [20620145] Drug Discov Today. 2010 Dec;15(23-24):997-1007 [20708096] Curr Drug Targets. 2011 Jun;12(6):774-82 [21275886] Environ Health Perspect. 2011 Aug;119(8):1142-8 [21543282] Adv Exp Med Biol. 2012;942:385-419 [22399433] Physiol Genomics. 2012 May 1;44(9):495-503 [22433785] Toxicol Sci. 2013 Jan;131(1):271-8 [22977170] Toxicol In Vitro. 2013 Mar;27(2):978-90 [23232461] Environ Health Perspect. 2013 Jul;121(7):756-65 [23603828] Drug Discov Today. 2013 Aug;18(15-16):716-23 [23732176] Chem Res Toxicol. 2013 Sep 16;26(9):1323-32 [23895456] Chem Res Toxicol. 2008 Apr;21(4):911-27 [18358007] Biol Chem. 1999 Oct;380(10):1157-66 [10595578] Eur J Cancer. 1999 Oct;35(10):1517-25 [10673981] J Bioenerg Biomembr. 1999 Dec;31(6):581-90 [10682916] Int J Radiat Biol. 2000 Oct;76(10):1323-33 [11057740] Biochem J. 2001 Jun 1;356(Pt 2):621-6 [11368793] J Mol Cell Cardiol. 2001 Jun;33(6):1065-89 [11444914] EMBO J. 2001 Aug 1;20(15):4107-21 [11483514] Toxicol Sci. 2002 Sep;69(1):131-8 [12215667] Antioxid Redox Signal. 2002 Oct;4(5):769-81 [12470504] Mol Pharmacol. 2003 Jan;63(1):232-42 [12488556] Biochem J. 1964 May;91(2):287-97 [4220923] J Biol Chem. 1973 Jan 25;248(2):610-8 [4684694] Mol Cell Biochem. 1982 May 28;45(1):13-31 [7050653] FEBS Lett. 1986 Jun 9;201(2):267-70 [3086126] Chem Biol Interact. 1987;62(2):179-89 [3594640] J Immunol Methods. 1993 Mar 15;160(1):81-8 [7680699] Microsc Res Tech. 1994 Feb 15;27(3):198-219 [8204911] Biochem Pharmacol. 1998 Jun 1;55(11):1907-14 [9714309] Biochim Biophys Acta. 1998 Aug 10;1366(1-2):53-67 [9714734] Leukemia. 1999 Aug;13(8):1273-80 [10450757] Nature. 1953 Jan 3;171(4340):30-2 [13025467] Nature. 1961 Jul 8;191:144-8 [13771349] J Biochem. 1964 Aug;56:151-6 [14228485] Curr Biol. 2006 Jul 25;16(14):R551-60 [16860735] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11473-8 [16864780] Neural Netw. 2006 Jul-Aug;19(6-7):723-33 [16774731] Comment In: Environ Health Perspect. 2015 Jan;123(1):A23 [25561610] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408642 ER - TY - JOUR T1 - Genistein disrupts glucocorticoid receptor signaling in human uterine endometrial Ishikawa cells. AN - 1643406894; 25136773 AB - 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. We evaluated the transcriptional response to genistein in Ishikawa cells and investigated the effects of genistein on GR-mediated target genes. 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. 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 ERα signaling, respectively. Using Ishikawa cells, we observed that exposure to genistein resulted in distinct changes in gene expression and unique differences in the GR transcriptome. 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 - 2015/01// PY - 2015 DA - January 2015 SP - 80 EP - 87 VL - 123 IS - 1 KW - Estrogen Receptor alpha KW - 0 KW - Phytoestrogens KW - Receptors, Glucocorticoid KW - estrogen receptor alpha, human KW - Estradiol KW - 4TI98Z838E KW - Dexamethasone KW - 7S5I7G3JQL KW - Genistein KW - DH2M523P0H KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Humans KW - Signal Transduction -- drug effects KW - Estradiol -- pharmacology KW - Microarray Analysis KW - Estrogen Receptor alpha -- drug effects KW - Cell Line, Tumor KW - Uterus -- drug effects KW - Female KW - Gene Expression -- drug effects KW - Receptors, Glucocorticoid -- drug effects KW - Genistein -- pharmacology KW - Phytoestrogens -- pharmacology KW - Gene Expression Regulation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1643406894?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=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=2015-01-01&rft.volume=123&rft.issue=1&rft.spage=80&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408437 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-22 N1 - Date created - 2015-01-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Hum Reprod. 2000 Jan;6(1):68-74 [10611263] Biol Reprod. 2013 Sep;89(3):66 [23843231] Am J Pathol. 2001 Mar;158(3):905-19 [11238039] J Chromatogr B Analyt Technol Biomed Life Sci. 2002 Sep 25;777(1-2):129-38 [12270206] Toxicology. 2002 Dec 27;181-182:371-82 [12505339] Proc Natl Acad Sci U S A. 1970 Mar;65(3):709-15 [4315614] J Biol Chem. 1987 Apr 25;262(12):5592-5 [3106339] Gastroenterology. 1987 Aug;93(2):225-33 [3297906] Mol Endocrinol. 1990 Oct;4(10):1427-37 [1704480] Epidemiol Rev. 1990;12:1-15 [2286214] J Steroid Biochem Mol Biol. 1992 Mar;41(3-8):331-7 [1314077] Acta Physiol Hung. 1994;82(3):195-200 [7717082] J Clin Invest. 1997 May 15;99(10):2342-50 [9153275] Reprod Biol Endocrinol. 2004 Oct 17;2:73 [15488153] Structure. 2004 Dec;12(12):2197-207 [15576033] Adv Exp Med Biol. 2004;546:121-65 [15584372] Environ Health Perspect. 2006 Jun;114(6):A352-8 [16759972] FASEB J. 2007 Feb;21(2):402-14 [17185747] Hum Reprod Update. 2008 Jan-Feb;14(1):59-72 [18070835] Nucleic Acids Res. 2008 Jan;36(Database issue):D102-6 [18006571] Mol Endocrinol. 2008 May;22(5):1032-43 [18258689] FASEB J. 2009 Nov;23(11):3649-58 [19567371] Aust Vet J. 1946 Feb;22:2-12 [21028682] Ann N Y Acad Sci. 2011 Mar;1221:98-102 [21401636] PLoS One. 2011;6(3):e18242 [21483825] Am J Reprod Immunol. 2011 Jul;66 Suppl 1:88-92 [21726343] Horm Metab Res. 2012 Jul;44(8):587-91 [22438212] Immunol Res. 2012 Dec;54(1-3):95-110 [22484990] PLoS One. 2012;7(10):e47979 [23110148] Genome Res. 2012 Nov;22(11):2153-62 [23019147] Endocrinology. 2013 Jan;154(1):499-510 [23183181] Trends Endocrinol Metab. 2013 Mar;24(3):109-19 [23312823] Cancer Res. 2013 Aug 15;73(16):5130-9 [23803465] Biofactors. 2000;12(1-4):209-15 [11216488] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408437 ER - TY - JOUR T1 - Perfluorochemicals and human semen quality: the LIFE study. AN - 1643406797; 25127343 AB - The relation between persistent environmental chemicals and semen quality is evolving, although limited data exist for men recruited from general populations. We examined the relation between perfluorinated chemicals (PFCs) and semen quality among 501 male partners of couples planning pregnancy. 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. 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. Select PFCs were associated with certain semen end points, with the most significant associations observed for PFOSA but with results in varying directions. JF - Environmental health perspectives AU - Louis, Germaine M Buck 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 - 2015/01// PY - 2015 DA - January 2015 SP - 57 EP - 63 VL - 123 IS - 1 KW - Environmental Pollutants KW - 0 KW - Fluorocarbons KW - Index Medicus KW - Humans KW - Linear Models KW - Adult KW - Environmental Exposure KW - Texas KW - Tandem Mass Spectrometry KW - Michigan KW - Male KW - Environmental Pollutants -- toxicity KW - Semen Analysis KW - Fluorocarbons -- toxicity KW - Semen -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1643406797?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Perfluorochemicals+and+human+semen+quality%3A+the+LIFE+study.&rft.au=Louis%2C+Germaine+M+Buck%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+M&rft.date=2015-01-01&rft.volume=123&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1307621 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-22 N1 - Date created - 2015-01-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Fertil Steril. 2000 Jan;73(1):43-50 [10632410] Paediatr Perinat Epidemiol. 2011 Sep;25(5):413-24 [21819423] Fertil Steril. 2001 Nov;76(5):879-83 [11704105] J Androl. 2002 Jan-Feb;23(1):25-43 [11780920] Best Pract Res Clin Endocrinol Metab. 2002 Jun;16(2):289-309 [12064894] J Androl. 2002 Sep-Oct;23(5):629-34 [12185096] Am J Epidemiol. 2003 Feb 15;157(4):355-63 [12578806] Environ Sci Technol. 2011 Oct 1;45(19):8037-45 [21469664] Toxicol Appl Pharmacol. 2012 Jan 15;258(2):248-55 [22119708] Reprod Toxicol. 2012 Jul;33(4):419-27 [21736937] Reprod Toxicol. 2012 Jul;33(4):577-83 [22449571] Hum Reprod. 2012 Aug;27(8):2532-40 [22647447] Methods Mol Biol. 2013;927:27-37 [22992901] Methods Mol Biol. 2013;927:147-64 [22992911] Hum Reprod. 2013 Jan;28(1):274-82 [23042799] Hum Reprod. 2013 Mar;28(3):599-608 [23250927] Environ Health Perspect. 2013 Apr;121(4):453-8 [23360585] Fertil Steril. 2013 Mar 1;99(3):673-7 [23391408] Urology. 2013 Dec;82(6):1296-9 [24094663] Chem Res Toxicol. 2003 Jun;16(6):775-81 [12807361] Environ Health Perspect. 2004 Jan;112(1):79-86 [14698935] Fertil Steril. 2004 Aug;82(2):358-66 [15302284] Crit Rev Toxicol. 2004 Jul-Aug;34(4):351-84 [15328768] J Androl. 1990 Jan-Feb;11(1):32-9 [2312397] Arch Androl. 1992 Sep-Oct;29(2):105-16 [1456832] Fertil Steril. 1994 Dec;62(6):1244-9 [7957992] Toxicol Appl Pharmacol. 1995 Sep;134(1):18-25 [7676454] Clin Chem. 1997 Dec;43(12):2281-91 [9439445] Am J Epidemiol. 1998 Nov 15;148(10):992-7 [9829871] Andrologia. 2004 Dec;36(6):337-45 [15541049] Anal Chem. 2005 Sep 15;77(18):6085-91 [16159145] Toxicology. 2005 Nov 5;215(1-2):126-48 [16146667] Environ Sci Technol. 2006 Jan 1;40(1):32-44 [16433330] Am J Epidemiol. 2006 Feb 15;163(4):374-83 [16394206] Epidemiology. 2006 Jul;17(4):440-9 [16755258] Hum Reprod. 2007 Jan;22(1):188-96 [16966350] Fertil Steril. 2007 Mar;87(3):554-64 [17140573] Reprod Biomed Online. 2007 Apr;14(4):418-21 [17425820] Toxicol Sci. 2007 Jul;98(1):206-15 [17400581] Science. 2007 Jul 13;317(5835):236-9 [17626882] Environ Health Perspect. 2007 Aug;115(8):1169-76 [17687443] Environ Health Perspect. 2007 Sep;115(9):1298-305 [17805419] Toxicol Sci. 2007 Oct;99(2):366-94 [17519394] Aquat Toxicol. 2007 Dec 30;85(4):267-77 [17980923] Environ Sci Technol. 2008 Feb 15;42(4):995-1003 [18351063] J Toxicol Environ Health B Crit Rev. 2008 Mar;11(3-4):188-220 [18368553] Risk Anal. 2008 Apr;28(2):251-69 [18419647] Int J Hyg Environ Health. 2009 May;212(3):239-70 [18565792] Environ Sci Technol. 2009 Jun 1;43(11):4037-43 [19569327] Environ Health Perspect. 2009 Jun;117(6):923-7 [19590684] Asian J Androl. 2010 Jan;12(1):99-103 [20111089] Crit Rev Toxicol. 2010 Aug;40(7):633-52 [20662712] Natl Med J India. 2010 May-Jun;23(3):134-6 [20949713] Fertil Steril. 2011 Jan;95(1):116-23 [20674912] J Urol. 2011 Feb;185(2):381-2 [21168161] Biol Reprod. 2011 May;84(5):1016-23 [21209418] Syst Biol Reprod Med. 2011 Jun;57(3):133-8 [21299480] J Androl. 2000 May-Jun;21(3):478-84 [10819457] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1307621 ER - TY - JOUR T1 - Preconception maternal and paternal exposure to persistent organic pollutants and birth size: the LIFE study. AN - 1643405640; 25095280 AB - Persistent organic pollutants (POPs) are developmental toxicants, but the impact of both maternal and paternal exposures on offspring birth size is largely unexplored. We examined associations between maternal and paternal serum concentrations of 63 POPs, comprising five major classes of pollutants, with birth size measures. 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. 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. Preconceptional maternal and paternal concentrations of several POPs were associated with statistically significant differences in birth size among offspring. 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 M Buck 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 - 2015/01// PY - 2015 DA - January 2015 SP - 88 EP - 94 VL - 123 IS - 1 KW - Environmental Pollutants KW - 0 KW - Hydrocarbons, Halogenated KW - Pesticides KW - Index Medicus KW - Hydrocarbons, Halogenated -- toxicity KW - Humans KW - Infant, Newborn KW - Texas KW - Hydrocarbons, Halogenated -- blood KW - Pregnancy KW - Pesticides -- toxicity KW - Body Size -- drug effects KW - Prenatal Exposure Delayed Effects -- chemically induced KW - Adult KW - Cohort Studies KW - Middle Aged KW - Michigan KW - Adolescent KW - Environmental Exposure -- adverse effects KW - Female KW - Male KW - Pesticides -- blood KW - Maternal Exposure -- adverse effects KW - Environmental Pollutants -- toxicity KW - Paternal Exposure -- adverse effects KW - Maternal Exposure -- statistics & numerical data KW - Birth Weight -- drug effects KW - Paternal Exposure -- statistics & numerical data KW - Environmental Pollutants -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1643405640?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=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+M+Buck&rft.aulast=Robledo&rft.aufirst=Candace&rft.date=2015-01-01&rft.volume=123&rft.issue=1&rft.spage=88&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1308016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-22 N1 - Date created - 2015-01-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2009 Apr;117(4):660-7 [19440508] Environ Health Perspect. 2009 Aug;117(8):1244-9 [19672404] Environ Sci Technol. 2010 Jan 15;44(2):813-9 [20000818] Am J Obstet Gynecol. 2010 Feb;202(2):103-23 [20113689] Environ Health Perspect. 2010 Feb;118(2):297-302 [20123616] Curr Opin Pediatr. 2010 Apr;22(2):208-18 [20216314] Epidemiol Rev. 2010;32:70-81 [20378629] Sci Total Environ. 2010 Nov 1;408(23):5758-67 [20832846] Horm Behav. 2011 Mar;59(3):306-14 [20620140] Pediatrics. 2011 Apr;127(4):734-41 [21382949] Paediatr Perinat Epidemiol. 2011 Sep;25(5):413-24 [21819423] Chemosphere. 2011 Sep;84(10):1301-9 [21663933] Am J Epidemiol. 2011 Oct 15;174(8):885-92 [21878423] J Expo Sci Environ Epidemiol. 2012 Jan-Feb;22(1):60-9 [21971379] Environ Int. 2012 Apr;40:162-9 [21820740] Environ Health Perspect. 2012 Feb;120(2):162-70 [21997443] Environ Sci Pollut Res Int. 2012 Jul;19(6):1936-43 [22767291] Environ Health. 2012;11:49 [22817616] Int J Hyg Environ Health. 2013 Mar;216(2):184-94 [22494936] Ultrasound Obstet Gynecol. 2013 Feb;41(2):136-45 [22648955] Environ Health Perspect. 2013 Feb;121(2):231-6 [23151773] BMC Pregnancy Childbirth. 2013;13 Suppl 1:S3 [23445768] FASEB J. 2013 Oct;27(10):4226-43 [23845863] Anal Chem. 2003 Jan 1;75(1):71-7 [12530820] J Pediatr Endocrinol Metab. 2003 Apr-May;16(4):537-40 [12793605] Environ Health Perspect. 2003 Jul;111(9):1249-52 [12842781] J Chromatogr B Analyt Technol Biomed Life Sci. 2003 Aug 25;794(1):137-48 [12888206] Environ Health Perspect. 2004 Jan;112(1):69-78 [14698934] Environ Health Perspect. 2004 Jul;112(10):1116-24 [15238287] Environ Health Perspect. 2004 Oct;112(14):1403-8 [15471733] Schizophr Res. 2004 Dec 1;71(2-3):417-26 [15474913] Arch Environ Contam Toxicol. 1989 Jul-Aug;18(4):495-500 [2505694] Clin Chim Acta. 1989 Oct 16;184(3):219-26 [2611996] Annu Rev Public Health. 1993;14:159-81 [7686758] Obstet Gynecol. 1995 Apr;85(4):625-30 [7898845] Semin Perinatol. 1995 Jun;19(3):222-40 [7570074] Clin Chem. 1997 Dec;43(12):2281-91 [9439445] Epidemiology. 1998 Mar;9(2):161-7 [9504284] Environ Health. 2004 Jan 28;3(1):1 [14748928] Epidemiology. 2005 Sep;16(5):641-7 [16135940] Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):506-13 [16039685] Anal Chem. 2005 Sep 15;77(18):6085-91 [16159145] Am J Epidemiol. 2005 Oct 15;162(8):717-25 [16120698] Am J Epidemiol. 2006 Feb 15;163(4):374-83 [16394206] Pediatr Res. 2007 Feb;61(2):243-50 [17237730] Environ Pollut. 2007 Mar;146(2):400-13 [16949712] Chemosphere. 2007 Jun;68(5):824-31 [17408721] Environ Health Perspect. 2007 Sep;115(9):1320-4 [17805422] Chemosphere. 2007 Oct;69(8):1295-304 [17617441] Environ Res. 2007 Nov;105(3):370-9 [17485077] Basic Clin Pharmacol Toxicol. 2008 Feb;102(2):176-81 [18226072] Fertil Steril. 2008 Feb;89(2 Suppl):e111-6; discussion e117 [18308050] BJOG. 2008 Jun;115(7):886-93 [18485168] Chemosphere. 2009 Jan;74(3):428-33 [18986677] Environ Health Perspect. 2009 Mar;117(3):488-94 [19337527] Reprod Toxicol. 2009 Jun;27(3-4):212-30 [19429401] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1308016 ER - TY - JOUR T1 - Insecticide residues in soil, water, and eggplant fruits and farmers' health effects due to exposure to pesticides. AN - 1643146328; 25413584 AB - 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. 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. 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(®) for 24 years at a rate of 10 ml/application, and Malathion(®) 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(®) and Magnum(®) 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. 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 VL - 20 IS - 1 KW - Insecticides KW - 0 KW - Pesticide Residues KW - Pesticides KW - Soil Pollutants KW - Water Pollutants, Chemical KW - Index Medicus KW - Cross-Sectional Studies KW - Water Pollutants, Chemical -- analysis KW - Humans KW - Food Contamination -- analysis KW - Interviews as Topic KW - Pesticide Residues -- analysis KW - Philippines -- epidemiology KW - Pesticides -- adverse effects KW - Soil Pollutants -- analysis KW - Insecticides -- adverse effects KW - Insecticides -- administration & dosage KW - Agricultural Workers' Diseases -- epidemiology KW - Agricultural Workers' Diseases -- chemically induced KW - Occupational Exposure -- adverse effects KW - Solanum melongena -- chemistry KW - Insecticides -- analysis KW - Occupational Exposure -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1643146328?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+and+preventive+medicine&rft.atitle=Insecticide+residues+in+soil%2C+water%2C+and+eggplant+fruits+and+farmers%27+health+effects+due+to+exposure+to+pesticides.&rft.au=Del+Prado-Lu%2C+Jinky+Leilanie&rft.aulast=Del+Prado-Lu&rft.aufirst=Jinky&rft.date=2015-01-01&rft.volume=20&rft.issue=1&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=Environmental+health+and+preventive+medicine&rft.issn=1347-4715&rft_id=info:doi/10.1007%2Fs12199-014-0425-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-27 N1 - Date created - 2015-01-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Sci Total Environ. 1997 Sep 15;203(3):229-44 [9260309] Sci Total Environ. 1992 Aug 12;123-124:63-76 [1439745] J Environ Sci Health B. 1987 Jun;22(3):347-77 [3655189] Environ Sci Technol. 2004 May 15;38(10):2752-9 [15212247] Int J Occup Environ Health. 2002 Jul-Sep;8(3):220-31 [12358078] Occup Med (Lond). 1997 Jul;47(5):301-8 [9302813] Chemosphere. 2008 Jun;72(5):781-4 [18471864] Arch Environ Contam Toxicol. 2010 Aug;59(2):175-81 [20162264] Residue Rev. 1970;32:29-92 [4924145] Ann Agric Environ Med. 2001;8(1):1-5 [11426918] Int J Occup Environ Health. 2002 Jan-Mar;8(1):41-5 [11843439] Occup Environ Med. 2002 Jun;59(6):387-93 [12040114] Ind Health. 2002 Apr;40(2):182-90 [12064560] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s12199-014-0425-3 ER - TY - JOUR T1 - Integrative genomic and transcriptomic characterization of matched primary and metastatic liver and colorectal carcinoma. AN - 1641858269; 25552933 AB - Metastasis is the main cause of cancer mortality but its process remains poorly understood and thus hampers more effective treatment and improved cancer prognosis. To search for metastasis driver genes responsible for tumor spread, we integrated genomic and transcriptomic profiles of 61 matched primary tumors and distant metastases of liver or colorectal carcinoma isolated by laser-capture microdissection and assayed by array-based technologies. We found that primary tumor lesions and their matched distant metastases were largely similar at the genomic and transcriptomic levels, but substantial differences could be found between primary tumors with or without accompanying metastases. Interestingly, metastasis genes were principally tumor type and organ site-specific. Despite distinct pathway enrichment, different metastasis gene sets shared common prognostic capacity and were predictive of hepatocellular carcinoma survival in an independent cohort. Thus, the metastatic propensity is inherent to the primary tumor and the lack of general metastasis genes necessitates the development of specific treatment modalities. JF - International journal of biological sciences AU - Roessler, Stephanie AU - Lin, Guoling AU - Forgues, Marshonna AU - Budhu, Anuradha AU - Hoover, Shelley AU - Simpson, R Mark AU - Wu, Xiaolin AU - He, Ping AU - Qin, Lun-Xiu AU - Tang, Zhao-You AU - Ye, Qing-Hai AU - Wang, Xin Wei AD - 1. Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, MD, USA; ; 1. Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, MD, USA; ; 2. Liver Cancer Institute, Fudan University, Shanghai, China; ; 3. Laboratory of Cancer Biology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA; ; 4. Laboratory of Molecular Technology, NCI-Frederick, SAIC-Frederick, Frederick, MD 21701, USA; ; 5. Division of Hematology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA. ; 2. Liver Cancer Institute, Fudan University, Shanghai, China; Y1 - 2015 PY - 2015 DA - 2015 SP - 88 EP - 98 VL - 11 IS - 1 KW - Index Medicus KW - Organ site-specific metastasis KW - Liver cancer KW - Colon cancer KW - Profiling. KW - Gene Expression Profiling KW - Comparative Genomic Hybridization KW - Humans KW - Microarray Analysis KW - Laser Capture Microdissection KW - China KW - Colorectal Neoplasms -- secondary KW - Neoplasm Metastasis -- genetics KW - Neoplasm Metastasis -- physiopathology KW - Colorectal Neoplasms -- genetics KW - Liver Neoplasms -- secondary KW - Liver Neoplasms -- genetics KW - Gene Expression Regulation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1641858269?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biological+sciences&rft.atitle=Integrative+genomic+and+transcriptomic+characterization+of+matched+primary+and+metastatic+liver+and+colorectal+carcinoma.&rft.au=Roessler%2C+Stephanie%3BLin%2C+Guoling%3BForgues%2C+Marshonna%3BBudhu%2C+Anuradha%3BHoover%2C+Shelley%3BSimpson%2C+R+Mark%3BWu%2C+Xiaolin%3BHe%2C+Ping%3BQin%2C+Lun-Xiu%3BTang%2C+Zhao-You%3BYe%2C+Qing-Hai%3BWang%2C+Xin+Wei&rft.aulast=Roessler&rft.aufirst=Stephanie&rft.date=2015-01-01&rft.volume=11&rft.issue=1&rft.spage=88&rft.isbn=&rft.btitle=&rft.title=International+journal+of+biological+sciences&rft.issn=1449-2288&rft_id=info:doi/10.7150%2Fijbs.10583 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-14 N1 - Date created - 2015-01-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Med. 2006 Aug;12(8):895-904 [16892035] Bioinformatics. 2005 Nov 15;21(22):4084-91 [16159913] Bioinformatics. 2007 Mar 15;23(6):657-63 [17234643] Nat Rev Genet. 2007 May;8(5):341-52 [17440531] Nat Rev Cancer. 2009 Apr;9(4):274-84 [19308067] Cancer Res. 2009 May 1;69(9):4059-66 [19366792] Nature. 2010 Feb 18;463(7283):899-905 [20164920] BMC Surg. 2010;10:27 [20875094] Cancer Res. 2010 Dec 15;70(24):10202-12 [21159642] Nat Rev Cancer. 2011 Feb;11(2):135-41 [21258397] Cell. 2011 Mar 4;144(5):646-74 [21376230] Nat Rev Cancer. 2011 Oct;11(10):735-48 [21941285] Cell. 2011 Oct 14;147(2):275-92 [22000009] N Engl J Med. 2012 Mar 8;366(10):883-92 [22397650] Gastroenterology. 2012 Apr;142(4):957-966.e12 [22202459] Nat Med. 2013 Nov;19(11):1423-37 [24202395] Ann Surg. 2002 Mar;235(3):373-82 [11882759] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349] Nat Genet. 2003 Jan;33(1):49-54 [12469122] J Cancer Res Clin Oncol. 2003 Jan;129(1):43-51 [12618900] Nat Med. 2003 Apr;9(4):416-23 [12640447] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15901-5 [14665696] Cancer Res. 1988 Apr 1;48(7):1943-8 [3349467] Surg Clin North Am. 1997 Feb;77(1):27-48 [9092116] J Clin Invest. 2005 Jan;115(1):44-55 [15630443] Cancer Cell. 2006 Aug;10(2):99-111 [16904609] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.7150/ijbs.10583 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 - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-22 N1 - Date created - 2014-12-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Anal Biochem. 1992 Sep;205(2):263-70 [1332541] Nature. 1993 Jun 3;363(6428):446-8 [8502296] N Engl J Med. 1999 Nov 4;341(19):1432-8 [10547406] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569] Lancet. 2007 Dec 22;370(9605):2127-37 [18156035] Adv Drug Deliv Rev. 2008 Sep15;60(12):1407-20 [18508155] Appl Environ Microbiol. 2008 Aug;74(15):4626-35 [18539799] Bull World Health Organ. 2008 Oct;86(10):805-12, A [18949218] Blood. 2009 Apr 16;113(16):3792-800 [18988862] Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873] J Infect Dis. 2010 Feb 15;201(4):499-504 [20088691] J Immunol Methods. 2010 Feb 28;353(1-2):78-86 [19932697] Sci Transl Med. 2009 Nov 18;1(7):7ra16 [20161655] Virology. 1996 Jan 1;215(1):101-6 [8553581] Antimicrob Agents Chemother. 1996 Feb;40(2):470-2 [8834901] Virology. 1996 Nov 1;225(1):213-5 [8918548] N Engl J Med. 1997 Oct 16;337(16):1105-11 [9329932] FEBS Lett. 1997 Sep 15;414(3):521-6 [9323027] EMBO J. 1998 Jul 1;17(13):3512-20 [9649422] Virol J. 2004;1:11 [15560847] AIDS. 2006 Jan 2;20(1):73-83 [16327322] Acta Derm Venereol. 2006;86(2):129-34 [16648915] Hybridoma (Larchmt). 2006 Aug;25(4):209-15 [16934017] Biotechnol Appl Biochem. 2007 Jan;46(Pt 1):41-9 [16848761] J Immunol Methods. 2007 Jul 31;324(1-2):13-25 [17568607] J Infect Dis. 2014 Aug 15;210(4):571-5 [24652496] Protein Expr Purif. 2002 Aug;25(3):400-8 [12182819] J Virol. 2003 Sep;77(17):9695-9 [12915581] N Engl J Med. 2004 Jan 1;350(1):11-20 [14702423] Methods Mol Biol. 2004;248:503-18 [14970517] Blood. 2004 Apr 1;103(7):2718-26 [14525789] Brain Res. 1981 Apr 27;211(1):235-41 [7225841] J Immunother. 2010 Apr;33(3):297-304 [20445350] Am J Reprod Immunol. 2011 Mar;65(3):308-16 [21214660] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054] Antiviral Res. 2011 Jun;90(3):143-50 [21440007] J Acquir Immune Defic Syndr. 2011 Jul 1;57(3):238-44 [21860356] BMC Biotechnol. 2011;11:86 [21933444] Mucosal Immunol. 2011 Nov;4(6):648-57 [21734653] FEBS J. 2011 Dec;278(23):4683-700 [21585657] J Clin Invest. 2011 Dec;121(12):4600-9 [22133885] Postepy Hig Med Dosw (Online). 2012;66:348-58 [22706121] Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11782-7 [22753489] Methods Mol Biol. 2012;911:277-86 [22886258] BMC Biotechnol. 2012;12:59 [22953695] Proc Natl Acad Sci U S A. 2012 Dec 18;109(51):E3597-603 [23213206] J Virol. 2013 Feb;87(3):1443-53 [23152529] Mol Cancer Ther. 2013 Jan;12(1):48-57 [23136186] Microb Pathog. 2013 May;58:45-54 [23159485] Elife. 2013;2:e00288 [23606943] J R Soc Interface. 2014 Jun 6;11(95):20140160 [24671939] MAbs. 2012 Mar-Apr;4(2):233-42 [22377676] Mol Med. 1998 Jun;4(6):384-91 [10780881] J Immunol Methods. 2000 Jun 23;240(1-2):185-95 [10854612] Int J Cancer. 2000 Jul 1;87(1):86-94 [10861457] Antimicrob Agents Chemother. 2001 Oct;45(10):2807-12 [11557473] Protein Sci. 2002 Mar;11(3):500-15 [11847273] Biochemistry. 2002 Mar 19;41(11):3628-36 [11888279] Int J Cancer. 2002 Mar 20;98(3):456-62 [11920600] Clin Cancer Res. 2002 Apr;8(4):995-1002 [11948105] Acta Crystallogr D Biol Crystallogr. 2002 May;58(Pt 5):836-8 [11976496] J Immunol Methods. 2002 May 1;263(1-2):97-109 [12009207] J Reprod Immunol. 2002 Jul-Aug;56(1-2):61-76 [12106884] J Virol. 1985 Jun;54(3):682-9 [2987522] JAMA. 1988 Feb 19;259(7):1048-50 [2828700] Proc Natl Acad Sci U S A. 1989 Mar;86(6):1987-91 [2538826] N1 - 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 - Autophagy/mitophagy and neurodegenerative diseases T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638898; 6327999 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 - Neurodegenerative diseases KW - Phagocytosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638898?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Autophagy%2Fmitophagy+and+neurodegenerative+diseases&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 - 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 - 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 - PINK1 is a ubiquitin kinase T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638763; 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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; 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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 - 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 - Structural studies into the mechanistic origin of microtubule dynamic instability T2 - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AN - 1647638458; 6327966 JF - 2014 American Society for Cell Biology and International Federation for Cell Biology Meeting (2014 ASCB/IFCB) AU - Alushin, G AU - Lander, G AU - Kellogg, E AU - Zhang, R AU - Baker, D AU - Nogales, E Y1 - 2014/12/06/ PY - 2014 DA - 2014 Dec 06 KW - Microtubules KW - Instability UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647638458?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Structural+studies+into+the+mechanistic+origin+of+microtubule+dynamic+instability&rft.au=Alushin%2C+G%3BLander%2C+G%3BKellogg%2C+E%3BZhang%2C+R%3BBaker%2C+D%3BNogales%2C+E&rft.aulast=Alushin&rft.aufirst=G&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 - 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 - 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 - Race and health profiles in the United States: an examination of the social gradient through the 2009 CHIS adult survey AN - 1665171654 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 ; The National Cancer Institute (NCI), Division of Cancer Control and Population Sciences (DCCPS), 9609 Medical Center Dr., Rockville, MD 20850-9761, USA ; The National Cancer Institute (NCI), Division of Cancer Control and Population Sciences (DCCPS), 9609 Medical Center Dr., Rm 3E638, Rockville, MD 20850-9761, USA Y1 - 2014/12// PY - 2014 DA - Dec 2014 SP - 1076 EP - 1086 CY - Houndsmill PB - Elsevier Science Ltd. VL - 128 IS - 12 SN - 0033-3506 KW - Public Health And Safety KW - Health disparities KW - SES KW - Race KW - Ethnicity KW - Social gradient KW - Academic achievement KW - Ethnic groups KW - Health behaviour KW - Health status KW - Income inequalities KW - Inequalities KW - National income KW - Socioeconomic status KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665171654?accountid=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&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=2014-12-01&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 - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-02-24 N1 - Last updated - 2016-05-12 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1016/j.puhe.2014.10.003 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 - 1660024893; 201507012 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 Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 548 EP - 549 PB - Cambridge University Press, New York NY VL - 37 IS - 6 SN - 0140-525X, 0140-525X KW - Brain KW - Communication KW - Social Factors KW - Language KW - article KW - 1330: sociology of language and the arts; sociology of language/sociolinguistics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660024893?accountid=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=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/10.1017%2FS0140525X13003968 LA - English DB - Sociological Abstracts N1 - Date revised - 2015-03-01 N1 - Number of references - 9 N1 - Last updated - 2016-09-28 N1 - CODEN - BBSCDH N1 - SubjectsTermNotLitGenreText - Language; Communication; Brain; Social Factors DO - http://dx.doi.org/10.1017/S0140525X13003968 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 - Identification of Fragile X Syndrome Specific Molecular Markers in Human Fibroblasts: A Useful Model to Test the Efficacy of Therapeutic Drugs AN - 1635035222; 21045979 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 p110 beta , 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. We show that primary fibroblasts from fragile X syndrome (FXS) patients have elevated rates of protein synthesis and increased levels of translational regulators, p-mTOR and p-S6K1. Treatment with inhibitors of S6K1 and PI3K reduces rates of protein synthesis in these cells. Our data suggest that primary fibroblasts from FXS patients can be a useful cell-based model for high-throughput drug screens, evaluation of potential therapeutic compounds and designing personalized treatment approaches. 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 - Dec 2014 SP - 1485 EP - 1494 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 35 IS - 12 SN - 1059-7794, 1059-7794 KW - Genetics Abstracts; Toxicology Abstracts KW - FMR1 protein KW - Translation KW - Protein biosynthesis KW - Data processing KW - RNA-binding protein KW - Brain KW - Catalytic subunits KW - Drug development KW - Toxicity KW - fragile X mental retardation protein KW - Drug screening KW - Clinical trials KW - Fibroblasts KW - 1-Phosphatidylinositol 3-kinase KW - Fragile X syndrome KW - Ribosomal protein S6 kinase KW - Mental retardation KW - Drugs KW - Autism KW - X 24310:Pharmaceuticals KW - G 07710:Chemical Mutagenesis & Radiation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635035222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+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=10597794&rft_id=info:doi/10.1002%2Fhumu.22699 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2015-03-04 N1 - SubjectsTermNotLitGenreText - Translation; FMR1 protein; Data processing; Protein biosynthesis; RNA-binding protein; Brain; Catalytic subunits; Drug development; Toxicity; Drug screening; fragile X mental retardation protein; Clinical trials; Fibroblasts; 1-Phosphatidylinositol 3-kinase; Fragile X syndrome; Ribosomal protein S6 kinase; Mental retardation; Autism; Drugs DO - http://dx.doi.org/10.1002/humu.22699 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 - Mitochondria, energetics, epigenetics, and cellular responses to stress. AN - 1629966890; 25127496 AB - 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. 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. 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. 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. Understanding mitochondria-cell signaling will provide insight into individual responses to environmental hazards, improving prediction of hazard and susceptibility to environmental stressors. 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 - 2014/12// PY - 2014 DA - December 2014 SP - 1271 EP - 1278 VL - 122 IS - 12 KW - DNA, Mitochondrial KW - 0 KW - Environmental Pollutants KW - Index Medicus KW - DNA, Mitochondrial -- drug effects KW - DNA Damage KW - Humans KW - Genome, Mitochondrial KW - DNA, Mitochondrial -- genetics KW - Environmental Pollutants -- toxicity KW - Mitochondria -- drug effects KW - Environmental Exposure KW - Environmental Pollutants -- administration & dosage KW - Mitochondria -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629966890?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=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=2014-12-01&rft.volume=122&rft.issue=12&rft.spage=1271&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408418 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-13 N1 - Date created - 2014-12-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Science. 2009 May 22;324(5930):1076-80 [19461003] Free Radic Biol Med. 2009 Jul 15;47(2):115-27 [19362589] Cell. 2009 Jul 10;138(1):18-20 [19596230] Nature. 2009 Jul 30;460(7255):587-91 [19641587] Mitochondrion. 2010 Jan;10(1):12-31 [19796712] Mol Cancer Res. 2010 Jan;8(1):67-79 [20068071] Mutat Res. 2010 Apr 1;686(1-2):57-67 [20096707] Methods. 2010 Aug;51(4):416-25 [20188838] Methods. 2010 Aug;51(4):452-7 [20347038] Nat Rev Mol Cell Biol. 2010 Sep;11(9):621-32 [20683470] Environ Health. 2010;9:48 [20696069] Mitochondrion. 2011 Mar;11(2):237-45 [21047563] Cell. 2011 Mar 4;144(5):646-74 [21376230] Cell Metab. 2011 May 4;13(5):517-26 [21531334] Mol Cell. 2011 May 20;42(4):426-37 [21596309] PLoS Genet. 2011 Jun;7(6):e1002080 [21655080] Antioxid Redox Signal. 2011 Jul 15;15(2):551-89 [20919933] Mitochondrion. 2011 Sep;11(5):686-92 [21635974] J Biol Chem. 2011 Sep 16;286(37):31975-83 [21768646] Chem Res Toxicol. 2011 Oct 17;24(10):1630-2 [21950265] Mol Cell. 2011 Oct 21;44(2):177-90 [21856199] Trends Biochem Sci. 2012 Jan;37(1):15-22 [22079189] Mol Syst Biol. 2012;8:565 [22252388] J Biol Chem. 2012 Jan 20;287(4):2819-29 [22130663] Environ Health Perspect. 2012 Feb;120(2):210-5 [22005026] Cell Metab. 2012 Jul 3;16(1):9-17 [22768835] Int J Biochem Cell Biol. 2012 Sep;44(9):1473-6 [22664327] J Inherit Metab Dis. 2008 Apr;31(2):205-16 [18392741] Autophagy. 2012 May 1;8(5):840-1 [22617444] Environ Health Perspect. 2012 Sep;120(9):1346-52 [22626541] Methods Mol Biol. 2012;920:111-32 [22941600] Nucleic Acids Res. 2012 Sep;40(16):7916-31 [22718972] Nat Rev Mol Cell Biol. 2012 Oct;13(10):659-71 [22992591] Neurobiol Aging. 2012 Dec;33(12):2881-91 [22445327] Nat Rev Genet. 2012 Nov;13(11):807-17 [23044826] NMR Biomed. 2012 Nov;25(11):1234-44 [22419606] Cell Stem Cell. 2012 Nov 2;11(5):589-95 [23122286] PLoS One. 2013;8(5):e64444 [23717615] Br J Pharmacol. 2013 Jul;169(5):1072-90 [23758163] Mol Cell Biol. 2013 Jul;33(14):2683-90 [23671186] Antioxid Redox Signal. 2013 Jul 20;19(3):240-2 [23432475] Toxicol Sci. 2013 Jul;134(1):1-17 [23629515] Stem Cells. 2013 Jul;31(7):1287-97 [23400930] PLoS One. 2013;8(7):e69229 [23922695] Mol Genet Metab. 2013 Sep-Oct;110(1-2):25-34 [23920043] Blood. 2012 Feb 9;119(6):1490-500 [22144182] Int J Epidemiol. 2012 Feb;41(1):79-105 [22253299] Nature. 2012 Mar 22;483(7390):479-83 [22343889] J Cell Sci. 2012 Feb 15;125(Pt 4):807-15 [22448037] Diabetologia. 2012 Jun;55(6):1689-98 [22396012] Oncogene. 2012 May 10;31(19):2491-8 [21996744] J Cell Physiol. 2012 Sep;227(9):3169-77 [22261928] PLoS Comput Biol. 2012;8(6):e1002576 [22761564] Nature. 2012 Nov 15;491(7424):364-73 [23151579] Nature. 2012 Nov 15;491(7424):374-83 [23151580] Best Pract Res Clin Endocrinol Metab. 2012 Dec;26(6):771-90 [23168279] Free Radic Biol Med. 2012 Dec 1;53(11):2178-87 [23022407] Cell. 2012 Dec 7;151(6):1185-99 [23217706] Int J Biochem Cell Biol. 2013 Jan;45(1):16-22 [22842533] Mol Cancer. 2012;11:76 [23043612] Mol Cell. 2013 Jan 24;49(2):346-58 [23273983] J Cell Sci. 2012 Dec 1;125(Pt 23):5745-57 [23015593] Biophys J. 2013 Jan 22;104(2):332-43 [23442855] Mol Cell Neurosci. 2013 Jul;55:77-86 [22940086] BMC Pharmacol Toxicol. 2013;14:9 [23374645] Mol Carcinog. 2013 May;52(5):329-37 [22228080] Cold Spring Harb Perspect Biol. 2013 May;5(5):a012641 [23637283] Cancer Discov. 2013 May;3(5):497-501 [23658298] Part Fibre Toxicol. 2013;10:17 [23628000] Part Fibre Toxicol. 2013;10:18 [23656717] Biochim Biophys Acta. 2013 Oct;1831(10):1533-41 [23500888] Proc Natl Acad Sci U S A. 2013 Sep 17;110(38):E3622-30 [24003133] Biochim Biophys Acta. 2013 Nov-Dec;1827(11-12):1346-61 [23220121] Cancer Epidemiol Biomarkers Prev. 2013 Oct;22(10):1722-9 [23885040] Cell Rep. 2013 Dec 26;5(6):1714-24 [24360959] DNA Repair (Amst). 2014 Jan;13:22-31 [24342190] Environ Health Perspect. 2015 Jan;123(1):49-56 [25302578] JAMA. 2013 Jun 12;309(22):2371-81 [23757085] Curr Opin Biotechnol. 2011 Feb;22(1):103-8 [20833526] Proc Natl Acad Sci U S A. 2011 Mar 1;108(9):3630-5 [21321201] NMR Biomed. 2013 Nov;26(11):1403-11 [23703831] DNA Res. 2013 Dec;20(6):537-47 [23804556] Eur J Biochem. 2000 Nov;267(21):6435-42 [11029587] J Acquir Immune Defic Syndr. 2003 Jun 1;33(2):175-83 [12794551] Nat Genet. 2003 Jul;34(3):267-73 [12808457] AIDS. 2004 Jan 23;18(2):137-51 [15075530] Mol Cell Endocrinol. 1998 Oct 25;145(1-2):81-8 [9922103] Mol Interv. 2005 Apr;5(2):94-111 [15821158] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517] DNA Repair (Amst). 2006 Feb 3;5(2):145-52 [15878696] Cancer Biol Ther. 2005 Dec;4(12):1367-73 [16294028] Mol Cell. 2006 Jul 21;23(2):207-17 [16857587] Mol Syst Biol. 2006;2:62 [17102807] Curr Top Dev Biol. 2007;77:87-111 [17222701] Am J Physiol Cell Physiol. 2007 Feb;292(2):C689-97 [16928776] Nucleic Acids Res. 2008 Mar;36(4):1369-79 [18187503] Genes Dev. 2008 Jun 15;22(12):1577-90 [18559474] Cancer Biol Ther. 2008 Aug;7(8):1182-90 [18458531] J Cell Physiol. 2009 Jan;218(1):58-65 [18767040] Am J Respir Crit Care Med. 2009 Apr 1;179(7):572-8 [19136372] Science. 2009 May 22;324(5930):1029-33 [19460998] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408418 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 - Cited By: Nitric Oxide. 2013 Apr 1;30:26-35 [23357401] Prostate. 2013 Jun;73(9):932-40 [23334979] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14753-8 [10611285] J Cell Physiol. 2000 Feb;182(2):150-62 [10623878] Anal Chem. 2000 Mar 15;72(6):1119-26 [10740848] J Mol Cell Cardiol. 2000 Apr;32(4):565-76 [10756114] Free Radic Biol Med. 2000 May 15;28(10):1463-9 [10927170] Endocr Relat Cancer. 2001 Mar;8(1):11-31 [11350724] Biochem J. 2001 Aug 1;357(Pt 3):593-615 [11463332] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10463-8 [11517312] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10845-50 [11526215] Mol Cancer Ther. 2005 Mar;4(3):399-412 [15767549] World J Gastroenterol. 2005 May 7;11(17):2539-44 [15849807] Ann N Y Acad Sci. 2005 May;1041:272-9 [15956717] World J Gastroenterol. 2005 Aug 14;11(30):4644-9 [16094703] J Biol Chem. 2002 Apr 5;277(14):12343-50 [11805088] Cell Death Differ. 2002 Oct;9(10):1160-2 [12232805] Early Hum Dev. 2002 Oct;69(1-2):57-64 [12324183] Semin Radiat Oncol. 2002 Oct;12(4):285-95 [12382187] Methods Enzymol. 2002;359:84-105 [12481562] Free Radic Biol Med. 2003 Jan 1;34(1):33-43 [12498977] Proc Natl Acad Sci U S A. 2003 Jan 7;100(1):143-8 [12518062] Mol Microbiol. 2003 Jan;47(2):463-9 [12519196] Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5537-42 [12704230] Circ Res. 2003 Jul 25;93(2):96-105 [12881475] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9196-201 [12865500] Ai Zheng. 2003 Sep;22(9):978-81 [12969533] Coron Artery Dis. 2003 Nov;14(7):477-90 [14561940] Oral Oncol. 2004 Mar;40(3):287-97 [14747060] Acta Neuropathol. 2004 Jul;108(1):43-8 [15088099] Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):8894-9 [15178764] Oncogene. 2004 Jun 24;23(29):4993-5003 [15048072] Carcinogenesis. 2004 Sep;25(9):1559-65 [15059928] Lab Invest. 2004 Sep;84(9):1112-25 [15208647] Mutat Res. 2004 Nov 2;555(1-2):107-19 [15476855] Anal Biochem. 1982 Oct;126(1):131-8 [7181105] Science. 1987 Jan 23;235(4787):473-6 [2432665] Proc Natl Acad Sci U S A. 1987 Sep;84(18):6369-73 [2819872] Biochem Biophys Res Commun. 1988 Nov 30;157(1):87-94 [3196352] J Exp Med. 1989 Mar 1;169(3):1011-20 [2784476] J Med Chem. 1991 Nov;34(11):3242-7 [1956043] J Pharmacol Exp Ther. 1992 Nov;263(2):546-51 [1331403] Clin Exp Immunol. 1993 Feb;91(2):277-81 [8428392] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3491-5 [7682706] J Surg Res. 1993 Oct;55(4):427-32 [7692140] Biochem Biophys Res Commun. 1993 Oct 29;196(2):707-13 [8240347] Cancer Res. 1994 Mar 1;54(5):1352-4 [7509718] Cardiovasc Res. 1994 Oct;28(10):1519-25 [8001040] Biochim Biophys Acta. 1994 Dec 30;1198(2-3):165-84 [7819273] J Exp Med. 1995 Apr 1;181(4):1333-43 [7535333] Proc Natl Acad Sci U S A. 1995 May 9;92(10):4392-6 [7538668] Br J Cancer. 1995 Jul;72(1):41-4 [7541238] Curr Top Microbiol Immunol. 1995;196:37-50 [7543398] Proc Natl Acad Sci U S A. 1996 Mar 19;93(6):2442-7 [8637893] Cancer Res. 1996 Feb 15;56(4):866-74 [8631026] Methods Enzymol. 1996;268:281-93 [8782594] Cancer Res. 1998 Jan 15;58(2):334-41 [9443414] Cancer Metastasis Rev. 1998 Mar;17(1):7-23 [9544420] Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8823-8 [9671763] Br J Cancer. 1998 Jul;78(2):233-9 [9683299] Naunyn Schmiedebergs Arch Pharmacol. 1998 Jul;358(1):113-22 [9721012] J Natl Cancer Inst. 1999 Jan 6;91(1):86-8 [9890175] Gynecol Oncol. 1999 May;73(2):257-64 [10329044] Curr Mol Med. 2004 Nov;4(7):741-51 [15579021] Biomed Res Int. 2014;2014:617868 [24804226] Mol Med Rep. 2014 Jul;10(1):341-6 [24756435] Annu Rev Physiol. 1999;61:391-415 [10099694] Hum Mol Genet. 2013 Mar 1;22(5):904-18 [23201752] Curr Top Med Chem. 2005;5(7):625-36 [16101424] Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13147-52 [16141331] J Med Chem. 2005 Dec 29;48(26):8220-8 [16366603] J Clin Oncol. 2006 Feb 1;24(4):688-94 [16446342] Antioxid Redox Signal. 2006 Jul-Aug;8(7-8):1329-37 [16910780] J Biol Chem. 2006 Sep 8;281(36):25984-93 [16829532] Arterioscler Thromb Vasc Biol. 2006 Dec;26(12):2666-72 [17023680] Clin Cancer Res. 2006 Nov 15;12(22):6748-57 [17121895] Trends Cell Biol. 2006 Dec;16(12):649-56 [17085050] Biochem Biophys Res Commun. 2013 Feb 22;431(4):647-51 [23337501] Clin Cancer Res. 2013 Mar 15;19(6):1340-6 [23271799] Cardiovasc Res. 2007 Feb 1;73(3):587-96 [17189622] Oncogene. 2007 May 14;26(22):3113-21 [17496910] Oncogene. 2007 May 14;26(22):3122-42 [17496911] Semin Oncol. 2007 Apr;34(2 Suppl 3):S10-6 [17512431] Org Lett. 2007 Aug 16;9(17):3409-12 [17658755] Br J Cancer. 2007 Oct 22;97(8):1099-105 [17895889] Int J Oncol. 2008 Feb;32(2):377-85 [18202760] Int J Cancer. 2008 Apr 15;122(8):1905-10 [18076071] Br J Pharmacol. 2008 May;154(1):13-24 [18362896] Free Radic Biol Med. 2008 Jul 1;45(1):18-31 [18439435] Nitric Oxide. 2008 Sep;19(2):199-204 [18486630] Proc Natl Acad Sci U S A. 2008 Jul 29;105(30):10513-8 [18663219] Hum Mutat. 2008 Aug;29(8):992-1006 [18470943] Free Radic Biol Med. 2008 Sep 1;45(5):578-84 [18503778] Int J Oncol. 2008 Nov;33(5):909-27 [18949354] Nitric Oxide. 2009 Feb;20(1):39-52 [18778787] Int J Hyperthermia. 2008 Dec;24(8):613-22 [18608577] Int J Cancer. 2009 Mar 1;124(5):1178-82 [19048628] Mol Carcinog. 2009 Feb;48(2):141-9 [18623111] Cell Stress Chaperones. 2009 May;14(3):301-10 [18987994] Urology. 2009 Oct;74(4):878-83 [19476985] Mol Cell Biochem. 2010 Jan;334(1-2):221-32 [20012469] Mol Cell. 2010 Jan 29;37(2):183-95 [20122401] Immunol Rev. 2010 Mar;234(1):90-104 [20193014] J Clin Invest. 2010 Nov;120(11):3843-54 [20978357] Oncol Rep. 2010 Dec;24(6):1455-61 [21042739] J Am Chem Soc. 2010 Nov 24;132(46):16526-32 [21033665] Clin Chem. 2011 Jan;57(1):18-32 [21059829] Nitric Oxide. 2011 Jan 1;24(1):1-7 [20933602] Cancer Biol Ther. 2010 Dec 15;10(12):1224-32 [21139417] Histochem Cell Biol. 2011 Apr;135(4):337-50 [21373891] Inorg Chem. 2011 Apr 18;50(8):3262-70 [21405089] J Leukoc Biol. 2011 Jun;89(6):873-91 [21233414] Clin Adv Hematol Oncol. 2011 May;9(5 Suppl 10):1-16 [21738118] Nitric Oxide. 2011 Aug 1;25(2):138-44 [21440655] Hum Pathol. 2011 Sep;42(9):1275-82 [21333324] Free Radic Biol Med. 2011 Nov 1;51(9):1765-73 [21875664] J Med Chem. 2011 Nov 24;54(22):7751-8 [22003962] ACS Chem Biol. 2011 Nov 18;6(11):1147-55 [21932836] Oral Dis. 2012 Jan;18(1):67-73 [21883708] Curr Med Chem. 2012;19(3):386-405 [22335514] BMC Cancer. 2012;12:120 [22452810] Biochem Biophys Res Commun. 1993 Jul 30;194(2):826-35 [7688228] Cancer Res. 2012 May 1;72(9):2394-404 [22436383] Immunol Invest. 2012;41(6-7):635-57 [23017139] Biofactors. 2012 Sep-Oct;38(5):320-8 [22628054] PLoS One. 2012;7(10):e47449 [23077620] Int J Cancer. 2013 Jan 1;132(1):9-18 [22618808] Cell Death Differ. 1999 Oct;6(10):969-75 [10556974] Semin Immunopathol. 2013 Mar;35(2):203-27 [22955327] Asia Pac J Clin Oncol. 2013 Mar;9(1):53-9 [22898264] J Natl Cancer Inst. 2013 Jun 19;105(12):849-59 [23704278] Tumour Biol. 2013 Aug;34(4):2175-81 [23625654] Curr Mol Med. 2013 Sep;13(8):1241-9 [23590833] Cancer Res. 2013 Sep 15;73(18):5821-33 [23832666] Breast Cancer Res Treat. 2013 Oct;141(3):353-63 [24062207] BMC Cancer. 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 - Comparative uterotrophic effects of endoxifen and tamoxifen in ovariectomized Sprague-Dawley rats. AN - 1628528403; 24670817 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 ≤ 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. © 2014 by The Author(s). 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. ; Charles River Laboratories Pathology Associates, Frederick, Maryland, USA Present address: Developmental Therapeutics Program, National Cancer Institute, Bethesda, MD, USA. ; Mayo Clinic, Rochester, Minnesota, USA. ; SRI International, Menlo Park, California, USA. ; Developmental Therapeutics Program, National Cancer Institute, Bethesda, Maryland, USA. Y1 - 2014/12// PY - 2014 DA - December 2014 SP - 1188 EP - 1196 VL - 42 IS - 8 KW - Tamoxifen KW - 094ZI81Y45 KW - 4-hydroxy-N-desmethyltamoxifen KW - 110025-28-0 KW - Index Medicus KW - tamoxifen KW - endoxifen KW - endometrial cell proliferation. KW - Rats KW - Cell Proliferation -- drug effects KW - Animals KW - Rats, Sprague-Dawley KW - Endometrium -- drug effects KW - Endometrium -- chemistry KW - Hypertrophy -- chemically induced KW - Histocytochemistry KW - Female KW - Organ Size -- drug effects KW - Tamoxifen -- toxicity KW - Uterus -- chemistry KW - Ovariectomy KW - Uterus -- drug effects KW - Tamoxifen -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1628528403?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=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=1533-1601&rft_id=info:doi/10.1177%2F0192623314525688 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-11 N1 - Date created - 2014-11-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2001 Aug;109(8):785-94 [11564613] Cancer Chemother Pharmacol. 2014 Dec;74(6):1271-8 [25318936] J Chromatogr B Analyt Technol Biomed Life Sci. 2003 Jul 5;791(1-2):245-53 [12798184] Environ Health Perspect. 2003 Sep;111(12):1527-9 [12948895] Environ Health Perspect. 2003 Sep;111(12):1530-49 [12948896] Environ Health Perspect. 2003 Sep;111(12):1550-8 [12948897] J Natl Cancer Inst. 2003 Dec 3;95(23):1758-64 [14652237] Breast Cancer Res Treat. 2004 May;85(2):151-9 [15111773] Reprod Biol Endocrinol. 2003 May 7;1:40 [12777179] Carcinogenesis. 1990 Dec;11(12):2245-51 [2265476] Drug Metab Dispos. 1991 Jan-Feb;19(1):36-43 [1673419] J Natl Cancer Inst. 1993 Nov 17;85(22):1850-5 [8230266] Carcinogenesis. 1994 Apr;15(4):589-93 [8149466] Eur J Clin Pharmacol. 1996;51(1):73-8 [8880055] Fundam Appl Toxicol. 1996 Oct;33(2):182-95 [8921337] Fundam Appl Toxicol. 1996 Dec;34(2):288-305 [8954758] Toxicol Sci. 1999 Apr;48(2):197-205 [10353311] J Natl Cancer Inst. 1999 Oct 6;91(19):1654-62 [10511593] J Natl Cancer Inst. 2005 Jan 5;97(1):30-9 [15632378] J Pharmacol Exp Ther. 2006 Aug;318(2):503-12 [16690721] Breast Cancer Res Treat. 2007 Jan;101(1):113-21 [17115111] Cancer Res. 2009 Mar 1;69(5):1722-7 [19244106] JAMA. 2009 Oct 7;302(13):1429-36 [19809024] BMJ. 2010;340:c693 [20142325] Breast Cancer Res Treat. 2010 Jul;122(2):579-84 [20052538] Clin Pharmacol Ther. 2010 Dec;88(6):814-7 [20981001] Breast Cancer Res. 2011;13(2):R27 [21392396] Cancer Treat Rev. 2012 Jun;38(4):318-28 [21775065] Clin Cancer Res. 2013 Jan 15;19(2):500-7 [23213055] PLoS One. 2013;8(1):e54613 [23382923] Breast Cancer Res Treat. 2013 Jun;139(2):553-60 [23686417] Anticancer Drugs. 2002 Oct;13(9):939-47 [12394257] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623314525688 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 - 1628528352; 24862797 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 F 1 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. © 2014 by The Author(s). JF - Toxicologic pathology AU - Foster, Paul M D 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 VL - 42 IS - 8 KW - Endocrine Disruptors KW - 0 KW - Index Medicus KW - female reproduction KW - male reproduction KW - reproductive system KW - safety assessment. KW - endocrine disrupters KW - developmental pathology KW - Endocrine Disruptors -- toxicity KW - Animals KW - Humans KW - Mice KW - Growth and Development -- drug effects KW - Reproduction -- drug effects KW - Toxicity Tests -- methods KW - Organisation for Economic Co-Operation and Development KW - Toxicity Tests -- standards UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1628528352?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=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+M+D&rft.aulast=Foster&rft.aufirst=Paul+M&rft.date=2014-12-01&rft.volume=42&rft.issue=8&rft.spage=1165&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623314534920 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-11 N1 - Date created - 2014-11-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Crit Rev Toxicol. 2006 Jan;36(1):69-98 [16708695] Toxicol Sci. 2010 Aug;116(2):640-6 [20484383] Environ Health Perspect. 2007 Sep;115(9):1351-6 [17805427] Toxicol Pathol. 2006;34(6):802-5 [17162538] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623314534920 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 - 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 - Inhibition of NANOG/NANOGP8 Downregulates MCL-1 in Colorectal Cancer Cells and Enhances the Therapeutic Efficacy of BH3 Mimetics AN - 1808625193; PQ0003452462 AB - Purpose: 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.Experimental Design: 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.Results: Clone A and CX-1 were sensitive to ABT-737 and ABT-199 at IC50s of 2 to 9 mu mol/L but LS174T was resistant with IC50s of 18 to 30 mu mol/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.Conclusions: 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. Clin Cancer Res; 20(21); 5446-55. copyright 2014 AACR. JF - Clinical Cancer Research AU - Mattoo, Abid R AU - Zhang, Jingyu AU - Espinoza, Luis A AU - Jessup, JMilburn AD - Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, jessupj@mail.nih.gov Y1 - 2014/11/01/ PY - 2014 DA - 2014 Nov 01 SP - 5446 EP - 5455 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 20 IS - 21 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Expression vectors KW - Cytotoxicity KW - Apoptosis KW - Gene therapy KW - Mcl-1 protein KW - Colorectal cancer KW - Colorectal carcinoma KW - Tumorigenicity KW - Bcl-2 protein KW - Xenografts KW - Cell proliferation KW - W 30905:Medical Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808625193?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=Inhibition+of+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+JMilburn&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&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-1134 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Expression vectors; Cytotoxicity; Apoptosis; Gene therapy; Mcl-1 protein; Colorectal cancer; Tumorigenicity; Colorectal carcinoma; Xenografts; Bcl-2 protein; Cell proliferation DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-1134 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 - 1660000349; llba-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 - Nov 2014 SP - 1189 EP - 1211 VL - 35 IS - 6 SN - 0142-7164, 0142-7164 KW - *Comprehension (13950) KW - *Dutch (20100) KW - *Bilingualism (08850) KW - *Children (11850) KW - *Language Acquisition (41600) KW - *Monolingualism (54850) KW - *French (25750) KW - *Vocabulary Size (94862) KW - article KW - 4026: psycholinguistics; bilingual language processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660000349?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&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 - ComDisDome N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-03-03 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 - 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 - A case-control study of occupational exposure to metalworking fluids and bladder cancer risk among men AN - 1808660494; PQ0003443722 AB - ObjectivesMetalworking 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.MethodsCases (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.ResultsBladder 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).ConclusionsExposure 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. 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 - Beane Freeman, Laura E 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 Y1 - 2014/10/20/ PY - 2014 DA - 2014 Oct 20 SP - 667 EP - 674 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 71 IS - 10 SN - 1351-0711, 1351-0711 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Risk assessment KW - Historical account KW - mineral oil KW - Data processing KW - Urinary bladder KW - Males KW - Employment KW - Carcinogens KW - Metal-working fluids KW - Cancer KW - Oil KW - Health risks KW - Smoking KW - Population control KW - USA, New England KW - Risk factors KW - Hybrids KW - Additives KW - Minerals KW - Occupational exposure KW - X 24380:Social Poisons & Drug Abuse KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808660494?accountid=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=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%3BBeane+Freeman%2C+Laura+E%3BMoore%2C+Lee+E%3BKoutros%2C+Stella%3BBaris%2C+Dalsu%3BSilverman%2C+Debra+T&rft.aulast=Colt&rft.aufirst=Joanne&rft.date=2014-10-20&rft.volume=71&rft.issue=10&rft.spage=667&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2013-102056 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Smoking; mineral oil; Data processing; Urinary bladder; Hybrids; Carcinogens; Occupational exposure; Cancer; Risk assessment; Historical account; Males; Employment; Metal-working fluids; Oil; Health risks; Population control; Risk factors; Minerals; Additives; USA, New England DO - http://dx.doi.org/10.1136/oemed-2013-102056 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 - 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 Acad Sci U S A. 2005 Nov 29;102(48):17342-7 [16293696] Biochemistry. 2006 Jan 17;45(2):498-512 [16401079] FEBS J. 2006 Feb;273(3):658-68 [16420488] J Biol Chem. 2006 Jan 27;281(4):2151-61 [16301322] Lancet. 2008 Jul 19;372(9634):216-23 [18640458] Neurobiol Aging. 2008 Sep;29(9):1334-47 [17403556] J Biol Chem. 2008 Oct 31;283(44):29615-9 [18650430] J Biol Chem. 2008 Oct 31;283(44):29639-43 [18723507] Biophys J. 2008 Nov 15;95(10):4631-42 [18708452] Proc Natl Acad Sci U S A. 2008 Nov 25;105(47):18349-54 [19015532] J Phys Chem B. 2009 Jan 29;113(4):1162-72 [19125574] J Mol Biol. 2009 Feb 27;386(3):869-77 [19038266] Biochemistry. 2008 Dec 2;47(48):12680-8 [18989933] Chem Phys Lipids. 2009 Mar;158(1):1-9 [19056366] Proc Natl Acad Sci U S A. 2009 Mar 24;106(12):4653-8 [19264960] Angew Chem Int Ed Engl. 2009;48(17):3030-59 [19330877] J Phys Chem B. 2009 Mar 12;113(10):2990-9 [19708161] J Am Chem Soc. 2009 Oct 21;131(41):14938-45 [19824733] J Phys Chem B. 2009 Oct 29;113(43):14480-6 [19807060] Biophys J. 2009 Dec 2;97(11):3029-37 [19948133] J Biol Chem. 2010 Feb 26;285(9):6071-9 [20018889] Biochemistry. 2010 Apr 13;49(14):3031-9 [20201586] Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6538-43 [20308552] Proc Natl Acad Sci U S A. 2010 May 25;107(21):9490-5 [20448202] Biophys J. 2010 Jun 2;98(11):2644-52 [20513409] Proc Natl Acad Sci U S A. 2012 Dec 11;109(50):20455-60 [23184970] J Phys Chem B. 2010 Jul 29;114(29):9445-51 [20608696] Adv Exp Med Biol. 2010;677:150-67 [20687488] Chem Rev. 2010 Aug 11;110(8):4820-38 [20402519] Proc Natl Acad Sci U S A. 2010 Aug 10;107(32):14128-33 [20660780] Angew Chem Int Ed Engl. 2010 Aug 2;49(33):5628-54 [20623810] Biochemistry. 2010 Oct 19;49(41):8967-77 [20731379] J Mol Biol. 2010 Dec 17;404(5):917-34 [20970427] Neurobiol Aging. 2011 Feb;32(2):235-48 [19324459] Biomacromolecules. 2014 Jan 13;15(1):122-31 [24313776] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14126-31 [12391326] Eur J Biochem. 2002 Nov;269(22):5642-8 [12423364] EMBO J. 2003 Feb 3;22(3):355-61 [12554637] J Clin Invest. 2003 Aug;112(3):415-22 [12897209] J Mol Biol. 2003 Sep 26;332(4):795-808 [12972252] J Biol Chem. 2003 Nov 14;278(46):46179-87 [12944403] Nature. 2003 Dec 18;426(6968):884-90 [14685248] Nature. 2003 Dec 18;426(6968):905-9 [14685252] Biochim Biophys Acta. 2010 Aug;1801(8):747-9 [20547302] Amyloid. 2001 Jun;8(2):94-100 [11409039] Nat Neurosci. 2001 Sep;4(9):887-93 [11528419] FASEB J. 2001 Nov;15(13):2433-44 [11689468] J Neurochem. 2001 Nov;79(3):595-605 [11701763] Nature. 2002 Apr 4;416(6880):535-9 [11932745] Amyloid. 2002 Mar;9(1):13-23 [12000193] Nature. 2002 Jul 18;418(6895):291 [12124613] Peptides. 2002 Jul;23(7):1311-5 [12128087] Biochim Biophys Acta. 2013 Feb;1828(2):327-39 [22975281] Biophys J. 2013 Jan 8;104(1):173-84 [23332070] Biochemistry. 2013 Feb 12;52(6):1089-100 [23331123] Curr Top Med Chem. 2012;12(22):2596-610 [23339310] Chem Commun (Camb). 2013 May 4;49(34):3582-4 [23527380] J Phys Chem B. 2013 Apr 18;117(15):3993-4002 [23537203] Phys Chem Chem Phys. 2013 Jun 21;15(23):8868-77 [23450150] Phys Chem Chem Phys. 2013 Jun 21;15(23):8908-15 [23493863] Phys Chem Chem Phys. 2013 Jun 21;15(23):8878-89 [23493873] J Mol Biol. 2013 Jun 26;425(12):2260-75 [23500806] Biophys J. 2013 Jun 18;104(12):2714-24 [23790380] J Mol Biol. 2013 Sep 23;425(18):3338-59 [23811057] PLoS Comput Biol. 2013;9(8):e1003211 [24009497] Biophys J. 2013 Sep 3;105(5):1227-35 [24010666] Biophys Chem. 2013 Dec 1;182:86-93 [23932412] Cell. 2013 Sep 12;154(6):1257-68 [24034249] J Comput Chem. 2013 Nov 5;34(29):2524-36 [24037720] Protein Sci. 2013 Oct;22(10):1320-35 [23904252] Sci Rep. 2013;3:2880 [24096987] J Am Chem Soc. 2013 Oct 9;135(40):15114-28 [23859103] Biophys J. 2013 Nov 5;105(9):2093-103 [24209854] Biophys J. 2013 Nov 19;105(10):2323-32 [24268144] Proc Natl Acad Sci U S A. 2013 Nov 26;110(48):19285-90 [24218609] Biochemistry. 2013 Jul 23;52(29):4971-80 [23855340] J Phys Chem B. 2013 Dec 5;117(48):14907-15 [24261958] Biochim Biophys Acta. 2014 Jan;1840(1):357-66 [24041993] J Neurochem. 2014 Jan;128(1):186-95 [23919567] J Phys Chem B. 2013 Dec 19;117(50):16066-75 [24245879] J Mol Biol. 2004 Jan 16;335(3):833-42 [14687578] J Am Chem Soc. 2004 Feb 25;126(7):1992-2005 [14971932] J Clin Invest. 2004 May;113(10):1456-64 [15146243] J Pept Sci. 2004 May;10(5):229-48 [15160835] Science. 1990 Jun 1;248(4959):1124-6 [2111584] Science. 1992 Apr 10;256(5054):184-5 [1566067] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):567-71 [8380642] Ann N Y Acad Sci. 1993 Sep 24;695:165-8 [8239277] Proc Natl Acad Sci U S A. 1993 Nov 15;90(22):10573-7 [7504270] Biophys J. 1993 Dec;65(6):2455-60 [7508762] J Biol Chem. 1994 Apr 15;269(15):10987-90 [8157623] Ann N Y Acad Sci. 1994 Dec 15;747:256-66 [7847675] Neuron. 1995 Feb;14(2):457-66 [7857653] Biochem J. 1995 Oct 1;311 ( Pt 1):1-16 [7575439] J Biol Chem. 1996 Jan 26;271(4):1988-92 [8567648] Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1710-5 [8643694] Am J Pathol. 1996 Aug;149(2):585-96 [8701997] J Biol Chem. 1996 Dec 27;271(52):33623-31 [8969231] J Biol Chem. 1997 Jan 3;272(1):44-7 [8995224] J Biol Chem. 1997 Aug 29;272(35):22364-72 [9268388] Adv Protein Chem. 1997;50:123-59 [9338080] J Biol Chem. 1998 May 29;273(22):13379-82 [9593665] J Mol Biol. 1999 Jan 15;285(2):755-73 [9878442] J Neurosci Res. 1999 Aug 15;57(4):458-66 [10440895] J Biol Chem. 2004 Nov 5;279(45):46363-6 [15385542] J Membr Biol. 2004 Nov;202(1):1-10 [15702375] Cell. 2005 Feb 25;120(4):545-55 [15734686] Protein Sci. 2005 Jun;14(6):1581-96 [15930005] J Phys Chem B. 2013 Oct 3;117(39):11518-29 [24000923] Proteins. 2014 Mar;82(3):399-404 [24038616] Chembiochem. 2006 Feb;7(2):257-67 [16444756] Curr Alzheimer Res. 2006 Feb;3(1):71-3 [16472206] Annu Rev Biochem. 2006;75:333-66 [16756495] Neuron. 2006 Oct 5;52(1):3-13 [17015223] Nature. 2006 Oct 19;443(7113):774-9 [17051203] Q Rev Biophys. 2006 May;39(2):167-201 [16978447] J Gen Physiol. 2006 Dec;128(6):637-47 [17101816] Chembiochem. 2007 Jan 22;8(2):163-5 [17195250] Nat Rev Mol Cell Biol. 2007 Feb;8(2):101-12 [17245412] J Neurosci. 2007 Jan 24;27(4):796-807 [17251419] J Biol Chem. 2007 Apr 13;282(15):11590-601 [17308309] Biochim Biophys Acta. 2007 Aug;1768(8):1966-75 [17553456] Biophys J. 2007 Sep 15;93(6):1938-49 [17526580] Biochim Biophys Acta. 2007 Sep;1768(9):2026-9 [17662957] Biochemistry. 2007 Nov 27;46(47):13523-32 [17973493] J Phys Chem B. 2008 Jan 10;112(1):100-9 [18072760] J Am Chem Soc. 2008 Jan 30;130(4):1376-83 [18179213] Trends Biochem Sci. 2008 Feb;33(2):91-100 [18182298] Ann Neurol. 2008 Mar;63(3):377-87 [18300294] J Am Chem Soc. 2008 May 14;130(19):6145-58 [18412346] Proteins. 2008 Jul;72(1):1-24 [18186465] J Mol Biol. 2008 Aug 1;381(1):221-8 [18597778] Chem Soc Rev. 2012 Jan 21;41(2):608-21 [21818468] Biochemistry. 2012 Jan 10;51(1):108-17 [22129303] Acc Chem Res. 2012 Jan 17;45(1):83-92 [21761818] Biochemistry. 2012 Jan 24;51(3):776-85 [22242635] J Phys Chem B. 2012 Feb 9;116(5):1728-35 [22217000] Biophys J. 2012 Feb 8;102(3):587-96 [22325282] Biophys J. 2012 Jan 18;102(2):315-24 [22339868] Cell. 2012 Mar 16;148(6):1188-203 [22424229] J Phys Chem B. 2012 Apr 5;116(13):4043-55 [22409719] Prog Mol Biol Transl Sci. 2012;107:295-325 [22482454] Biochemistry. 2012 Apr 10;51(14):3031-8 [22413858] PLoS One. 2012;7(4):e34345 [22509291] J Am Chem Soc. 2012 Jun 20;134(24):10271-8 [22656332] J Chem Phys. 2012 Jun 28;136(24):245105 [22755606] J Biol Chem. 2012 Jul 13;287(29):24765-73 [22547072] J Mol Biol. 2012 Aug 10;421(2-3):172-84 [22119878] Biophys J. 2012 Aug 22;103(4):702-10 [22947931] Prion. 2012 Sep-Oct;6(4):339-45 [22874669] Biochim Biophys Acta. 2012 Dec;1818(12):3121-30 [22935354] Biochemistry. 2012 Oct 2;51(39):7676-84 [22970795] Biophys J. 2012 Oct 3;103(7):1411-3 [23062332] J Am Chem Soc. 2011 Mar 2;133(8):2742-8 [21299220] Nat Chem. 2009 Jul;1(4):326-31 [20703363] J Am Chem Soc. 2011 Mar 16;133(10):3390-400 [21341665] J Biol Chem. 2011 Apr 1;286(13):11555-62 [21292768] Nat Rev Neurosci. 2011 May;12(5):284-96 [21448224] Biochem Biophys Res Commun. 2011 Jul 29;411(2):312-6 [21726530] Nat Struct Mol Biol. 2007 Dec;14(12):1157-64 [18059284] FEBS J. 2011 Oct;278(20):3905-17 [21722314] J Am Chem Soc. 2011 Oct 12;133(40):16013-22 [21882806] J Cell Biol. 2011 Oct 31;195(3):515-24 [22024165] J Biol Chem. 2011 Nov 11;286(45):38825-32 [21965666] J Chem Phys. 2011 Nov 28;135(20):205101 [22128957] Stroke. 2000 Feb;31(2):534-8 [10657433] J Neurosci Res. 2000 May 15;60(4):490-4 [10797551] FASEB J. 2000 Jun;14(9):1233-43 [10834945] J Struct Biol. 2000 Jun;130(2-3):88-98 [10940217] J Biol Chem. 2000 Sep 1;275(35):27110-6 [10821838] Trends Neurosci. 2001 Apr;24(4):219-24 [11250006] Ann Neurol. 2001 Jun;49(6):697-705 [11409420] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1039/c3cs60459d ER - TY - JOUR T1 - Michael acceptor approach to the design of new salvinorin A-based high affinity ligands for the kappa-opioid receptor. 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 Exp Pharmacol Physiol. 2004 Dec;31(12):862-7 [15659050] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009] J Biol Chem. 1999 Oct 29;274(44):31648-54 [10531373] Biochem Pharmacol. 1999 Nov 15;58(10):1625-9 [10535754] Cancer. 2000 Jan 15;88(2):318-23 [10640963] Eur J Cancer. 2000 Jan;36(2):249-56 [10741285] J Pharmacol Exp Ther. 2000 May;293(2):677-85 [10773044] Cancer Chemother Pharmacol. 1980;4(4):249-58 [7438327] Cancer. 1981 Feb 15;47(4):645-8 [7194729] J Cell Biol. 1981 Nov;91(2 Pt 1):479-87 [6118377] Cancer Treat Rep. 1982 Dec;66(12):2013-20 [6890409] Cancer. 1983 Dec 1;52(11):2007-10 [6684986] Cancer Treat Rep. 1985 Mar;69(3):319-21 [3884153] Cancer Treat Rev. 1985 Sep;12 Suppl A:125-36 [3002623] Obstet Gynecol. 1986 Feb;67(2):265-8 [2418394] Cancer. 1987 Dec 15;60(12):2869-72 [2824016] Ann Intern Med. 1989 Aug 15;111(4):273-9 [2569287] J Biol Chem. 1990 Mar 5;265(7):3623-7 [2303468] Cancer. 1990 Jun 1;65(11):2478-81 [1970948] J Clin Oncol. 1990 Jun;8(6):1056-62 [2112183] Invest New Drugs. 1991 Feb;9(1):59-64 [1673965] Cancer. 1991 Jun 15;67(12):2984-7 [2044044] J Urol. 1991 Nov;146(5):1284-7 [1719241] J Natl Cancer Inst. 1991 Dec 18;83(24):1797-805 [1683908] J Cell Physiol. 2002 Jul;192(1):1-15 [12115731] Mol Pharmacol. 2002 Nov;62(5):1154-9 [12391279] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14298-302 [12370430] J Biol Chem. 2002 Nov 8;277(45):43377-88 [12218054] Science. 2002 Dec 6;298(5600):1911-2 [12471242] Biochem J. 2003 Mar 1;370(Pt 2):361-71 [12495431] J Biol Chem. 2003 Mar 14;278(11):9100-6 [12509415] Br J Cancer. 2003 Apr 22;88(8):1199-206 [12698184] Mol Cancer Ther. 2003 May;2(5):471-8 [12748309] Expert Opin Pharmacother. 2003 Jun;4(6):889-901 [12783586] Nat Rev Cancer. 2003 Jul;3(7):502-16 [12835670] Semin Nephrol. 2003 Sep;23(5):460-4 [13680535] Cancer Res. 1997 Sep 1;57(17):3759-64 [9288784] FEBS Lett. 1997 Sep 15;414(3):552-6 [9323034] Cell. 1997 Nov 14;91(4):443-6 [9390553] Nephrol Dial Transplant. 1997 Dec;12(12):2478-80 [9430835] Int J Cancer. 1998 Oct 23;79(5):468-75 [9761114] Oncogene. 1998 Dec 24;17(25):3237-45 [9916986] Ann Oncol. 1998 Dec;9(12):1347-9 [9932167] Cancer. 1999 Jan 15;85(2):295-301 [10023695] Br J Cancer. 1999 Mar;79(7-8):1104-10 [10098743] Biochem Biophys Res Commun. 1999 Apr 13;257(2):361-8 [10198218] Clin Cancer Res. 1999 May;5(5):1007-14 [10353733] Lancet Oncol. 2008 Mar;9(3):215-21 [18282805] Pharmacol Res. 2008 Feb;57(2):125-31 [18282716] JAMA. 2008 Apr 23;299(16):1914-21 [18430910] J Clin Oncol. 2008 Jul 20;26(21):3552-9 [18506026] J Thorac Oncol. 2008 Aug;3(8):819-31 [18670299] J Clin Oncol. 2009 Mar 20;27(9):1401-4 [19204194] Mol Oncol. 2009 Apr;3(2):97-137 [19383374] Lancet Oncol. 2009 May;10(5):459-66 [19269895] Food Chem Toxicol. 2009 Jun;47(6):1176-1183 [19425235] Proc Natl Acad Sci U S A. 2009 Sep 22;106(38):16281-6 [19805294] Curr Med Chem. 2009;16(32):4314-27 [19754416] J Clin Oncol. 2009 Dec 20;27(36):6243-50 [19826112] Exp Toxicol Pathol. 2010 Jan;62(1):45-52 [19268559] Neoplasia. 2010 Feb;12(2):128-38 [20126471] Crit Rev Toxicol. 2010 Apr;40(4):347-59 [20163198] N Engl J Med. 2010 Apr 8;362(14):1273-81 [20375404] Am J Respir Cell Mol Biol. 2013 Aug;49(2):241-50 [23526220] Mol Cell Biol. 2000 Jul;20(14):4979-89 [10866655] Invest New Drugs. 2000 Aug;18(3):281-9 [10958599] Cancer Res. 2000 Nov 1;60(21):5988-94 [11085518] J Biol Chem. 2000 Dec 15;275(50):39435-43 [10993883] J Clin Oncol. 2001 Jan 1;19(1):119-26 [11134204] Nature. 2001 Mar 1;410(6824):37-40 [11242034] Neoplasma. 2001;48(2):99-103 [11478701] Anticancer Res. 2001 May-Jun;21(3B):1925-9 [11497279] J Am Chem Soc. 2001 Sep 26;123(38):9378-87 [11562220] Trends Biochem Sci. 2001 Nov;26(11):657-64 [11701324] Cancer Chemother Pharmacol. 2001 Nov;48(5):383-8 [11761456] Cancer Res. 2002 Feb 1;62(3):924-31 [11830553] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585] Crit Rev Oncol Hematol. 2002 Apr;42(1):1-3 [11923064] Biochem Pharmacol. 2002 Apr 15;63(8):1423-30 [11996883] J Am Chem Soc. 2002 May 22;124(20):5834-42 [12010058] Crit Rev Oncol Hematol. 2002 Jun;42(3):317-25 [12050023] Curr Pharm Des. 2010 Jun;16(16):1813-25 [20337575] Cell Cycle. 2010 Oct 1;9(19):4005-12 [20935493] Cell. 1995 Jan 27;80(2):179-85 [7834738] Anticancer Res. 2011 Nov;31(11):3789-97 [22110201] Proc Natl Acad Sci U S A. 2011 Feb 1;108(5):1850-5 [21233423] Mol Cancer Ther. 2011 Jul;10(7):1161-72 [21566064] Antioxid Redox Signal. 2012 Jun 1;16(11):1295-322 [22117137] Pharmacol Rev. 2012 Jul;64(3):706-21 [22659329] Biochem Biophys Res Commun. 2012 Jul 13;423(4):819-25 [22713472] Anticancer Res. 2013 Feb;33(2):433-44 [23393334] Br J Cancer. 2013 Feb 19;108(3):579-86 [23370212] Mol Cancer Res. 2013 Feb;11(2):140-8 [23239809] Oncol Rep. 2013 Apr;29(4):1540-6 [23338680] Nihon Hinyokika Gakkai Zasshi. 2013 Jan;104(1):33-7 [23457933] Biomed Pharmacother. 2013 Mar;67(2):116-21 [23433853] Biochem Pharmacol. 2013 Apr 15;85(8):1077-90 [23396090] Oncol Rep. 2013 Jun;29(6):2332-40 [23525453] Arch Pharm Res. 2013 May;36(5):619-25 [23494564] Oncogene. 2003 Oct 20;22(47):7265-79 [14576837] Annu Rev Pharmacol Toxicol. 2004;44:27-42 [14744237] Toxicology. 2004 Feb 15;195(2-3):221-30 [14751677] Cancer Treat Rev. 2004 Feb;30(1):53-81 [14766126] Cell Death Differ. 2004 Mar;11(3):290-300 [14657961] Oncogene. 2004 Apr 12;23(16):2774-84 [15077141] J Am Chem Soc. 2004 May 19;126(19):5999-6004 [15137764] Pharmacol Res. 2004 Sep;50(3):287-90 [15225672] Mol Pharmacol. 2004 Oct;66(4):789-93 [15385639] J Bacteriol. 1973 Dec;116(3):1247-52 [4584807] Mutat Res. 1978 Jul;51(1):121-32 [672924] Gan. 1979 Apr;70(2):209-14 [381088] J Clin Oncol. 1992 Jul;10(7):1165-70 [1376773] J Clin Oncol. 1992 Nov;10(11):1748-53 [1357110] Science. 1992 Oct 23;258(5082):607-14 [1411571] J Urol. 1992 Nov;148(5):1625-6 [1433578] J Natl Cancer Inst. 1993 Mar 3;85(5):384-8 [8094466] J Cell Biochem. 1993 Feb;51(2):151-6 [8440749] J Histochem Cytochem. 1993 Jul;41(7):1053-73 [8515048] Int J Cancer. 1993 Sep 30;55(3):521-7 [8375936] Drugs. 1993 Sep;46(3):360-77 [7693428] Pharmacol Ther. 1993 Sep;59(3):257-80 [8309991] J Clin Oncol. 1994 Feb;12(2):360-7 [8113844] Semin Oncol. 1994 Oct;21(5 Suppl 8):49-52 [7939763] Drug Metab Dispos. 1995 Feb;23(2):178-84 [7736908] EMBO J. 1995 Nov 15;14(22):5579-88 [8521815] N Engl J Med. 1996 Jan 4;334(1):1-6 [7494563] Exp Cell Res. 1996 Jul 10;226(1):133-9 [8660948] J Clin Oncol. 1997 Jan;15(1):297-303 [8996156] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078] Nat Rev Drug Discov. 2005 Apr;4(4):307-20 [15789122] Toxicol Ind Health. 2005 May;21(3-4):67-73 [15986578] J Clin Oncol. 2005 Jul 20;23(21):4602-8 [16034041] Biochem Biophys Res Commun. 2005 Sep 9;334(4):1068-73 [16039614] Endocr Rev. 2005 Aug;26(5):662-87 [15798098] Ann Clin Lab Sci. 2005 Summer;35(3):329-35 [16081592] Chest. 2005 Oct;128(4):2268-73 [16236883] J Appl Toxicol. 2006 Jan-Feb;26(1):42-6 [16158393] Nucleic Acids Res. 2006;34(2):543-54 [16434701] Pharmacol Res. 2006 Mar;53(3):278-86 [16436331] Endocrinology. 2006 Apr;147(4):1761-9 [16396982] Mol Pharmacol. 2006 Apr;69(4):1383-8 [16394183] Stem Cells. 2006 Mar;24(3):514-5 [16582013] Int J Mol Med. 2006 Sep;18(3):511-6 [16865238] Mol Pharmacol. 2006 Oct;70(4):1390-4 [16847145] J Biochem Mol Biol. 2006 Nov 30;39(6):656-61 [17129399] Oncogene. 2006 Nov 30;25(56):7381-90 [16785992] Toxicology. 2007 Feb 12;230(2-3):256-64 [17196726] Basic Clin Pharmacol Toxicol. 2007 Mar;100(3):145-50 [17309516] EMBO J. 2007 Apr 18;26(8):2115-26 [17380123] Cell Signal. 2007 Aug;19(8):1633-42 [17537614] Biochem J. 2007 Aug 1;405(3):617-23 [17521288] Nat Rev Cancer. 2007 Aug;7(8):573-84 [17625587] J Pharm Sci. 2007 Sep;96(9):2181-96 [17593552] Am J Med Sci. 2007 Aug;334(2):115-24 [17700201] Chem Biol Interact. 2007 Dec 15;170(3):177-86 [17850778] Cancer Lett. 2008 Feb 18;260(1-2):96-108 [18036733] Mol Cell. 2008 Feb 15;29(3):350-61 [18280240] Oncol Res. 2007;16(11):497-506 [18306929] Eur J Pharmacol. 2014 Jan 15;723:156-66 [24333218] Asian Pac J 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 - The Role of Acculturation and Collectivism in Cancer Screening for Vietnamese American Women AN - 1660021242; 201507973 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. Adapted from the source document. JF - Health Care for Women International AU - Nguyen, Anh B AU - Clark, Trenette T AD - Division of Cancer Control and Population Sciences, The National Cancer Institute, Rockville, Maryland, USA Y1 - 2014/10/03/ PY - 2014 DA - 2014 Oct 03 SP - 1162 EP - 1180 PB - Taylor & Francis, Philadelphia PA VL - 35 IS - 10 SN - 0739-9332, 0739-9332 KW - Attitudes KW - Acculturation KW - Collectivism KW - Tests KW - Breast Cancer KW - Asian Americans KW - Empowerment KW - Females KW - Sociodemographic Factors KW - article KW - 2045: sociology of health and medicine; sociology of medicine & health care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660021242?accountid=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=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=2014-10-03&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 - Sociological Abstracts N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-09-28 N1 - CODEN - HCWIDQ N1 - SubjectsTermNotLitGenreText - Tests; Females; Acculturation; Collectivism; Attitudes; Breast Cancer; Empowerment; Sociodemographic Factors; Asian Americans DO - http://dx.doi.org/10.1080/07399332.2013.863317 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 -